SlideShare a Scribd company logo
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
METABOLISM OF CARBOHYDRATES
GLYCOLYSIS / EMBDEN-MEYERHOF PATHWAY
 Glycolysis ("splitting sugars") oxidation of glucose to pyruvate or lactate is called
glycolysis.
 It occurs in all tissues. Erythrocytes & nervous tissues derive its energy mainly from
glycolysis.
Reactions of glycolysis:
 In glycolysis, glucose (a six carbon sugar) is split into two molecules of three-carbon
sugar (pyruvate) mainly occurs in ten steps.
 In the preparatory phase first glucose is converted into glucose -6-p by the enzyme
glucokinase or hexokinase.
 Glucose-6-phosphate is converted to fructose 6-P by isomerase enzyme, then it forms
fructose-1, 6-bis phosphate by phosphofructokinase.
 The enzyme aldolase split Fructose 1, 6-bisphosphate to dihydroxy acetone phosphate
(DHAP) & glyceraldehyde -3-p, both triose phosphates are inter convertible sugars.
 DHAP is converted to glyceraldehyde -3-p then is converted to 1,3 bisphosphoglycerate
by glyceraldehyde -3-p dehydrogenase, which is NAD+ dependent, then converted to 3-
phosphoglycerate by the enzyme phoshoglycerate kinase. High energy phosphate is
formed.
 Then 3-phosphoglycerate is converted to 2- phosphoglycerate, then phosphoenolpyruvate.
Further phosphoenolpyruvate is converted to pyruvate; this reaction is catalyzed by
pyruvate kinase.
 The high energy phosphate of Phosphoenolpyruvate is directly transferred to ADP
producing ATP, and then it is converted to pyruvate.

Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Glucose (6C)
Glucose -6-Phosphate (6C)
Fructose -6-Phoshate (6C)
Fructose -1,6-BisPhoshate (6C)
Dihydroxyacetone
Phosphate (3C)
1,3 Bisphosphoglycerate (2 molecules)
ATP
ADP
Hexokinase /
Glucokinase
Isomerase
ATP
ADP
Phospho fructokinase
Aldolase
Glyceraldehyde 3-Phosphate
(3C)
Triose Phosphate
isomerase
Gly-3-P Dehydrogenase
Phoshoglycerate Kinase
Mutase
Enolase
3-Phosphoglycerate (2 molecules)
2- Phoshoglycerate (2 molecules)
Phosphoenolpyruvate (2 molecules)
Pyruvate (3C)
(2 molecules)
Pyruvate Kinase
NAD+ + Pi
ADP
ATP
ADP
ATP Lactate
(Anaerobic phase)
Acetyl CoA
(Aerobic phase)
Reactions of Glycolysis
NADH + H+
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Anaerobic phase:
In absence of oxygen, reoxidation of NADH by conversion of pyruvate to lactate (with out
production of ATP)
Energy yield per glucose molecule oxidation:
Hexokinase or glucokinase (1ATP→1ADP) -1 ATP
Phosphofructokinase (1ATP→1ADP) -1 ATP
Glyceraldehyde 3-P dehydrogenase (2 NADH) [1 NADH= 2.5ATPs] + 5 ATP
Phosphogycerokinase (2ADP + Pi → 2ATP) +2ATPs
Pyruvate kinase (2ADP + Pi → 2ATP) + 2 ATPs
Net gain 09 – 2 = 7 ATPs
Significance of glycolysis:
 This pathway for the production of energy.
 It’s importance in skeletal muscle as glycolysis provides ATP even in absence of O2.
 It generates precursors for biosynthetic pathways like
o Pyruvate gives alanine (amino acids), acetyl- CoA for fatty acid
biosynthesis.
o Glycerol -3-Phosphate forms the backbone of triacylglycerol
Regulation of glycolysis:
 Hormonal- Insulin and glucocorticoids stimulates, glucagon, epinephrine inhibits
glycolysis process.
 Allosteric regulation- AMPs stimulates & citrate, ATPs inhibits phosphofructokinase on
glycolysis process.
Inhibitors Enzymes of glycolysis
Bromo hydroxy acetone Phospho triose Isomerase
Arsenate Glyceraldehyde 3-P dehydrogenase
Fluoride Enolase
Oxamate Lactate dehydrogenase
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Metabolic fate of pyruvate:
Formation of Acetyl CoA:
 Pyruvate is end product of aerobic glycolysis. It occurs in cytoplasm, further pyruvate is
transported into mitochondria by a pyruvate transporter.
 Under aerobic conditions, pyruvate is converted to acetyl CoA, which enters the TCA
cycle to be oxidized to CO2 & energy.
Pyruvate dehydrogenase (PDH) complex:
 The PDH complex is comprises of multiple copies of 3 separate enzymes & coenzymes.
1) Pyruvate dehydrogenase (PDH)
2) Dihydrolipoamide S-acetyltransferase (DLAT)
3) Dihydrolipoamide dehydrogenase (DLD).
 The complex also requires 5 different coenzymes: CoA, NAD+
, FAD+
, thiamine
pyrophosphate (TPP) and lipoic acid
Fate of Acetyl CoA:
PYRUVATE
Glucogenic amino
acid (Gly, Ser, Cys,
Thr)
Alanine (Deamination)
Glucose (Gluconeogenesis)
Acetyl -CoA
Glucose (Glycolysis)
Lactate (anaerobic)
Alanine (Transamination)
TCA cycle
CO2& ATP
Oxaloacetate (decarboxylation)
Acetyl CoA
Synthesis of Cholesterol
Detoxification (acetylation
reactions)
Synthesis of
Melatonin
Formation of
Acetyl choline
Formation of ketone
bodies
Oxidation of TCA cycle
Denovo synthesis of Fatty
acids
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
CITRIC ACID CYCLE / KREBS CYCLE/ TCA CYCLE
The citric acid cycle is the central metabolic hub of the cell. It is the gateway to the aerobic
metabolism of any molecule that can be transformed into an acetyl group or dicarboxylic
acid.
 The aerobic processing of glucose starts with the complete oxidation to CO2.
 This oxidation takes place in the citric acid cycle, a series of reactions known as the
“tricarboxylic acid (TCA) cycle” or the “Krebs cycle”.
 The citric acid cycle is the final common pathway for the oxidation of fuel molecules –
amino acids, carbohydrates & fatty acids that enter the cycle as acetyl CoA. The enzymes
of citric acid cycle are located in the mitochondrial matrix.
Reactions of the TCA Cycle
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 Condensation of Acetyl-CoA with oxaloacetate to form citrate by citrate synthase.
 Citrate is isomerized to isocitrate by the enzyme aconitase. The reaction occurs in
two steps, dehydration to cis-aconitate & rehydration to isocitrate.
 Isocitrate is dehydration to oxalosuccinate initially, then decarboxylation to give α-
ketoglutarate by isocitrate dehydrogenase
 Alpha-ketoglutarate (α-KG) is oxidative decarboxylated to Succinyl -CoA by the α-
ketoglutarate dehydrogenase& it generates NADH [equal to 2.5ATPs].
 The Succinyl-CoA is converted to succinate by Succinyl-CoA thiokinase. This
reaction produces GTP [equal to 1ATP].
 Succinate dehydrogenase catalyzes the oxidation of succinate to form fumarate and
it generates FADH2 [equal to 1.5 ATPs].
 The fumarase catalyzed by the addition of water to fumarate to gives malate.
 The final enzyme, forwards the reaction of the TCA cycle, the oxidation of malate to
oxaloacetate (OAA) by malate dehydrogenase, and this reaction produces NADH
[equal to 2.5ATPs].
Finally oxaloacetate is regenerated, thus two carbon atoms form acetyl-coA enter the
cycle.
Energetics of TCA cycle:
Isocitrate dehydrogenase (NADH+H+
) +2.5 ATP
α-Ketoglutarate Dehydrogenase (NADH+H+
) + 2.5ATP
Succinyl Thiokinase [GTP = 1ATP)] + 1 ATPs
Succinate Dehydrogenase [FADH2 = 1.5 ATP)] + 1.5 ATPs
Malate Dehydrogenase (NADH+H+
) +2.5 ATP
one molecule of acetyl CoA produced no. of ATPs in TCA cycle 10 ATPs
Regulation:
 Alpha ketoglutarate dehydrogenase is inhibited by NADH, Succinyl-CoA and Arsenate.
 Aconitase enzyme is inhibited by fluoroacetate
 The key enzymes of the TCA cycle are also regulated allosterically by Ca2+
, ATP and
ADP.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Energetics on complete oxidation of glucose:
Pathways Total ATPs
A. Glycolysis 7 ATPs
B. Oxidative decarboxylation of 2 pyruvate to 2 Acetyl CoA [2 x NADH] 5 ATPs
C. TCA cycle (2 molecules of acetyl CoA involved 2x10) 20ATPs
one molecule of glucose produced total ATPs 32 ATPs
Significance of the TCA Cycle:
 Final common oxidative pathway and integration of major metabolic pathways
 Carbon skeleton of amino acids finally enter the TCA cycle
 The TCA cycle is an important source of precursors for the building blocks of many
molecules such as amino acids, Nucleotide bases (Purines & Pyrimidines), Cholesterol,
and Porphyrin (the organic component of heme).
Anabolic and Catabolic nature of TCA cycle
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Amphibolic nature of TCA cycle:
Amphibolic nature of the TCA cycle is both catabolic and anabolic in nature
o Oxaloacetate is precursor for aspartate
o Alpha ketoglutarate can be transaminated to glutamate
o Succinyl CoA is used for synthesis of heme
o Citrate (mitochondrial) is transported to cytoplasm and provides substrate for fatty
acid synthesis
Anapleurotic reaction:
The reactions concerned to replenish or fill up the intermediates of citric acid cycle are
called anapleurotic reactions
o Pyruvate carboxylase catalyses conversion of pyruvate to oxaloacetate
o Pyruvate is converted to malate by NADP+
dependent Malate dehydrogenase
(Malic enzyme)
o Alpha ketoglutarate is also synthesized from glutamate by glutamate
dehydrogenase
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
GLYCOGEN METABOLISM
Glycogen is the principal storage form of glucose in human body and it is found mainly in
cytoplasm of liver and muscle.
Stores of glycogen in the liver are considered the main buffer of blood glucose levels.
Glycogen metabolism mainly consists of two pathways
1) Anabolic part is glycogenesis
2) Catabolic part is glycogenolysis
GLYCOGENESIS (GLYCOGEN SYNTHESIS)
Definition:
The formation of glycogen from glucose is known as Glycogenesis.
Reactions:
 Glucose by the enzyme
glucokinase or hexokinase to
form glucose -6- phosphate
then it is converted to
glucose-1-P catalysed by
phosphoglucomutase
enzyme.
 UDP glucose is formed from
glucose -1 phosphate & UTP
by Glucose-1- phosphate
uridyl transferase. UDP
glucose acts as a donor of
glucose.
 Activated glucose units are
sequentially added by the
enzyme glycogen synthase. The glucose moiety from UDP-glucose is transfused to a
glycogen primer molecule. Glucose units is added to the non reducing end of the
glycogen primer to form an α-1,4-glycosidic linkage and then UDP is liberated
 The glycogen synthase can add glucose units only in α-1, 4 linkage.
 A branching enzyme is needed to created the α-1, 6 glycosidic linkage.
Glucose (6C)
Glucose -6-Phosphate (6C)
Glucose -1-Phospate
UDP-Glucose
Glycogen
ATP
ADP
Hexokinase /
Glucokinase
Phosphoglucomutase
UTP
PPi
Glu-1-P-Uridyl transferase
1,4-Glycosyl Units
Glycogen synthase
Branching Enzyme
Glycogen Primer
Reactions of Glycogenesis
Glycogenin
UDP
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 To these newly created branches, further glucose units can be make the molecule more
globular and less space consuming, finally it forms glycogen.
Regulation of Glycogen Synthesis
 Glycogenesis regulated through glycogen synthase enzyme, it is stimulated by high
conc. of glucose & insulin, leads to increased synthesis of glycogen.
 Glycogen synthase is inhibited by low conc. of glucose, glucagon and epinephrine, leads
to decreased synthesis of glycogen.
II. GLYCOGENOLYSIS:
Definition: Formation of glucose from storage glycogen is known as glycogenolysis.
Reactions:
 Glycogen Phosphorylase is involved in
the conversion of glycogen to glucose-1-
phosphate by phosphorolytic cleavage.
This enzyme removes glucose units one at
a time from the non reducing end of the
glycogen molecules.
 Phosphorylase sequentially attack α-(1,4)-
linkages, till it reaches a glucose residue 3
to 4 glucose units away from a branch point
but it doesn’t attack the α-1,6 linkage at
branch point, the final product is a highly
branched molecule – limit dextrin.
 Then a few glucose residues are transferred
from the branching point to another branch
by enzyme is α-(1, 4) → α-(1, 4) glucose
transferase. The branch point is free.
 Debranching enzyme α-(1, 6 glucosidase) can hydrolyze the remaining glucosyl unit
held in α-(1, 6) linkage at the branch point, it gives free glucose molecules.
 Transferase & de branching enzyme will together convert the branch point to a linear one
with the removal of branches.
 Phosphoglucomutase enzyme converts Glucose-1-phosphate to glucose-6-phosphate.
Debranching Enzyme
Phosphoglucomutase
Limit Dextrin
Glucose-1-Phosphate
Glucose-6-Phosphate
Glucose
Glucose-6-Phasphatase
Pi
H2O
Pi
Glycogen
Glycogen Phosphorylase
Glucose
Reactions of Glycogenolysis
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 Glucose-6-phasphatase hydrolyses glucose -6-P to glucose. Glucose is released to the
blood stream for maintaining blood glucose levels. Glucose-6-Phasphatase enzyme is
present in liver only.
 The conversion of glucose-6-phosphate to glucose does not occur in skeletal muscle
because of absence of this enzyme.
Regulation of Glycogenolysis
 Glycogenolysis regulated by phosphorylase enzyme, it is stimulated by glucagon
&adrenaline, leads to increased synthesis of glucose from glycogen.
 Phosphorylase is inhibited by high conc. of glucose, insulin, leads to inactivates
glycogenolysis.
Glycogen Storage Diseases
 It is a genetic disorder in which abnormal quantities of glycogen are deposited in the
liver, kidney, heart and muscle.
Name Enzyme Defect Affected Organ Manifestations
TYPE-I : Von
Gierke‘s Diseases
Glucose-6-
phosphatase
Liver, Kidney and
Intestine.
Hepatomegaly, renal disease,
growth retardation & delayed
puberty
TYPE-II: Pompe’s
Diseases
Lysosomal Acid
maltase
Skeletal &
Cardiac muscle
Myopathy, muscular
dystrophy
TYPE-III: Cori ‘s
Diseases
Debranching
enzyme
Liver, skeletal &
cardiac muscle
Infant hepatomegaly,
myopathy
TYPE-IV: Andersen
Diseases
Branching enzyme Liver, muscle Hepatosplenomegaly,
cirrhosis
TYPE-V: McArdle
Diseases
Muscle
phosphorylase
Skeletal muscle Induced cramps and pain,
Myoglobinuria
TYPE-VI: Her’s
Diseases
Liver
phosphorylase
Liver Hepatomegaly, mild
hypoglycemia,
Hyperlipidemia and ketosis.
TYPE-VII: Tarui’s
Diseases
Muscle PFK-1 Muscle, RBC's Cramps and pain,
myoglobinuria , also
hemolytic anemia
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
GLUCONEOGENESIS
Definition:
Synthesis of new glucose (i.e. not glucose from glycogen) from non carbohydrate precursors
(pyruvate, lactate, glycerol, alanine), a process called gluconeogenesis.
The liver is the major site of gluconeogenesis; however, the kidney also has an important
part to play in this process.
From pyruvate:
In gluconeogenesis, three new steps bypass these are irreversible reactions of glycolysis.
 Phosphoenolpyruvate (PEP) is formed from pyruvate via oxaloacetate through the
action of pyruvate carboxylase & phosphoenolpyruvate carboxylase.
 Fructose -6-phosphate is formed from fructose – 1, 6-bisphosphate by hydrolysis of
the phosphate ester at C1. It catalyzed by Fructose -1, 6-bis-phosphatase.
 This reaction is a major point of control of gluconeogenesis
 Glucose is formed by hydrolysis of glucose -6- Phosphate in a reaction catalyzed by
glucose-6-phosphatase.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Since skeletal muscle lacks glucose-6-phosphatase, it cannot deliver free glucose to
the blood and undergoes gluconeogenesis exclusively as a mechanism to generate glucose
for storage as glycogen.
From Lactate / Cori cycle:
 Lactate is a predominate source of carbon atoms for glucose synthesis by during
anaerobic glycolysis occurs in skeletal muscle, pyruvate is reduced to lactate by
lactate dehydrogenase (LDH).
 After formation of lactate, then released to the blood stream and transported to the
liver where it is converted to glucose by gluconeogenesis process.
 The glucose is then returned to the blood for use by muscle as an energy source and
to replenish glycogen stores. This cycle is called Cori cycle.
 The Cori cycle involves the utilization of lactate, produced by glycolysis in non-
hepatic tissues, (such as muscle and erythrocytes) as a carbon source for hepatic
gluconeogenesis.
From Alanine / Glucose-Alanine Cycle:
 Pyruvate, generated in muscle and other peripheral tissues, can be transaminated to
alanine which is returned to the liver for gluconeogenesis. This pathway is termed as
glucose-alanine cycle.
 Glucose oxidation produces pyruvate which can undergo transamination to alanine.
This reaction is catalyzed by alanine transaminase (ALT). Additionally, during the
fasting, skeletal muscle protein is degraded for the energy value of the amino acid
carbons and alanine is a major amino acid in protein.
 The alanine then enters the blood stream and is transported to the liver. Within the
liver alanine is converted back to pyruvate which is then a source of carbon atoms for
gluconeogenesis.
 The newly formed glucose can then enter the blood for delivery back to the muscle.
The amino group transported from the muscle to the liver in the form of alanine is
converted to urea in the urea cycle and excreted.
From Glycerol:
 The glycerol backbone of lipids can be used for gluconeogenesis. This requires
phosphorylation to glycerol-3-phosphate by glycerol kinase and dehydrogenation to
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
dihydroxyacetone phosphate (DHAP) by glyceraldehyde-3-phosphate
dehydrogenase (G3PDH).
 The G3PDH reaction is the same as that used in the transport of cytosolic reducing
equivalents into the mitochondrion for use in oxidative phosphorylation. This
transport pathway is called the glycerol-phosphate shuttle.
Regulation of Gluconeogenesis:
 Gluconeogenesis stimulated by acetyl CoA, glucagon, glucocorticoids, epinephrine,
oxaloacetate, high conc. of citrates and ATPs.
 This process inhibited by insulin, ADP, AMP, low conc. of citrates
GALACTOSE METABOLISM
Galactose is obtained from the milk sugar, lactose (a disaccharide of glucose and
galactose), enters glycolysis by its conversion to glucose-1-phosphate.
Steps:
 First the galactose is phosphorylated by galactokinase to yield galactose-1-phosphate.
 Epimerization of galactose-1-P to Glucose-1-P requires the transfer of UDP from UDP-
glucose catalyzed by galactose-1-phosphate uridyl transferase. This generates UDP-
galactose and Glucose-1-P.
 UDP-galactose is epimerized to UDP-glucose by UDP-galactose-4 epimerase.
 The UDP portion is exchanged for phosphate generating glucose-1-phosphate, which
then is converted to Glucose – 6-phosphate by phosphoglucose mutase.
 Glucose -6-phosphate then converted to glucose by glucose-6-phosphatase.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Biomedical importance:
 Galactose is required by lactating mammary gland for synthesis of lactose of milk.
 Galactose is required for the synthesis of mucopolysaccharides (keratan sulphate &
chondroitin sulphate) and glycolipids (Cerebrosides & Gangliosides).
 It is mainly used as a test for liver functions called galactose tolerance test.
Clinical Significances:
Galactosaemia:
 It is a rare congenital disease in infants.
 Accumulation of galactose & galactose-1-P in blood due to the defect of uridyl
transferase and galactokinase. Leads to failure of growth in newborn.
 Accumulation of galactose in liver, brain & eye lenses causes liver failure, mental
retardation and cataract formation respectively.
 Treatment: To decrease lactose in the diet (milk or milk products).
Galactosuria:
 Galactose is excreted in the urine.
 Urine, gives a positive test for reducing substances but a negative test for glucose.
FRUCTOSE METABOLISM
Reactions:
 Hepatic Fructokinases
phosphorylates fructose
on C1 yielding fructose-
1-phosphate by
fructokinase.
 In the liver aldolase-B
enzyme, splits fructose-
1-phosphate and
generates DHAP and
glyceraldehyde.
 The DHAP is converted,
by triose phosphate
isomerase, to
Glyceraldehyde-3-P and enters glycolysis.
 Glyceraldehyde is phosphorylated to glyceraldehyde-3-P by glyceraldehyde kinase.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 Glyceraldehyde-3-P further enters to the glycolytic pathway.
Biomedical importance:
 Seminal fluid is rich in fructose & spermatozoa utilize fructose for energy.
 It is easily metabolized & good source of energy.
Clinical Significances:
Essential fructosuria:
 It is a metabolic disorder caused by the lack of fructokinase, which is normally
present in the liver, pancreatic islets and kidney cortex.
Hereditary fructose intolerance:
 It is a disorder resulting from a lack of aldolase B.
 It is characterized by severe hypoglycemia and vomiting
 Prolonged intake of fructose by infants with this defect leads to vomiting, poor
feeding, hepatic failure and death.
HEXOSE MONOPHOSPHATE SHUNT PATHWAY (HMP SHUNT PATHWAY)
 It is also called as pentose phosphate pathway.
 It is an alternative pathway to glycolysis and TCA cycle for the oxidation of glucose.
 HMP Shunt is found in all cells and enzymes of this pathway are present in cytosol.
 This pathway is divided into two phases.
1. Oxidative phase
2. Non oxidative phase
In Oxidative phase,
 Glucose -6-P undergoes dehydrogenation and decarboxylation to give pentose sugar,
ribulose-5-P with generation of NADPH.
In non oxidation phase:
 All the reactions are reversible, Ribulose -5- phosphate further converted to fructose -
6-phosphate and glyceraldehyde-3- phosphate by a series of reactions of
epimerization, isomerization, transketolation, transaldolation and transketolation.
 Fructose -6 -P & glyceraldehyde-3- phosphate can be further catabolized through
glycolysis and TCA cycle.
Regulation:
 The first step in this pathway, catalyzed by glucose- 6-phosphate dehydrogenase is
rate limiting step.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 Insulin, well fed state and low levels of NADPH stimulates HMP shunt.
 Starvation & diabetes mellitus and high levels of NADPH inhibits HMP shunt
pathway.
Significance of HMP shunt pathway:
 HMP shunt pathway produced pentoses (ribose-5-P), it required for the biosynthesis
of nucleotide & nucleic acid (DNA and RNA).
Glucose (6C)
6-Phosphogluconolactone
6-Phosphogluconate
Ribulose-5-P
Xylulose-5-P
Xylulose -5-P
Glucose -6-P-Dehydrogenase
Hydrolase
s
Dehydrogenase
Epimeras
e
Ribose-5-P
Isomerase
Trans Ketolases
Trans Aldolase
Glyceraldehyde -3-P
Sedoheptulose -7-P
HMP shunt Pathway
NADP+
Erythrose-4-P Fructose-6-P
Trans Ketolases
Fructose-6-P
Glyceraldehyde -3-P
NADPH + H+
NADPH + H+
NADP+
Oxidative Phase
Non Oxidative
Phase
H2O
+ CO2
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 It provides a route for the interconversion of pentoses and hexoses.
 It generates NADPH, which plays an important for biosynthesis of fatty acids,
cholesterol and also involved in detoxification reaction.
URONIC ACID PATHWAY (GLUCURONIC ACID CYCLE)
Definition:
 It is an alternative oxidative pathway for glucose but does not generate ATPs.

