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CARBOHYDRATES
AND LIPIDS
BY- SANCHIT DHANKHAR
1. Introduction to biochemistry: Cell and its biochemical organization,
transport process across the cell membranes. Energy rich compounds: ATP,
Cyclic AMP and their biological significance.
2. Biological oxidation: Coenzyme system involved in Biological oxidation.
Electron transport chain (its mechanism in energy capture: regulation and
inhibition): Uncouplers of ETC: Oxidative phosphorylation.
3. Enzymes: Definition: Nomenclature, IUB classification, Factor affecting
enzyme activity, Enzyme action, enzyme inhibition. Isoenzymes and their
therapeutic and diagnostic applications, Coenzymes and their biochemical role
and deficiency diseases.
4. Carbohydrate metabolism: Glycolysis, Citric acid cycle (TCA cycle), HMP
shunt, Glycogenolysis, gluconeogenesis, glycogenesis. Metabolic disorders of
carbohydrate metabolism (diabetes mellitus and glycogen storage diseases):
Glucose, Galactose tolerance test and their significance, hormonal regulation of
carbohydrate metabolism.
5. Lipid metabolism: Oxidation of saturated ( -oxidation): Ketogenesis and
ketolysis, biosynthesis of fatty acids, lipids, metabolism of cholesterol,
Hormonal regulation of lipid metabolism. Defective metabolism of lipids
(Atherosclerosis, fatty liver, hypercholesterolemia).
6. Protein and amino acid metabolism: protein turn over, nitrogen balance,
Catabolism of Amino acids (Transamination, deamination & decarboxylation).Urea
cycle and its metabolic disorders, production of bile pigments,
hyperbilirubinemia, porphoria, jaundice. Metabolic disorder of Amino acids.
7. Nucleic acid metabolism: Metabolism of purine and pyrimidine nucleotides,
Protein synthesis, inhibition of protein synthesis
8. Introduction to clinical chemistry:
a) Urine analysis (macroscopic and physical examination, quantitative and
semi quantitative tests).
b) Test for NPN constituents. (Creatinine /urea clearance, determination of
blood and urine creatinine, urea and uric acid).
c) Test for hepatic dysfunction-Bile pigments metabolism.
d) Test for hepatic function: test- Serum bilirubin, urine bilirubin and urine
urobilinogen.
e) Lipid profile tests: Lipoproteins, composition, functions. Determination of
serum lipids, total cholesterol, HDL cholesterol, LDL cholesterol and
triglycerides.
CARBOHYDRATE
Carbohydrate metabolism: Glycolysis, Citric acid cycle (TCA cycle), HMP
shunt, Glycogenolysis, gluconeogenesis, glycogenesis. Metabolic disorders of
carbohydrate metabolism (diabetes mellitus and glycogen storage diseases):
Glucose, Galactose tolerance test and their significance, hormonal
regulation of carbohydrate metabolism.
METABOLISM OF CARBOHYDRATE
 DEFINATION
 CLASSIFICATION
 GLYCO-LYSIS = (glucose+ -lysis degradation) {glucose to pyruvate}
 GLYCO-NEO-GENESIS= Generation of glucose from non- carbohydrate carbon substrate
such pyruvate,lactate,glycerol,etc {glucose to pyruvate}
 CITRIC ACID (TCA) Tri-carboxylic-acid cycle or Krebs cycle {From pyruvate}
 HMP SHUNT (Hexose-mono-phosphate) or(Phospho-gluconate-pathway)
Is an alternative route for the metabolism of glucose.it does not lead to formation of ATP
but has two major function : 1. formation of NADPH for synthesis of fatty acid and
steroid
2. synthesis of ribose for nucleotide and nuclic acid
formation
 GLYCO-GENESIS = Process of glycogen synthesis, in which glucose molecule are added to
chains of glycogen for storage. {glucose to glycogen}
 GLYCO-GENO-LYSIS= Break down of glycogen(n) to glucose-1-phosphate & glycoge( n-1)
{glycogen to glucose}
Metabolicdisorders-
 Dibetic mellitus.
 Glycogen storage
 Glucose & galactose tolerance test. and significance
 Hormonal regulation of Carb. Meta
 A reducing sugar is any sugar that either has an aldehyde group or is capable of
forming one in solution through isomerism
 A reducing sugar is any sugar that either has an aldehyde group or is capable of forming
one in solution through isomerism.
 The aldehyde functional group allows the sugar to act as a reducing agent, for example
in the Tollens' test or Benedict's reagent, or the Maillard reaction, important in the
browning of many foods.
 The cyclic hemiacetal forms of aldoses can open to reveal an aldehyde and
certain ketoses can undergo tautomerization to become aldoses. However, acetals,
including those found in polysaccharide linkages, cannot easily become free aldehydes.
 Monosaccharides which contain an aldehyde group are known as aldoses, and
those with a ketone group are known as ketoses. The aldehyde can be oxidized
via a redox reaction in which another compound is reduced. Thus, a reducing
sugar is one that reduces certain chemicals.
Nonreducing sugar A sugar that cannot donate electrons to other
molecules and therefore cannot act as a reducing agent.