In this pathway glucose produces glucuronic acid, ascorbic acid (except in humans) and
pentoses
Reactions:
 Glucose-6-P is converted to
glucose-1-phosphate then
reacts with UTP to form
UDP-Glucose catalysed by
mutase and
pyrophosphorylase enzymes
respectively.
 UDP-glucose is oxidized to
glucuronate via UDP
glucuronate catalyzed by
UDP glucose
dehydrogenase, further
glucuronate is form ascorbic
acid (Vitamin-C) and
Xylulose, in lower animals.
 Xylulose then enters into the
HMP shunt pathway to
produced pentose sugars.
Significance of uronic acid
pathway:
 Uronic acid pathway is a source of UDP-glucuronate.
 UDP glucuronate is a precursor in the biosynthesis of glycosaminoglycans,
proteoglycans and glycoproteins.
Glucose -6-Phosphate
Glucose -1-Phosphate
UDP- Glucose
UDP-Glucuronate
Ascorbic acid
(Vitamin-C)
UTP
PPi
Phosphogluco-
mutase
UDP-Glucose
Pyrophosphorylase
2NAD+ + H2O
UDP- Glucose
Dehydrogenas
e
Glucuronate
H2O
Uronic Acid Pathway
UDP
2NADH+ + 2H+
Xylulose
Pentose Phosphate
Pathway
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 It is a source of UDP-glucose, which is used for glycogen formation.
 It involved in detoxification reactions via conjugation reactions (bilirubin).
Disorders:
Essential pentosuria:
 This condition is inherited in an autosomal recessive disorder.
 It is a condition characterized by high levels of L-xylulose in urine. Due to defect of
NADP+
dependent L-xylulose dehydrogenase enzyme.
 L-xylulose cannot be converted to xylitol so excrete large amount of L-xylulose
excreted.
REGULATION OF BLOOD SUGAR LEVELS
Blood sugar regulation is the process by which levels of blood sugar (glucose), are
maintained by the body. The blood glucose is regulated by several metabolic pathways,
which are mainly regulated through many hormones.
Normal ranges of blood sugars:
Fasting blood sugars (FBS) – 70 – 110 mg/dl
Post prandial blood sugars (PPBS) – 70 – 140 mg/dl
Random blood sugars (RBS) – 70 – 160 mg/dl
Mechanisms of blood sugar regulation
The glucose levels in the blood are monitored by the cells in the pancreas.
In Fasting condition (before food):
 If the blood glucose level falls below normal levels, the α-cells of the pancreas
release glucagon.
 Glucagon increases the blood glucose levels. Converts glycogen into glucose
(glycogenolysis), thus increasing the blood sugar levels.
 Prolonged fasting condition, glucose is synthesized by gluconeogenesis. Liver is the
central organ, which maintains blood glucose levels.
In Post prandial condition (after food):
 Blood glucose level rises after the meal; insulin hormone is released by the β- cells in
the islets of langerhans of the pancreas.
 Insulin stimulates the liver to convert more glucose into glycogen (glycogenesis),
formation of fat (lipogenesis), thus decreasing the blood sugar.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Hormonal regulations of blood glucose levels:
Hormones that influence blood glucose level are
a) Hypoglycemic hormones:
Insulin only hormone decrease the blood glucose levels in the body.
 Insulin hormone produced by β- cells of islets of langerhans of pancrease.
Action -
Stimulates the uptake of glucose into muscle & other tissues (glycolysis)
It promotes the conversion of glucose to glycogen (Glycogenesis)
Inhibits the glucose production by the liver (decreased gluconeogenesis)
Suppresses breakdown of proteins into amino acids
Inhibits the lipolysis in adipose tissue into free fatty acids
b) Hyper glycemic hormones:
These hormones increase the blood glucose levels in the body.
Glucagon:
It is a polypeptide hormone secreted by α- cells of pancreas.
Action-
It stimulates the production of glucose in the liver by glycogenolysis &
Gluconeogenesis
Inhibits glycolysis
Decreases glycogen synthesis
Enhance synthesis of glucose from amino acids and fatty acids.
Other hormones:
Hormones Action
Epinephrine
(synthesized by adrenal
medulla hormone)
 Enhances glycogenolysis
 Decreases glycolysis.
 Enhances release of fatty acids from adipose tissues.
Growth hormone
Anterior pituitary gland
 It stimulates Gluconeogenesis & lipolysis.
Cortisol
(secreted by adrenal cortex)
 Stimulate gluconeogenesis
 Increases the breakdown of protein & fats.
ACTH
(Anterior pituitary)
 Enhances release of fatty acids from adipose tissues
(lipolysis).
Thyroxine
(Thyroid gland)
 Increases the rate of intestinal glucose absorption.
 Enhances glycogenolysis
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
DIABETES MELLITUS
 It is a metabolic disorder of carbohydrate metabolism, in which glucose levels are
increased in blood, leading to producing hyperglycemia.
 Diabetes is classified into
A. Type 1, Insulin dependent Diabetes mellitus (IDDM) or juvenile onset diabetes.
B. Type II, Non Insulin dependent Diabetes mellitus (NIDDM) or adult diabetes
Type 1, Diabetes mellitus:
 Onset usually occurs in children & youth, less than 20years old.
 Due to less production of insulin.
 Type-I diabetes due to acute immune destruction of β-cells of pancreas.
Symptoms:
 Polyuria: production of abnormally large volume of urine.
 Polydypsia: increase intake of water (thirst).
 Polyphagia: person eats more frequently (hunger).
 Lipid & proteins breakdown is increased, it leads to weight loss.
 Complication is cataract, neuropathy & nephropathy.
Type 2, Diabetes mellitus:
 This type usually occurs after the age of 40 years.
 It is a result due to loss or less production of insulin..
 Patients are not dependent on insulin injections is called as non insulin dependent
diabetes mellitus
 This type of diabetes can be managed by proper nutrition, exercise, lifestyle changes,
oral medication, and insulin, if necessary.
Complications of diabetes mellitus
 In eyes: Cataract formation
 Retinopathy – retinol micro vascular abnormalities, leads to blindness
 Neuropathy- dysfunction of one or more peripheral nerves, It is highly risk of foot
ulcers and gangrene
 Angiopathy- Damage to basement membrane of blood vessels.
 Nephropathy- Damage to the glomerulus of kidneys.
 And also seen in hyperlipidemia and ketoacidosis
 Diabetic Complicating pregnancy:
o Diabetic mothers tend to have big babies.
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
o Anabolic hormone insulin defect leads to abortion, premature birth &
intrauterine death of fetus
Symptoms of diabetes
 Increased thirst, dry mouth, Weakness & anorexia
 Hunger (especially after eating)
 Frequent urination
 Unexplained weight loss (appetite is normal)
 Blurred vision
 Tingling of the hands or feet
 Slow healing sores or cuts
Diabetes risk factors
 A family history of diabetes, elderly persons, overweight,
 History of hypertension (high blood pressure), abnormal blood cholesterol or
triglyceride levels and alcoholics.
Management of Diabetes:
o To follow a healthy meals plan
o Regular exercise
o Take proper medication
o Test blood suger regularly
Diagnosis of Diabetes Mellitus
Fasting Blood Glucose
(mg/dl)
Hb A1c
(%)
OGTT
(mg/dl)
Normal < 110 < 5.7 < 140
Pre-diabetic state 100 to 125 5.7 to 6.4 140 to 199
Diabetes Mellitus > 126 > 6.5 > 200
Glucose Challenge Test (GCT):
• Glucose Challenge Test (GCT) mainly used for screening of gestational diabetes
mellitus.
• Usually done this test during 24-28 weeks of gestation
• 75 gm of glucose dissolved in 250 ml water was giving to pregnant women during
this test
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
• Blood sugar estimated after 1 hour
• If value >140 mg/dL, GDM is suspected
• Diagnosis confirmed by OGTT
Interpretation of GCT:
Screening: During 24-28 weeks
 Negative: Less than 140 mg/dL
 Positive: More than 141 mg/dL
Confirm Diagnosis: If GCT positive conform by GTT
GLUCOSE TOLERANCE TEST (GTT):
Glucose tolerance test is a simple and standard test to determine the ability of a person to
metabolize a given load of glucose.
Definition:
 The ability of the body to tolerate the excess load of glucose and to dispose of an
additional load of glucose given within the time.
 Used to measure changes in blood glucose after glucose load.
Preparation of the patient
 Good carbohydrate diet for 3
days prior to the test
 Diet containing about 30-50
g of carbohydrate should be
taken on the evening prior to
the test.
 Avoid drugs likely to
influence the blood glucose
levels for at least 2 days
prior to the test.
 Avoided smoking & exercise
on the previous day.
 No food after 8 pm the
previous night to ensure 12
hours fasting.
Procedure:
The patient is asked to report after an overnight fast
(10-12 hours) in the morning (8am)
↓
Fasting samples (blood & urine) is collected (1st
sample)
↓
75gm of glucose dissolved in 250-300 ml of water, is
given orally (1.75g/Kg body weight for children)
within 5 min
↓
Samples are collected at intervals of 30, 60, 90, 120
and 150 minutes.
↓
All the blood & Urine samples (6 samples)–
estimated for sugar
↓
Blood sugar concentration are plotted in a graph
paper against time
Note: GOD - POD methods is commonly used for
estimation of blood sugar & In urine sugar used benedict’s
qualitative method or GOD method (strip method)
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
Significance of GTT:
GTT useful to diagnose diabetes mellitus in doubtful cases of.
– Asymptomatic hyperglycemia or glycosuria
– Useful in diagnosis of mild Diabetes
– To rule out gestational diabetes mellitus – short GTT during pregnancy
– To rule out benign renal glucosuria
– Patients with symptoms of diabetes mellitus but with no glycosuria and normal
fasting level.
– Person with a strong family history of diabetes mellitus but with no symptoms of
diabetes mellitus.
OGTT respondances:
Normal OGTT
• Fasting blood glucose is 75-110mg/dl
• Oral glucose load(1g/kg wt.) the concentration increases and the peak value (140mg/dl) is
seen in less than an hour, it returns to normal by two hours
• Glucose is not detected in the urine sample.
In Uncontrolled Diabetes Mellitus / Severe Diabetes Mellitus
0
20
40
60
80
100
120
140
160
180
200
0 ½ 1 1 ½ 2 2 ½
Blood
Glucose
mg%
Time in hours
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 Fasting blood sample itself is more than normal range
 All the blood samples show higher values
 Last blood sample does not return to fasting level
 All the urine sugars are positive
Renal Glycosuria
 Due to defective renal reabsorption and decreased renal threshold
 Blood glucose is normal in all the samples
 Urine sugar is positive in more than one sample
Significance of GTT:
It is mainly used in the detection of diabetes mellitus under the conditions of
0
20
40
60
80
100
120
140
160
180
200
0 ½ 1 1 ½ 2 2 ½
Blood
Glucose
mg%
time in hours
Lower renal threshold
0
50
100
150
200
250
300
350
400
0 ½ 1 1 ½ 2 2 ½
Blood
glucose
(mg%)
Time in hours
Metabolism of Carbohydrates & its Disorders
Dr. Santhosh Kumar N/ Associate Professor of Biochemistry
 This test is useful in distinguishing a person with a normal glucose tolerance from a
person who has increased or decreased tolerance. It is of great value in detecting renal
glycosuria and endocrine malfunction.
 Patients with transient or sustained glycosuria, who have no clinical symptoms of
diabetes and with normal, fasting and post prandial blood glucose level.
 Patients whose glycosuria is associated with pregnancy, Thyrotoxicosis, liver disease and
infections.

More Related Content

What's hot

HM-01 HEME BIOSYNTHESIS & Porphyrias .pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias .pptxHM-01 HEME BIOSYNTHESIS & Porphyrias .pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias .pptx
Dr. Santhosh Kumar. N
 
Digestion & absorption of lipids by Dr. Santhosh Kumar N.pptx
Digestion & absorption of lipids by Dr. Santhosh Kumar N.pptxDigestion & absorption of lipids by Dr. Santhosh Kumar N.pptx
Digestion & absorption of lipids by Dr. Santhosh Kumar N.pptx
Dr. Santhosh Kumar. N
 
URONIC ACID PATHWAY
URONIC ACID PATHWAYURONIC ACID PATHWAY
URONIC ACID PATHWAY
Rabia Khan Baber
 
4 integration of metabolism
4   integration of metabolism4   integration of metabolism
4 integration of metabolism
MUBOSScz
 
Aminoacid metabolism
Aminoacid metabolismAminoacid metabolism
Aminoacid metabolism
Naresh Panigrahi
 
C-A&P 03 Classification and properties of proteins
C-A&P 03 Classification and properties of proteinsC-A&P 03 Classification and properties of proteins
C-A&P 03 Classification and properties of proteins
Dr. Santhosh Kumar. N
 
Class 10 uronic acid pathway
Class 10 uronic acid pathwayClass 10 uronic acid pathway
Class 10 uronic acid pathway
Dhiraj Trivedi
 
INTEGRATION OF METABOLISM
INTEGRATION OF METABOLISMINTEGRATION OF METABOLISM
INTEGRATION OF METABOLISM
YESANNA
 
Protein & Amino Acid Metabolism
Protein & Amino Acid MetabolismProtein & Amino Acid Metabolism
Protein & Amino Acid Metabolism
SmitaPakhmode1
 
carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...
carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...
carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...
RajkumarKumawat11
 
Uronic acid pathway
Uronic acid pathwayUronic acid pathway
Uronic acid pathway
Ashok Katta
 
class-3 Derived lipids (steorids).pptx
class-3   Derived lipids (steorids).pptxclass-3   Derived lipids (steorids).pptx
class-3 Derived lipids (steorids).pptx
Dr. Santhosh Kumar. N
 
Met of glycine
Met of glycineMet of glycine
Met of glycine
ranjani n
 
URONIC ACID PATHWAY
URONIC ACID PATHWAYURONIC ACID PATHWAY
URONIC ACID PATHWAY
YESANNA
 
CL- 01: Fatty acid (Derived lipids)
CL- 01: Fatty acid (Derived lipids)CL- 01: Fatty acid (Derived lipids)
CL- 01: Fatty acid (Derived lipids)
Dr. Santhosh Kumar. N
 
Integration of metabolism for medical school
Integration of metabolism for medical schoolIntegration of metabolism for medical school
Integration of metabolism for medical school
Ravi Kiran
 
METHIONINE METABOLISM
METHIONINE METABOLISMMETHIONINE METABOLISM
METHIONINE METABOLISM
YESANNA
 
Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)
Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)
Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)
Ashok Katta
 
Metabolism of carbohydrates
Metabolism of carbohydratesMetabolism of carbohydrates
Metabolism of carbohydrates
Towkir Ahmed Ove
 
CH-03. Glycogen metabolism.pptx
CH-03. Glycogen metabolism.pptxCH-03. Glycogen metabolism.pptx
CH-03. Glycogen metabolism.pptx
Dr. Santhosh Kumar. N
 

What's hot (20)

HM-01 HEME BIOSYNTHESIS & Porphyrias .pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias .pptxHM-01 HEME BIOSYNTHESIS & Porphyrias .pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias .pptx
 
Digestion & absorption of lipids by Dr. Santhosh Kumar N.pptx
Digestion & absorption of lipids by Dr. Santhosh Kumar N.pptxDigestion & absorption of lipids by Dr. Santhosh Kumar N.pptx
Digestion & absorption of lipids by Dr. Santhosh Kumar N.pptx
 
URONIC ACID PATHWAY
URONIC ACID PATHWAYURONIC ACID PATHWAY
URONIC ACID PATHWAY
 
4 integration of metabolism
4   integration of metabolism4   integration of metabolism
4 integration of metabolism
 
Aminoacid metabolism
Aminoacid metabolismAminoacid metabolism
Aminoacid metabolism
 
C-A&P 03 Classification and properties of proteins
C-A&P 03 Classification and properties of proteinsC-A&P 03 Classification and properties of proteins
C-A&P 03 Classification and properties of proteins
 
Class 10 uronic acid pathway
Class 10 uronic acid pathwayClass 10 uronic acid pathway
Class 10 uronic acid pathway
 
INTEGRATION OF METABOLISM
INTEGRATION OF METABOLISMINTEGRATION OF METABOLISM
INTEGRATION OF METABOLISM
 
Protein & Amino Acid Metabolism
Protein & Amino Acid MetabolismProtein & Amino Acid Metabolism
Protein & Amino Acid Metabolism
 
carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...
carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...
carbohydrate metabolism, Glycolysis, metabolic process of carbohydrates, EMP ...
 
Uronic acid pathway
Uronic acid pathwayUronic acid pathway
Uronic acid pathway
 
class-3 Derived lipids (steorids).pptx
class-3   Derived lipids (steorids).pptxclass-3   Derived lipids (steorids).pptx
class-3 Derived lipids (steorids).pptx
 
Met of glycine
Met of glycineMet of glycine
Met of glycine
 
URONIC ACID PATHWAY
URONIC ACID PATHWAYURONIC ACID PATHWAY
URONIC ACID PATHWAY
 
CL- 01: Fatty acid (Derived lipids)
CL- 01: Fatty acid (Derived lipids)CL- 01: Fatty acid (Derived lipids)
CL- 01: Fatty acid (Derived lipids)
 
Integration of metabolism for medical school
Integration of metabolism for medical schoolIntegration of metabolism for medical school
Integration of metabolism for medical school
 
METHIONINE METABOLISM
METHIONINE METABOLISMMETHIONINE METABOLISM
METHIONINE METABOLISM
 
Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)
Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)
Metabolism of Basic Amino Acids (Arginine, Histidine, Lysine)
 
Metabolism of carbohydrates
Metabolism of carbohydratesMetabolism of carbohydrates
Metabolism of carbohydrates
 
CH-03. Glycogen metabolism.pptx
CH-03. Glycogen metabolism.pptxCH-03. Glycogen metabolism.pptx
CH-03. Glycogen metabolism.pptx
 

Similar to Basic notes of Metabolism of Carbohydrates-1.docx

4.2 glycolysis & TCA cycle.ppt
4.2 glycolysis & TCA cycle.ppt4.2 glycolysis & TCA cycle.ppt
4.2 glycolysis & TCA cycle.ppt
Dr. Neelam H. Zaidi
 
Central Metabolism
Central MetabolismCentral Metabolism
Krebs cycle/Citric acid cycle
Krebs cycle/Citric acid cycleKrebs cycle/Citric acid cycle
Krebs cycle/Citric acid cycle
IshaTariq8
 
Carbohydrate 3
Carbohydrate 3Carbohydrate 3
Carbohydrate 3
Pharmacy Universe
 
Crebs cycle 2013
Crebs cycle 2013Crebs cycle 2013
PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)
PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)
PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)
YESANNA
 
Carbo metabolism
Carbo metabolismCarbo metabolism
Carbo metabolism
Gaurav Saxena
 
Biochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathway
Biochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathwayBiochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathway
Biochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathway
Rengesh Balakrishnan
 
Carbohydrates metabolism, part 2
Carbohydrates metabolism, part 2Carbohydrates metabolism, part 2
Carbohydrates metabolism, part 2
enamifat
 
Tca cycle b.pharm
Tca cycle b.pharmTca cycle b.pharm
Tca cycle b.pharm
Kamlesh Yadav
 
Carbohydrate metabolism
Carbohydrate metabolismCarbohydrate metabolism
Carbohydrate metabolism
Devipriya Viswambharan
 
TCA cycle/Krebs cycle/Citric acid cycle
TCA cycle/Krebs cycle/Citric acid cycleTCA cycle/Krebs cycle/Citric acid cycle
TCA cycle/Krebs cycle/Citric acid cycle
RoshanKumarMahat
 
Lec05 tc acycle
Lec05 tc acycleLec05 tc acycle
Lec05 tc acycle
dream10f
 
2. TCA cycle and fate of pyruvate & acetyl CoA.pptx
2. TCA cycle and fate of pyruvate & acetyl CoA.pptx2. TCA cycle and fate of pyruvate & acetyl CoA.pptx
2. TCA cycle and fate of pyruvate & acetyl CoA.pptx
Dr. Santhosh Kumar. N
 
glycolisis.docx
glycolisis.docxglycolisis.docx
glycolisis.docx
sunilsharmavet
 
Citric Acid Cycle
Citric Acid Cycle Citric Acid Cycle
Citric Acid Cycle
Hamid Ur-Rahman
 
Cellular Energy Transfer (Glycolysis and Krebs Cycle) and ATP
Cellular Energy Transfer (Glycolysis and Krebs Cycle) and ATPCellular Energy Transfer (Glycolysis and Krebs Cycle) and ATP
Cellular Energy Transfer (Glycolysis and Krebs Cycle) and ATP
muhammad aleem ijaz
 
Kerb's cycle.
Kerb's cycle.Kerb's cycle.
Kerb's cycle.
Prakash Pokhrel
 
Glycolysis.pptx
Glycolysis.pptxGlycolysis.pptx
Glycolysis.pptx
SUBHOJITPANJA
 
POWEPOINT PRESENTATION ON GLYCOLYSIS.pptx
POWEPOINT PRESENTATION ON GLYCOLYSIS.pptxPOWEPOINT PRESENTATION ON GLYCOLYSIS.pptx
POWEPOINT PRESENTATION ON GLYCOLYSIS.pptx
SoudeepBanerjee1
 

Similar to Basic notes of Metabolism of Carbohydrates-1.docx (20)

4.2 glycolysis & TCA cycle.ppt
4.2 glycolysis & TCA cycle.ppt4.2 glycolysis & TCA cycle.ppt
4.2 glycolysis & TCA cycle.ppt
 
Central Metabolism
Central MetabolismCentral Metabolism
Central Metabolism
 
Krebs cycle/Citric acid cycle
Krebs cycle/Citric acid cycleKrebs cycle/Citric acid cycle
Krebs cycle/Citric acid cycle
 
Carbohydrate 3
Carbohydrate 3Carbohydrate 3
Carbohydrate 3
 
Crebs cycle 2013
Crebs cycle 2013Crebs cycle 2013
Crebs cycle 2013
 
PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)
PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)
PYRUVATE DEHYDROGENASE COMPLEX (PDH-MULTI-ENZYME COMPLEX)
 
Carbo metabolism
Carbo metabolismCarbo metabolism
Carbo metabolism
 
Biochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathway
Biochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathwayBiochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathway
Biochemistry lecture notes metabolism_glycolysis &amp; pentose phosphate pathway
 
Carbohydrates metabolism, part 2
Carbohydrates metabolism, part 2Carbohydrates metabolism, part 2
Carbohydrates metabolism, part 2
 
Tca cycle b.pharm
Tca cycle b.pharmTca cycle b.pharm
Tca cycle b.pharm
 
Carbohydrate metabolism
Carbohydrate metabolismCarbohydrate metabolism
Carbohydrate metabolism
 
TCA cycle/Krebs cycle/Citric acid cycle
TCA cycle/Krebs cycle/Citric acid cycleTCA cycle/Krebs cycle/Citric acid cycle
TCA cycle/Krebs cycle/Citric acid cycle
 
Lec05 tc acycle
Lec05 tc acycleLec05 tc acycle
Lec05 tc acycle
 
2. TCA cycle and fate of pyruvate & acetyl CoA.pptx
2. TCA cycle and fate of pyruvate & acetyl CoA.pptx2. TCA cycle and fate of pyruvate & acetyl CoA.pptx
2. TCA cycle and fate of pyruvate & acetyl CoA.pptx
 
glycolisis.docx
glycolisis.docxglycolisis.docx
glycolisis.docx
 
Citric Acid Cycle
Citric Acid Cycle Citric Acid Cycle
Citric Acid Cycle
 
Cellular Energy Transfer (Glycolysis and Krebs Cycle) and ATP
Cellular Energy Transfer (Glycolysis and Krebs Cycle) and ATPCellular Energy Transfer (Glycolysis and Krebs Cycle) and ATP
Cellular Energy Transfer (Glycolysis and Krebs Cycle) and ATP
 
Kerb's cycle.
Kerb's cycle.Kerb's cycle.
Kerb's cycle.
 
Glycolysis.pptx
Glycolysis.pptxGlycolysis.pptx
Glycolysis.pptx
 
POWEPOINT PRESENTATION ON GLYCOLYSIS.pptx
POWEPOINT PRESENTATION ON GLYCOLYSIS.pptxPOWEPOINT PRESENTATION ON GLYCOLYSIS.pptx
POWEPOINT PRESENTATION ON GLYCOLYSIS.pptx
 

More from Dr. Santhosh Kumar. N

Alcohol metabolism and alcoholism & Fatty liver.pptx
Alcohol metabolism and alcoholism & Fatty liver.pptxAlcohol metabolism and alcoholism & Fatty liver.pptx
Alcohol metabolism and alcoholism & Fatty liver.pptx
Dr. Santhosh Kumar. N
 
M-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptxM-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptx
Dr. Santhosh Kumar. N
 
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptxMetabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Dr. Santhosh Kumar. N
 
Metabolism , Metabolic Fate& disorders of cholesterol.pptx
Metabolism , Metabolic Fate& disorders of cholesterol.pptxMetabolism , Metabolic Fate& disorders of cholesterol.pptx
Metabolism , Metabolic Fate& disorders of cholesterol.pptx
Dr. Santhosh Kumar. N
 
Metabolism of Galactose & fructose .pptx
Metabolism of Galactose & fructose .pptxMetabolism of Galactose & fructose .pptx
Metabolism of Galactose & fructose .pptx
Dr. Santhosh Kumar. N
 
HM-02 Heme catabolism & Genetic defects.pptx
HM-02 Heme catabolism & Genetic defects.pptxHM-02 Heme catabolism & Genetic defects.pptx
HM-02 Heme catabolism & Genetic defects.pptx
Dr. Santhosh Kumar. N
 
HM-01 HEME BIOSYNTHESIS & Porphyrias.pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias.pptxHM-01 HEME BIOSYNTHESIS & Porphyrias.pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias.pptx
Dr. Santhosh Kumar. N
 
class -2 Simple & Compound lipids.pptx
class -2  Simple & Compound lipids.pptxclass -2  Simple & Compound lipids.pptx
class -2 Simple & Compound lipids.pptx
Dr. Santhosh Kumar. N
 
OFT 04- AFTs.pptx
OFT 04- AFTs.pptxOFT 04- AFTs.pptx
OFT 04- AFTs.pptx
Dr. Santhosh Kumar. N
 
0FT 02. RFT.pptx
0FT 02. RFT.pptx0FT 02. RFT.pptx
0FT 02. RFT.pptx
Dr. Santhosh Kumar. N
 
OFT 03. TFT.pptx
OFT 03. TFT.pptxOFT 03. TFT.pptx
OFT 03. TFT.pptx
Dr. Santhosh Kumar. N
 
DIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docx
DIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docxDIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docx
DIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docx
Dr. Santhosh Kumar. N
 
1.Digestion & absorption of carbohydrate.pptx
1.Digestion & absorption of carbohydrate.pptx1.Digestion & absorption of carbohydrate.pptx
1.Digestion & absorption of carbohydrate.pptx
Dr. Santhosh Kumar. N
 
Thiamine & Riboflavin.pptx
Thiamine & Riboflavin.pptxThiamine & Riboflavin.pptx
Thiamine & Riboflavin.pptx
Dr. Santhosh Kumar. N
 
Vitamin - B3 and B6.pptx
Vitamin - B3 and B6.pptxVitamin - B3 and B6.pptx
Vitamin - B3 and B6.pptx
Dr. Santhosh Kumar. N
 
Vitamine -E & K.pptx
Vitamine -E & K.pptxVitamine -E & K.pptx
Vitamine -E & K.pptx
Dr. Santhosh Kumar. N
 
DIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docx
DIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docxDIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docx
DIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docx
Dr. Santhosh Kumar. N
 
class -3: Compound lipids .pptx
class -3:  Compound lipids .pptxclass -3:  Compound lipids .pptx
class -3: Compound lipids .pptx
Dr. Santhosh Kumar. N
 
CL-02: lipid classification & Simple lipids by Santhosh Kumar .pptx
CL-02:  lipid classification & Simple lipids by Santhosh Kumar .pptxCL-02:  lipid classification & Simple lipids by Santhosh Kumar .pptx
CL-02: lipid classification & Simple lipids by Santhosh Kumar .pptx
Dr. Santhosh Kumar. N
 
class - 1: Fatty Acid (Derived lipids).pptx
class - 1:  Fatty Acid (Derived lipids).pptxclass - 1:  Fatty Acid (Derived lipids).pptx
class - 1: Fatty Acid (Derived lipids).pptx
Dr. Santhosh Kumar. N
 

More from Dr. Santhosh Kumar. N (20)

Alcohol metabolism and alcoholism & Fatty liver.pptx
Alcohol metabolism and alcoholism & Fatty liver.pptxAlcohol metabolism and alcoholism & Fatty liver.pptx
Alcohol metabolism and alcoholism & Fatty liver.pptx
 
M-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptxM-2- General Reactions of amino acids.pptx
M-2- General Reactions of amino acids.pptx
 
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptxMetabolism of  lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
Metabolism of lipoproteins & its disorders(Chylomicron & VLDL & LDL).pptx
 
Metabolism , Metabolic Fate& disorders of cholesterol.pptx
Metabolism , Metabolic Fate& disorders of cholesterol.pptxMetabolism , Metabolic Fate& disorders of cholesterol.pptx
Metabolism , Metabolic Fate& disorders of cholesterol.pptx
 
Metabolism of Galactose & fructose .pptx
Metabolism of Galactose & fructose .pptxMetabolism of Galactose & fructose .pptx
Metabolism of Galactose & fructose .pptx
 
HM-02 Heme catabolism & Genetic defects.pptx
HM-02 Heme catabolism & Genetic defects.pptxHM-02 Heme catabolism & Genetic defects.pptx
HM-02 Heme catabolism & Genetic defects.pptx
 
HM-01 HEME BIOSYNTHESIS & Porphyrias.pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias.pptxHM-01 HEME BIOSYNTHESIS & Porphyrias.pptx
HM-01 HEME BIOSYNTHESIS & Porphyrias.pptx
 
class -2 Simple & Compound lipids.pptx
class -2  Simple & Compound lipids.pptxclass -2  Simple & Compound lipids.pptx
class -2 Simple & Compound lipids.pptx
 
OFT 04- AFTs.pptx
OFT 04- AFTs.pptxOFT 04- AFTs.pptx
OFT 04- AFTs.pptx
 
0FT 02. RFT.pptx
0FT 02. RFT.pptx0FT 02. RFT.pptx
0FT 02. RFT.pptx
 
OFT 03. TFT.pptx
OFT 03. TFT.pptxOFT 03. TFT.pptx
OFT 03. TFT.pptx
 
DIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docx
DIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docxDIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docx
DIGESTION, ABSORPTION AND METABOLISM OF LIPIDS.docx
 
1.Digestion & absorption of carbohydrate.pptx
1.Digestion & absorption of carbohydrate.pptx1.Digestion & absorption of carbohydrate.pptx
1.Digestion & absorption of carbohydrate.pptx
 
Thiamine & Riboflavin.pptx
Thiamine & Riboflavin.pptxThiamine & Riboflavin.pptx
Thiamine & Riboflavin.pptx
 
Vitamin - B3 and B6.pptx
Vitamin - B3 and B6.pptxVitamin - B3 and B6.pptx
Vitamin - B3 and B6.pptx
 
Vitamine -E & K.pptx
Vitamine -E & K.pptxVitamine -E & K.pptx
Vitamine -E & K.pptx
 
DIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docx
DIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docxDIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docx
DIGESTION & ABSORPTION OF BIOMOLECULES by Dr. Santhosh Kumar N.docx
 
class -3: Compound lipids .pptx
class -3:  Compound lipids .pptxclass -3:  Compound lipids .pptx
class -3: Compound lipids .pptx
 
CL-02: lipid classification & Simple lipids by Santhosh Kumar .pptx
CL-02:  lipid classification & Simple lipids by Santhosh Kumar .pptxCL-02:  lipid classification & Simple lipids by Santhosh Kumar .pptx
CL-02: lipid classification & Simple lipids by Santhosh Kumar .pptx
 
class - 1: Fatty Acid (Derived lipids).pptx
class - 1:  Fatty Acid (Derived lipids).pptxclass - 1:  Fatty Acid (Derived lipids).pptx
class - 1: Fatty Acid (Derived lipids).pptx
 

Recently uploaded

BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...
BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...
BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...
Nguyen Thanh Tu Collection
 
The History of Stoke Newington Street Names
The History of Stoke Newington Street NamesThe History of Stoke Newington Street Names
The History of Stoke Newington Street Names
History of Stoke Newington
 
Leveraging Generative AI to Drive Nonprofit Innovation
Leveraging Generative AI to Drive Nonprofit InnovationLeveraging Generative AI to Drive Nonprofit Innovation
Leveraging Generative AI to Drive Nonprofit Innovation
TechSoup
 
Life upper-Intermediate B2 Workbook for student
Life upper-Intermediate B2 Workbook for studentLife upper-Intermediate B2 Workbook for student
Life upper-Intermediate B2 Workbook for student
NgcHiNguyn25
 
Chapter 4 - Islamic Financial Institutions in Malaysia.pptx
Chapter 4 - Islamic Financial Institutions in Malaysia.pptxChapter 4 - Islamic Financial Institutions in Malaysia.pptx
Chapter 4 - Islamic Financial Institutions in Malaysia.pptx
Mohd Adib Abd Muin, Senior Lecturer at Universiti Utara Malaysia
 
Hindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdfHindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdf
Dr. Mulla Adam Ali
 
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPLAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
RAHUL
 
PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.
Dr. Shivangi Singh Parihar
 
MARY JANE WILSON, A “BOA MÃE” .
MARY JANE WILSON, A “BOA MÃE”           .MARY JANE WILSON, A “BOA MÃE”           .
MARY JANE WILSON, A “BOA MÃE” .
Colégio Santa Teresinha
 
How to Make a Field Mandatory in Odoo 17
How to Make a Field Mandatory in Odoo 17How to Make a Field Mandatory in Odoo 17
How to Make a Field Mandatory in Odoo 17
Celine George
 
How to Create a More Engaging and Human Online Learning Experience
How to Create a More Engaging and Human Online Learning Experience How to Create a More Engaging and Human Online Learning Experience
How to Create a More Engaging and Human Online Learning Experience
Wahiba Chair Training & Consulting
 
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptxC1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
mulvey2
 
Pengantar Penggunaan Flutter - Dart programming language1.pptx
Pengantar Penggunaan Flutter - Dart programming language1.pptxPengantar Penggunaan Flutter - Dart programming language1.pptx
Pengantar Penggunaan Flutter - Dart programming language1.pptx
Fajar Baskoro
 
NEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptx
NEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptxNEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptx
NEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptx
iammrhaywood
 
clinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdfclinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdf
Priyankaranawat4
 
South African Journal of Science: Writing with integrity workshop (2024)
South African Journal of Science: Writing with integrity workshop (2024)South African Journal of Science: Writing with integrity workshop (2024)
South African Journal of Science: Writing with integrity workshop (2024)
Academy of Science of South Africa
 
Wound healing PPT
Wound healing PPTWound healing PPT
Wound healing PPT
Jyoti Chand
 
Présentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptx
Présentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptxPrésentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptx
Présentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptx
siemaillard
 
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...
Dr. Vinod Kumar Kanvaria
 
What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...
What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...
What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...
GeorgeMilliken2
 

Recently uploaded (20)

BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...
BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...
BÀI TẬP BỔ TRỢ TIẾNG ANH LỚP 9 CẢ NĂM - GLOBAL SUCCESS - NĂM HỌC 2024-2025 - ...
 
The History of Stoke Newington Street Names
The History of Stoke Newington Street NamesThe History of Stoke Newington Street Names
The History of Stoke Newington Street Names
 
Leveraging Generative AI to Drive Nonprofit Innovation
Leveraging Generative AI to Drive Nonprofit InnovationLeveraging Generative AI to Drive Nonprofit Innovation
Leveraging Generative AI to Drive Nonprofit Innovation
 
Life upper-Intermediate B2 Workbook for student
Life upper-Intermediate B2 Workbook for studentLife upper-Intermediate B2 Workbook for student
Life upper-Intermediate B2 Workbook for student
 
Chapter 4 - Islamic Financial Institutions in Malaysia.pptx
Chapter 4 - Islamic Financial Institutions in Malaysia.pptxChapter 4 - Islamic Financial Institutions in Malaysia.pptx
Chapter 4 - Islamic Financial Institutions in Malaysia.pptx
 
Hindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdfHindi varnamala | hindi alphabet PPT.pdf
Hindi varnamala | hindi alphabet PPT.pdf
 
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UPLAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
 
PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.PCOS corelations and management through Ayurveda.
PCOS corelations and management through Ayurveda.
 
MARY JANE WILSON, A “BOA MÃE” .
MARY JANE WILSON, A “BOA MÃE”           .MARY JANE WILSON, A “BOA MÃE”           .
MARY JANE WILSON, A “BOA MÃE” .
 
How to Make a Field Mandatory in Odoo 17
How to Make a Field Mandatory in Odoo 17How to Make a Field Mandatory in Odoo 17
How to Make a Field Mandatory in Odoo 17
 
How to Create a More Engaging and Human Online Learning Experience
How to Create a More Engaging and Human Online Learning Experience How to Create a More Engaging and Human Online Learning Experience
How to Create a More Engaging and Human Online Learning Experience
 
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptxC1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
C1 Rubenstein AP HuG xxxxxxxxxxxxxx.pptx
 
Pengantar Penggunaan Flutter - Dart programming language1.pptx
Pengantar Penggunaan Flutter - Dart programming language1.pptxPengantar Penggunaan Flutter - Dart programming language1.pptx
Pengantar Penggunaan Flutter - Dart programming language1.pptx
 
NEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptx
NEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptxNEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptx
NEWSPAPERS - QUESTION 1 - REVISION POWERPOINT.pptx
 
clinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdfclinical examination of hip joint (1).pdf
clinical examination of hip joint (1).pdf
 
South African Journal of Science: Writing with integrity workshop (2024)
South African Journal of Science: Writing with integrity workshop (2024)South African Journal of Science: Writing with integrity workshop (2024)
South African Journal of Science: Writing with integrity workshop (2024)
 
Wound healing PPT
Wound healing PPTWound healing PPT
Wound healing PPT
 
Présentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptx
Présentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptxPrésentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptx
Présentationvvvvvvvvvvvvvvvvvvvvvvvvvvvv2.pptx
 
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...
 
What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...
What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...
What is Digital Literacy? A guest blog from Andy McLaughlin, University of Ab...
 

Basic notes of Metabolism of Carbohydrates-1.docx

  • 1. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry METABOLISM OF CARBOHYDRATES GLYCOLYSIS / EMBDEN-MEYERHOF PATHWAY  Glycolysis ("splitting sugars") oxidation of glucose to pyruvate or lactate is called glycolysis.  It occurs in all tissues. Erythrocytes & nervous tissues derive its energy mainly from glycolysis. Reactions of glycolysis:  In glycolysis, glucose (a six carbon sugar) is split into two molecules of three-carbon sugar (pyruvate) mainly occurs in ten steps.  In the preparatory phase first glucose is converted into glucose -6-p by the enzyme glucokinase or hexokinase.  Glucose-6-phosphate is converted to fructose 6-P by isomerase enzyme, then it forms fructose-1, 6-bis phosphate by phosphofructokinase.  The enzyme aldolase split Fructose 1, 6-bisphosphate to dihydroxy acetone phosphate (DHAP) & glyceraldehyde -3-p, both triose phosphates are inter convertible sugars.  DHAP is converted to glyceraldehyde -3-p then is converted to 1,3 bisphosphoglycerate by glyceraldehyde -3-p dehydrogenase, which is NAD+ dependent, then converted to 3- phosphoglycerate by the enzyme phoshoglycerate kinase. High energy phosphate is formed.  Then 3-phosphoglycerate is converted to 2- phosphoglycerate, then phosphoenolpyruvate. Further phosphoenolpyruvate is converted to pyruvate; this reaction is catalyzed by pyruvate kinase.  The high energy phosphate of Phosphoenolpyruvate is directly transferred to ADP producing ATP, and then it is converted to pyruvate. 
  • 2. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Glucose (6C) Glucose -6-Phosphate (6C) Fructose -6-Phoshate (6C) Fructose -1,6-BisPhoshate (6C) Dihydroxyacetone Phosphate (3C) 1,3 Bisphosphoglycerate (2 molecules) ATP ADP Hexokinase / Glucokinase Isomerase ATP ADP Phospho fructokinase Aldolase Glyceraldehyde 3-Phosphate (3C) Triose Phosphate isomerase Gly-3-P Dehydrogenase Phoshoglycerate Kinase Mutase Enolase 3-Phosphoglycerate (2 molecules) 2- Phoshoglycerate (2 molecules) Phosphoenolpyruvate (2 molecules) Pyruvate (3C) (2 molecules) Pyruvate Kinase NAD+ + Pi ADP ATP ADP ATP Lactate (Anaerobic phase) Acetyl CoA (Aerobic phase) Reactions of Glycolysis NADH + H+
  • 3. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Anaerobic phase: In absence of oxygen, reoxidation of NADH by conversion of pyruvate to lactate (with out production of ATP) Energy yield per glucose molecule oxidation: Hexokinase or glucokinase (1ATP→1ADP) -1 ATP Phosphofructokinase (1ATP→1ADP) -1 ATP Glyceraldehyde 3-P dehydrogenase (2 NADH) [1 NADH= 2.5ATPs] + 5 ATP Phosphogycerokinase (2ADP + Pi → 2ATP) +2ATPs Pyruvate kinase (2ADP + Pi → 2ATP) + 2 ATPs Net gain 09 – 2 = 7 ATPs Significance of glycolysis:  This pathway for the production of energy.  It’s importance in skeletal muscle as glycolysis provides ATP even in absence of O2.  It generates precursors for biosynthetic pathways like o Pyruvate gives alanine (amino acids), acetyl- CoA for fatty acid biosynthesis. o Glycerol -3-Phosphate forms the backbone of triacylglycerol Regulation of glycolysis:  Hormonal- Insulin and glucocorticoids stimulates, glucagon, epinephrine inhibits glycolysis process.  Allosteric regulation- AMPs stimulates & citrate, ATPs inhibits phosphofructokinase on glycolysis process. Inhibitors Enzymes of glycolysis Bromo hydroxy acetone Phospho triose Isomerase Arsenate Glyceraldehyde 3-P dehydrogenase Fluoride Enolase Oxamate Lactate dehydrogenase
  • 4. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Metabolic fate of pyruvate: Formation of Acetyl CoA:  Pyruvate is end product of aerobic glycolysis. It occurs in cytoplasm, further pyruvate is transported into mitochondria by a pyruvate transporter.  Under aerobic conditions, pyruvate is converted to acetyl CoA, which enters the TCA cycle to be oxidized to CO2 & energy. Pyruvate dehydrogenase (PDH) complex:  The PDH complex is comprises of multiple copies of 3 separate enzymes & coenzymes. 1) Pyruvate dehydrogenase (PDH) 2) Dihydrolipoamide S-acetyltransferase (DLAT) 3) Dihydrolipoamide dehydrogenase (DLD).  The complex also requires 5 different coenzymes: CoA, NAD+ , FAD+ , thiamine pyrophosphate (TPP) and lipoic acid Fate of Acetyl CoA: PYRUVATE Glucogenic amino acid (Gly, Ser, Cys, Thr) Alanine (Deamination) Glucose (Gluconeogenesis) Acetyl -CoA Glucose (Glycolysis) Lactate (anaerobic) Alanine (Transamination) TCA cycle CO2& ATP Oxaloacetate (decarboxylation) Acetyl CoA Synthesis of Cholesterol Detoxification (acetylation reactions) Synthesis of Melatonin Formation of Acetyl choline Formation of ketone bodies Oxidation of TCA cycle Denovo synthesis of Fatty acids
  • 5. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry CITRIC ACID CYCLE / KREBS CYCLE/ TCA CYCLE The citric acid cycle is the central metabolic hub of the cell. It is the gateway to the aerobic metabolism of any molecule that can be transformed into an acetyl group or dicarboxylic acid.  The aerobic processing of glucose starts with the complete oxidation to CO2.  This oxidation takes place in the citric acid cycle, a series of reactions known as the “tricarboxylic acid (TCA) cycle” or the “Krebs cycle”.  The citric acid cycle is the final common pathway for the oxidation of fuel molecules – amino acids, carbohydrates & fatty acids that enter the cycle as acetyl CoA. The enzymes of citric acid cycle are located in the mitochondrial matrix. Reactions of the TCA Cycle
  • 6. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  Condensation of Acetyl-CoA with oxaloacetate to form citrate by citrate synthase.  Citrate is isomerized to isocitrate by the enzyme aconitase. The reaction occurs in two steps, dehydration to cis-aconitate & rehydration to isocitrate.  Isocitrate is dehydration to oxalosuccinate initially, then decarboxylation to give α- ketoglutarate by isocitrate dehydrogenase  Alpha-ketoglutarate (α-KG) is oxidative decarboxylated to Succinyl -CoA by the α- ketoglutarate dehydrogenase& it generates NADH [equal to 2.5ATPs].  The Succinyl-CoA is converted to succinate by Succinyl-CoA thiokinase. This reaction produces GTP [equal to 1ATP].  Succinate dehydrogenase catalyzes the oxidation of succinate to form fumarate and it generates FADH2 [equal to 1.5 ATPs].  The fumarase catalyzed by the addition of water to fumarate to gives malate.  The final enzyme, forwards the reaction of the TCA cycle, the oxidation of malate to oxaloacetate (OAA) by malate dehydrogenase, and this reaction produces NADH [equal to 2.5ATPs]. Finally oxaloacetate is regenerated, thus two carbon atoms form acetyl-coA enter the cycle. Energetics of TCA cycle: Isocitrate dehydrogenase (NADH+H+ ) +2.5 ATP α-Ketoglutarate Dehydrogenase (NADH+H+ ) + 2.5ATP Succinyl Thiokinase [GTP = 1ATP)] + 1 ATPs Succinate Dehydrogenase [FADH2 = 1.5 ATP)] + 1.5 ATPs Malate Dehydrogenase (NADH+H+ ) +2.5 ATP one molecule of acetyl CoA produced no. of ATPs in TCA cycle 10 ATPs Regulation:  Alpha ketoglutarate dehydrogenase is inhibited by NADH, Succinyl-CoA and Arsenate.  Aconitase enzyme is inhibited by fluoroacetate  The key enzymes of the TCA cycle are also regulated allosterically by Ca2+ , ATP and ADP.
  • 7. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Energetics on complete oxidation of glucose: Pathways Total ATPs A. Glycolysis 7 ATPs B. Oxidative decarboxylation of 2 pyruvate to 2 Acetyl CoA [2 x NADH] 5 ATPs C. TCA cycle (2 molecules of acetyl CoA involved 2x10) 20ATPs one molecule of glucose produced total ATPs 32 ATPs Significance of the TCA Cycle:  Final common oxidative pathway and integration of major metabolic pathways  Carbon skeleton of amino acids finally enter the TCA cycle  The TCA cycle is an important source of precursors for the building blocks of many molecules such as amino acids, Nucleotide bases (Purines & Pyrimidines), Cholesterol, and Porphyrin (the organic component of heme). Anabolic and Catabolic nature of TCA cycle
  • 8. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Amphibolic nature of TCA cycle: Amphibolic nature of the TCA cycle is both catabolic and anabolic in nature o Oxaloacetate is precursor for aspartate o Alpha ketoglutarate can be transaminated to glutamate o Succinyl CoA is used for synthesis of heme o Citrate (mitochondrial) is transported to cytoplasm and provides substrate for fatty acid synthesis Anapleurotic reaction: The reactions concerned to replenish or fill up the intermediates of citric acid cycle are called anapleurotic reactions o Pyruvate carboxylase catalyses conversion of pyruvate to oxaloacetate o Pyruvate is converted to malate by NADP+ dependent Malate dehydrogenase (Malic enzyme) o Alpha ketoglutarate is also synthesized from glutamate by glutamate dehydrogenase
  • 9. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry GLYCOGEN METABOLISM Glycogen is the principal storage form of glucose in human body and it is found mainly in cytoplasm of liver and muscle. Stores of glycogen in the liver are considered the main buffer of blood glucose levels. Glycogen metabolism mainly consists of two pathways 1) Anabolic part is glycogenesis 2) Catabolic part is glycogenolysis GLYCOGENESIS (GLYCOGEN SYNTHESIS) Definition: The formation of glycogen from glucose is known as Glycogenesis. Reactions:  Glucose by the enzyme glucokinase or hexokinase to form glucose -6- phosphate then it is converted to glucose-1-P catalysed by phosphoglucomutase enzyme.  UDP glucose is formed from glucose -1 phosphate & UTP by Glucose-1- phosphate uridyl transferase. UDP glucose acts as a donor of glucose.  Activated glucose units are sequentially added by the enzyme glycogen synthase. The glucose moiety from UDP-glucose is transfused to a glycogen primer molecule. Glucose units is added to the non reducing end of the glycogen primer to form an α-1,4-glycosidic linkage and then UDP is liberated  The glycogen synthase can add glucose units only in α-1, 4 linkage.  A branching enzyme is needed to created the α-1, 6 glycosidic linkage. Glucose (6C) Glucose -6-Phosphate (6C) Glucose -1-Phospate UDP-Glucose Glycogen ATP ADP Hexokinase / Glucokinase Phosphoglucomutase UTP PPi Glu-1-P-Uridyl transferase 1,4-Glycosyl Units Glycogen synthase Branching Enzyme Glycogen Primer Reactions of Glycogenesis Glycogenin UDP
  • 10. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  To these newly created branches, further glucose units can be make the molecule more globular and less space consuming, finally it forms glycogen. Regulation of Glycogen Synthesis  Glycogenesis regulated through glycogen synthase enzyme, it is stimulated by high conc. of glucose & insulin, leads to increased synthesis of glycogen.  Glycogen synthase is inhibited by low conc. of glucose, glucagon and epinephrine, leads to decreased synthesis of glycogen. II. GLYCOGENOLYSIS: Definition: Formation of glucose from storage glycogen is known as glycogenolysis. Reactions:  Glycogen Phosphorylase is involved in the conversion of glycogen to glucose-1- phosphate by phosphorolytic cleavage. This enzyme removes glucose units one at a time from the non reducing end of the glycogen molecules.  Phosphorylase sequentially attack α-(1,4)- linkages, till it reaches a glucose residue 3 to 4 glucose units away from a branch point but it doesn’t attack the α-1,6 linkage at branch point, the final product is a highly branched molecule – limit dextrin.  Then a few glucose residues are transferred from the branching point to another branch by enzyme is α-(1, 4) → α-(1, 4) glucose transferase. The branch point is free.  Debranching enzyme α-(1, 6 glucosidase) can hydrolyze the remaining glucosyl unit held in α-(1, 6) linkage at the branch point, it gives free glucose molecules.  Transferase & de branching enzyme will together convert the branch point to a linear one with the removal of branches.  Phosphoglucomutase enzyme converts Glucose-1-phosphate to glucose-6-phosphate. Debranching Enzyme Phosphoglucomutase Limit Dextrin Glucose-1-Phosphate Glucose-6-Phosphate Glucose Glucose-6-Phasphatase Pi H2O Pi Glycogen Glycogen Phosphorylase Glucose Reactions of Glycogenolysis
  • 11. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  Glucose-6-phasphatase hydrolyses glucose -6-P to glucose. Glucose is released to the blood stream for maintaining blood glucose levels. Glucose-6-Phasphatase enzyme is present in liver only.  The conversion of glucose-6-phosphate to glucose does not occur in skeletal muscle because of absence of this enzyme. Regulation of Glycogenolysis  Glycogenolysis regulated by phosphorylase enzyme, it is stimulated by glucagon &adrenaline, leads to increased synthesis of glucose from glycogen.  Phosphorylase is inhibited by high conc. of glucose, insulin, leads to inactivates glycogenolysis. Glycogen Storage Diseases  It is a genetic disorder in which abnormal quantities of glycogen are deposited in the liver, kidney, heart and muscle. Name Enzyme Defect Affected Organ Manifestations TYPE-I : Von Gierke‘s Diseases Glucose-6- phosphatase Liver, Kidney and Intestine. Hepatomegaly, renal disease, growth retardation & delayed puberty TYPE-II: Pompe’s Diseases Lysosomal Acid maltase Skeletal & Cardiac muscle Myopathy, muscular dystrophy TYPE-III: Cori ‘s Diseases Debranching enzyme Liver, skeletal & cardiac muscle Infant hepatomegaly, myopathy TYPE-IV: Andersen Diseases Branching enzyme Liver, muscle Hepatosplenomegaly, cirrhosis TYPE-V: McArdle Diseases Muscle phosphorylase Skeletal muscle Induced cramps and pain, Myoglobinuria TYPE-VI: Her’s Diseases Liver phosphorylase Liver Hepatomegaly, mild hypoglycemia, Hyperlipidemia and ketosis. TYPE-VII: Tarui’s Diseases Muscle PFK-1 Muscle, RBC's Cramps and pain, myoglobinuria , also hemolytic anemia
  • 12. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry GLUCONEOGENESIS Definition: Synthesis of new glucose (i.e. not glucose from glycogen) from non carbohydrate precursors (pyruvate, lactate, glycerol, alanine), a process called gluconeogenesis. The liver is the major site of gluconeogenesis; however, the kidney also has an important part to play in this process. From pyruvate: In gluconeogenesis, three new steps bypass these are irreversible reactions of glycolysis.  Phosphoenolpyruvate (PEP) is formed from pyruvate via oxaloacetate through the action of pyruvate carboxylase & phosphoenolpyruvate carboxylase.  Fructose -6-phosphate is formed from fructose – 1, 6-bisphosphate by hydrolysis of the phosphate ester at C1. It catalyzed by Fructose -1, 6-bis-phosphatase.  This reaction is a major point of control of gluconeogenesis  Glucose is formed by hydrolysis of glucose -6- Phosphate in a reaction catalyzed by glucose-6-phosphatase.
  • 13. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Since skeletal muscle lacks glucose-6-phosphatase, it cannot deliver free glucose to the blood and undergoes gluconeogenesis exclusively as a mechanism to generate glucose for storage as glycogen. From Lactate / Cori cycle:  Lactate is a predominate source of carbon atoms for glucose synthesis by during anaerobic glycolysis occurs in skeletal muscle, pyruvate is reduced to lactate by lactate dehydrogenase (LDH).  After formation of lactate, then released to the blood stream and transported to the liver where it is converted to glucose by gluconeogenesis process.  The glucose is then returned to the blood for use by muscle as an energy source and to replenish glycogen stores. This cycle is called Cori cycle.  The Cori cycle involves the utilization of lactate, produced by glycolysis in non- hepatic tissues, (such as muscle and erythrocytes) as a carbon source for hepatic gluconeogenesis. From Alanine / Glucose-Alanine Cycle:  Pyruvate, generated in muscle and other peripheral tissues, can be transaminated to alanine which is returned to the liver for gluconeogenesis. This pathway is termed as glucose-alanine cycle.  Glucose oxidation produces pyruvate which can undergo transamination to alanine. This reaction is catalyzed by alanine transaminase (ALT). Additionally, during the fasting, skeletal muscle protein is degraded for the energy value of the amino acid carbons and alanine is a major amino acid in protein.  The alanine then enters the blood stream and is transported to the liver. Within the liver alanine is converted back to pyruvate which is then a source of carbon atoms for gluconeogenesis.  The newly formed glucose can then enter the blood for delivery back to the muscle. The amino group transported from the muscle to the liver in the form of alanine is converted to urea in the urea cycle and excreted. From Glycerol:  The glycerol backbone of lipids can be used for gluconeogenesis. This requires phosphorylation to glycerol-3-phosphate by glycerol kinase and dehydrogenation to
  • 14. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry dihydroxyacetone phosphate (DHAP) by glyceraldehyde-3-phosphate dehydrogenase (G3PDH).  The G3PDH reaction is the same as that used in the transport of cytosolic reducing equivalents into the mitochondrion for use in oxidative phosphorylation. This transport pathway is called the glycerol-phosphate shuttle. Regulation of Gluconeogenesis:  Gluconeogenesis stimulated by acetyl CoA, glucagon, glucocorticoids, epinephrine, oxaloacetate, high conc. of citrates and ATPs.  This process inhibited by insulin, ADP, AMP, low conc. of citrates GALACTOSE METABOLISM Galactose is obtained from the milk sugar, lactose (a disaccharide of glucose and galactose), enters glycolysis by its conversion to glucose-1-phosphate. Steps:  First the galactose is phosphorylated by galactokinase to yield galactose-1-phosphate.  Epimerization of galactose-1-P to Glucose-1-P requires the transfer of UDP from UDP- glucose catalyzed by galactose-1-phosphate uridyl transferase. This generates UDP- galactose and Glucose-1-P.  UDP-galactose is epimerized to UDP-glucose by UDP-galactose-4 epimerase.  The UDP portion is exchanged for phosphate generating glucose-1-phosphate, which then is converted to Glucose – 6-phosphate by phosphoglucose mutase.  Glucose -6-phosphate then converted to glucose by glucose-6-phosphatase.
  • 15. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Biomedical importance:  Galactose is required by lactating mammary gland for synthesis of lactose of milk.  Galactose is required for the synthesis of mucopolysaccharides (keratan sulphate & chondroitin sulphate) and glycolipids (Cerebrosides & Gangliosides).  It is mainly used as a test for liver functions called galactose tolerance test. Clinical Significances: Galactosaemia:  It is a rare congenital disease in infants.  Accumulation of galactose & galactose-1-P in blood due to the defect of uridyl transferase and galactokinase. Leads to failure of growth in newborn.  Accumulation of galactose in liver, brain & eye lenses causes liver failure, mental retardation and cataract formation respectively.  Treatment: To decrease lactose in the diet (milk or milk products). Galactosuria:  Galactose is excreted in the urine.  Urine, gives a positive test for reducing substances but a negative test for glucose. FRUCTOSE METABOLISM Reactions:  Hepatic Fructokinases phosphorylates fructose on C1 yielding fructose- 1-phosphate by fructokinase.  In the liver aldolase-B enzyme, splits fructose- 1-phosphate and generates DHAP and glyceraldehyde.  The DHAP is converted, by triose phosphate isomerase, to Glyceraldehyde-3-P and enters glycolysis.  Glyceraldehyde is phosphorylated to glyceraldehyde-3-P by glyceraldehyde kinase.
  • 16. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  Glyceraldehyde-3-P further enters to the glycolytic pathway. Biomedical importance:  Seminal fluid is rich in fructose & spermatozoa utilize fructose for energy.  It is easily metabolized & good source of energy. Clinical Significances: Essential fructosuria:  It is a metabolic disorder caused by the lack of fructokinase, which is normally present in the liver, pancreatic islets and kidney cortex. Hereditary fructose intolerance:  It is a disorder resulting from a lack of aldolase B.  It is characterized by severe hypoglycemia and vomiting  Prolonged intake of fructose by infants with this defect leads to vomiting, poor feeding, hepatic failure and death. HEXOSE MONOPHOSPHATE SHUNT PATHWAY (HMP SHUNT PATHWAY)  It is also called as pentose phosphate pathway.  It is an alternative pathway to glycolysis and TCA cycle for the oxidation of glucose.  HMP Shunt is found in all cells and enzymes of this pathway are present in cytosol.  This pathway is divided into two phases. 1. Oxidative phase 2. Non oxidative phase In Oxidative phase,  Glucose -6-P undergoes dehydrogenation and decarboxylation to give pentose sugar, ribulose-5-P with generation of NADPH. In non oxidation phase:  All the reactions are reversible, Ribulose -5- phosphate further converted to fructose - 6-phosphate and glyceraldehyde-3- phosphate by a series of reactions of epimerization, isomerization, transketolation, transaldolation and transketolation.  Fructose -6 -P & glyceraldehyde-3- phosphate can be further catabolized through glycolysis and TCA cycle. Regulation:  The first step in this pathway, catalyzed by glucose- 6-phosphate dehydrogenase is rate limiting step.
  • 17. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  Insulin, well fed state and low levels of NADPH stimulates HMP shunt.  Starvation & diabetes mellitus and high levels of NADPH inhibits HMP shunt pathway. Significance of HMP shunt pathway:  HMP shunt pathway produced pentoses (ribose-5-P), it required for the biosynthesis of nucleotide & nucleic acid (DNA and RNA). Glucose (6C) 6-Phosphogluconolactone 6-Phosphogluconate Ribulose-5-P Xylulose-5-P Xylulose -5-P Glucose -6-P-Dehydrogenase Hydrolase s Dehydrogenase Epimeras e Ribose-5-P Isomerase Trans Ketolases Trans Aldolase Glyceraldehyde -3-P Sedoheptulose -7-P HMP shunt Pathway NADP+ Erythrose-4-P Fructose-6-P Trans Ketolases Fructose-6-P Glyceraldehyde -3-P NADPH + H+ NADPH + H+ NADP+ Oxidative Phase Non Oxidative Phase H2O + CO2
  • 18. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  It provides a route for the interconversion of pentoses and hexoses.  It generates NADPH, which plays an important for biosynthesis of fatty acids, cholesterol and also involved in detoxification reaction. URONIC ACID PATHWAY (GLUCURONIC ACID CYCLE) Definition:  It is an alternative oxidative pathway for glucose but does not generate ATPs.  In this pathway glucose produces glucuronic acid, ascorbic acid (except in humans) and pentoses Reactions:  Glucose-6-P is converted to glucose-1-phosphate then reacts with UTP to form UDP-Glucose catalysed by mutase and pyrophosphorylase enzymes respectively.  UDP-glucose is oxidized to glucuronate via UDP glucuronate catalyzed by UDP glucose dehydrogenase, further glucuronate is form ascorbic acid (Vitamin-C) and Xylulose, in lower animals.  Xylulose then enters into the HMP shunt pathway to produced pentose sugars. Significance of uronic acid pathway:  Uronic acid pathway is a source of UDP-glucuronate.  UDP glucuronate is a precursor in the biosynthesis of glycosaminoglycans, proteoglycans and glycoproteins. Glucose -6-Phosphate Glucose -1-Phosphate UDP- Glucose UDP-Glucuronate Ascorbic acid (Vitamin-C) UTP PPi Phosphogluco- mutase UDP-Glucose Pyrophosphorylase 2NAD+ + H2O UDP- Glucose Dehydrogenas e Glucuronate H2O Uronic Acid Pathway UDP 2NADH+ + 2H+ Xylulose Pentose Phosphate Pathway
  • 19. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  It is a source of UDP-glucose, which is used for glycogen formation.  It involved in detoxification reactions via conjugation reactions (bilirubin). Disorders: Essential pentosuria:  This condition is inherited in an autosomal recessive disorder.  It is a condition characterized by high levels of L-xylulose in urine. Due to defect of NADP+ dependent L-xylulose dehydrogenase enzyme.  L-xylulose cannot be converted to xylitol so excrete large amount of L-xylulose excreted. REGULATION OF BLOOD SUGAR LEVELS Blood sugar regulation is the process by which levels of blood sugar (glucose), are maintained by the body. The blood glucose is regulated by several metabolic pathways, which are mainly regulated through many hormones. Normal ranges of blood sugars: Fasting blood sugars (FBS) – 70 – 110 mg/dl Post prandial blood sugars (PPBS) – 70 – 140 mg/dl Random blood sugars (RBS) – 70 – 160 mg/dl Mechanisms of blood sugar regulation The glucose levels in the blood are monitored by the cells in the pancreas. In Fasting condition (before food):  If the blood glucose level falls below normal levels, the α-cells of the pancreas release glucagon.  Glucagon increases the blood glucose levels. Converts glycogen into glucose (glycogenolysis), thus increasing the blood sugar levels.  Prolonged fasting condition, glucose is synthesized by gluconeogenesis. Liver is the central organ, which maintains blood glucose levels. In Post prandial condition (after food):  Blood glucose level rises after the meal; insulin hormone is released by the β- cells in the islets of langerhans of the pancreas.  Insulin stimulates the liver to convert more glucose into glycogen (glycogenesis), formation of fat (lipogenesis), thus decreasing the blood sugar.
  • 20. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Hormonal regulations of blood glucose levels: Hormones that influence blood glucose level are a) Hypoglycemic hormones: Insulin only hormone decrease the blood glucose levels in the body.  Insulin hormone produced by β- cells of islets of langerhans of pancrease. Action - Stimulates the uptake of glucose into muscle & other tissues (glycolysis) It promotes the conversion of glucose to glycogen (Glycogenesis) Inhibits the glucose production by the liver (decreased gluconeogenesis) Suppresses breakdown of proteins into amino acids Inhibits the lipolysis in adipose tissue into free fatty acids b) Hyper glycemic hormones: These hormones increase the blood glucose levels in the body. Glucagon: It is a polypeptide hormone secreted by α- cells of pancreas. Action- It stimulates the production of glucose in the liver by glycogenolysis & Gluconeogenesis Inhibits glycolysis Decreases glycogen synthesis Enhance synthesis of glucose from amino acids and fatty acids. Other hormones: Hormones Action Epinephrine (synthesized by adrenal medulla hormone)  Enhances glycogenolysis  Decreases glycolysis.  Enhances release of fatty acids from adipose tissues. Growth hormone Anterior pituitary gland  It stimulates Gluconeogenesis & lipolysis. Cortisol (secreted by adrenal cortex)  Stimulate gluconeogenesis  Increases the breakdown of protein & fats. ACTH (Anterior pituitary)  Enhances release of fatty acids from adipose tissues (lipolysis). Thyroxine (Thyroid gland)  Increases the rate of intestinal glucose absorption.  Enhances glycogenolysis
  • 21. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry DIABETES MELLITUS  It is a metabolic disorder of carbohydrate metabolism, in which glucose levels are increased in blood, leading to producing hyperglycemia.  Diabetes is classified into A. Type 1, Insulin dependent Diabetes mellitus (IDDM) or juvenile onset diabetes. B. Type II, Non Insulin dependent Diabetes mellitus (NIDDM) or adult diabetes Type 1, Diabetes mellitus:  Onset usually occurs in children & youth, less than 20years old.  Due to less production of insulin.  Type-I diabetes due to acute immune destruction of β-cells of pancreas. Symptoms:  Polyuria: production of abnormally large volume of urine.  Polydypsia: increase intake of water (thirst).  Polyphagia: person eats more frequently (hunger).  Lipid & proteins breakdown is increased, it leads to weight loss.  Complication is cataract, neuropathy & nephropathy. Type 2, Diabetes mellitus:  This type usually occurs after the age of 40 years.  It is a result due to loss or less production of insulin..  Patients are not dependent on insulin injections is called as non insulin dependent diabetes mellitus  This type of diabetes can be managed by proper nutrition, exercise, lifestyle changes, oral medication, and insulin, if necessary. Complications of diabetes mellitus  In eyes: Cataract formation  Retinopathy – retinol micro vascular abnormalities, leads to blindness  Neuropathy- dysfunction of one or more peripheral nerves, It is highly risk of foot ulcers and gangrene  Angiopathy- Damage to basement membrane of blood vessels.  Nephropathy- Damage to the glomerulus of kidneys.  And also seen in hyperlipidemia and ketoacidosis  Diabetic Complicating pregnancy: o Diabetic mothers tend to have big babies.
  • 22. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry o Anabolic hormone insulin defect leads to abortion, premature birth & intrauterine death of fetus Symptoms of diabetes  Increased thirst, dry mouth, Weakness & anorexia  Hunger (especially after eating)  Frequent urination  Unexplained weight loss (appetite is normal)  Blurred vision  Tingling of the hands or feet  Slow healing sores or cuts Diabetes risk factors  A family history of diabetes, elderly persons, overweight,  History of hypertension (high blood pressure), abnormal blood cholesterol or triglyceride levels and alcoholics. Management of Diabetes: o To follow a healthy meals plan o Regular exercise o Take proper medication o Test blood suger regularly Diagnosis of Diabetes Mellitus Fasting Blood Glucose (mg/dl) Hb A1c (%) OGTT (mg/dl) Normal < 110 < 5.7 < 140 Pre-diabetic state 100 to 125 5.7 to 6.4 140 to 199 Diabetes Mellitus > 126 > 6.5 > 200 Glucose Challenge Test (GCT): • Glucose Challenge Test (GCT) mainly used for screening of gestational diabetes mellitus. • Usually done this test during 24-28 weeks of gestation • 75 gm of glucose dissolved in 250 ml water was giving to pregnant women during this test
  • 23. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry • Blood sugar estimated after 1 hour • If value >140 mg/dL, GDM is suspected • Diagnosis confirmed by OGTT Interpretation of GCT: Screening: During 24-28 weeks  Negative: Less than 140 mg/dL  Positive: More than 141 mg/dL Confirm Diagnosis: If GCT positive conform by GTT GLUCOSE TOLERANCE TEST (GTT): Glucose tolerance test is a simple and standard test to determine the ability of a person to metabolize a given load of glucose. Definition:  The ability of the body to tolerate the excess load of glucose and to dispose of an additional load of glucose given within the time.  Used to measure changes in blood glucose after glucose load. Preparation of the patient  Good carbohydrate diet for 3 days prior to the test  Diet containing about 30-50 g of carbohydrate should be taken on the evening prior to the test.  Avoid drugs likely to influence the blood glucose levels for at least 2 days prior to the test.  Avoided smoking & exercise on the previous day.  No food after 8 pm the previous night to ensure 12 hours fasting. Procedure: The patient is asked to report after an overnight fast (10-12 hours) in the morning (8am) ↓ Fasting samples (blood & urine) is collected (1st sample) ↓ 75gm of glucose dissolved in 250-300 ml of water, is given orally (1.75g/Kg body weight for children) within 5 min ↓ Samples are collected at intervals of 30, 60, 90, 120 and 150 minutes. ↓ All the blood & Urine samples (6 samples)– estimated for sugar ↓ Blood sugar concentration are plotted in a graph paper against time Note: GOD - POD methods is commonly used for estimation of blood sugar & In urine sugar used benedict’s qualitative method or GOD method (strip method)
  • 24. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry Significance of GTT: GTT useful to diagnose diabetes mellitus in doubtful cases of. – Asymptomatic hyperglycemia or glycosuria – Useful in diagnosis of mild Diabetes – To rule out gestational diabetes mellitus – short GTT during pregnancy – To rule out benign renal glucosuria – Patients with symptoms of diabetes mellitus but with no glycosuria and normal fasting level. – Person with a strong family history of diabetes mellitus but with no symptoms of diabetes mellitus. OGTT respondances: Normal OGTT • Fasting blood glucose is 75-110mg/dl • Oral glucose load(1g/kg wt.) the concentration increases and the peak value (140mg/dl) is seen in less than an hour, it returns to normal by two hours • Glucose is not detected in the urine sample. In Uncontrolled Diabetes Mellitus / Severe Diabetes Mellitus 0 20 40 60 80 100 120 140 160 180 200 0 ½ 1 1 ½ 2 2 ½ Blood Glucose mg% Time in hours
  • 25. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  Fasting blood sample itself is more than normal range  All the blood samples show higher values  Last blood sample does not return to fasting level  All the urine sugars are positive Renal Glycosuria  Due to defective renal reabsorption and decreased renal threshold  Blood glucose is normal in all the samples  Urine sugar is positive in more than one sample Significance of GTT: It is mainly used in the detection of diabetes mellitus under the conditions of 0 20 40 60 80 100 120 140 160 180 200 0 ½ 1 1 ½ 2 2 ½ Blood Glucose mg% time in hours Lower renal threshold 0 50 100 150 200 250 300 350 400 0 ½ 1 1 ½ 2 2 ½ Blood glucose (mg%) Time in hours
  • 26. Metabolism of Carbohydrates & its Disorders Dr. Santhosh Kumar N/ Associate Professor of Biochemistry  This test is useful in distinguishing a person with a normal glucose tolerance from a person who has increased or decreased tolerance. It is of great value in detecting renal glycosuria and endocrine malfunction.  Patients with transient or sustained glycosuria, who have no clinical symptoms of diabetes and with normal, fasting and post prandial blood glucose level.  Patients whose glycosuria is associated with pregnancy, Thyrotoxicosis, liver disease and infections.