Sucrose is the most common nonreducing sugar.
The linkage between the glucose and fructose units in sucrose, which
involves aldehyde and ketone groups, is responsible for the inability of
sucrose to act as a reducing sugar.
reducing sugar (elctron accept & change to alde & keto)
Non-reducingsugar
GLYCO-LYSIS (glucose+ -lysis degradation)
01
KINASE is a type of enzyme that catalyzes the transfer of phosphate groups from
high-energy, phosphate-donating molecules to specific substrates
ISOMERASES are a general class of enzymes which convert a molecule from one
isomer to another. Isomerases can either facilitate intramolecular
rearrangements in which bonds are broken and formed or they can catalyze
conformational changes. The general form of such a reaction is as follows:
A–B → B–A
ALDOLASE is an enzyme that catalyses a reversible aldol reaction: The substrate,
fructose 1,6-bisphosphate (F-1,6-BP) is broken down into glyceraldehyde 3-
phosphate and dihydroxyacetone phosphate (DHAP). This reaction is a part of
glycolysis.
MUTASE is an enzyme of the isomerase class that catalyzes the shifting of a
functional group from one position to another within the same molecule.
PATHWAY
GLUCONEOGENESIS
 DEFINITION
The literal meaning of Gluconeogenesis is
GLUCO – glucose; NEO – new; GENESIS – creation.
Thus Gluconeogenesis is a biochemical term that describes the
synthesis of glucose or glycogen from substances which are not
carbohydrates.
Gluconeogenesis is the procedure that generates the energy giving fuel ’
glucose’ from substances other than carbohydrates, which are stored
in the body , when the carbohydrate substrates are not sufficiently
available as in starvation or when they are of great demand as in
intense physical exertion.
02
PATHWAY
HMP Shunt
OXIDATIVE
NON-OXIDATIVE
REGULATION
04
Oxidative phase
In this phase, two molecules of NADP+ are reduced to NADPH, utilizing the energy from the conversion of glucose-
6-phosphate into ribulose 5-phosphate.
Oxidative phase of pentose phosphate pathway.
Glucose-6-phosphate (1), 6-phosphoglucono-δ-lactone (2), 6-phosphogluconate (3), ribulose 5-phosphate (4)
2-PATHWAY
GLYCO-GENESIS = Process of glycogen synthesis, in which glucose
molecule are added to chains of glycogen for storage.(glucose to glycogen)
Definition
 Glycogenesis is the biosynthesis of glycogen, the major
storage form of carbohydrate in animals similar to starch
in plants. Glucose is the major source of energy to the
cells.
 Glucose and its precursors like starch are supplied
through the food we eat and are not reliable and
continuous sources.
 Therefore our body has a built in mechanism which
stores the excess carbohydrates we consume, in the form
of glycogen which could be broken down to glucose
when needed.
05
 Glycogen comes to rescue when the blood glucose drops down, a situation
which prevails between our daily meals.
 The major sites of storage of glycogen are liver and muscle.
 Although the glycogen content of liver is greater than that of muscle, three
quarter of total glycogen is stored in muscles due to their mass.
What is Glycogen ?
Glycogen is a homopolymer made up of repeated units of α D glucose and each
molecule is linked to each other by 1→4 glycosidic bond which is a link connecting
the 1st C atom of the active glucose residue to the 6th C atom of the approaching
glucose molecule.
Once there is a chain consisting of 8 to 10 glycosidic residues in the glycogen
fragment, branching begins by 1→6 linkages. Liver glycogen is synthesized in well
fed states.
Muscle glycogen is synthesized when the muscle glucose get depleted in intense
physical exercise.
 Glycogenenesis pathway is made up of series of steps resulting in the formation of
complex glycogen molecule from α D glucose in the cytoplasm of liver and muscle
cells.
PATHWAY
GLYCO-GENO-LYSIS= Break down of glycogen(n) to glucose-1-
phosphate {glycogen to glucose}
& glycogen( n-1)
 Glycogenolysis is the process of degradation of glycogen to glucose 1
phosphate and glucose in liver and muscle.
 Glycogen serves as the storage form of carbohydrate in our body
corresponding to starch in plants.
 When there is more supply of glucose to our body, immediately after meals,
it gets stored in the form of glycogen in liver and muscles.
 The stored Glycogen comes to rescue when the blood glucose drops down,
a situation which prevails between our daily meals.
Glycogenolysis Pathway
1. Glycogenolysis happens in the major storage organs of glycogen – liver and muscle,
when the body is need of more energy or when the blood glucose is low.
2. Glycogenolysis is not the reversal of Glycogenesis.
It is catalyzed by different set of enzymes. In this process, the
linkages between the glucose residues are broken down, forming glucose 6 phosphate
or free glucose so that it could be used for producing energy.
06
PATHWAY
Role of different hormones in
carbohydrate metabolism:
 The carbohydrate metabolism is regulated & the normal blood sugar level
maintained by a balance between the actions of insulin, Glucocorticoids,
growth hormones, adrenalin & thyroid hormones.
Insulin:
 Insulin increases utilization of glucose in energy production & lipogenesis,
decreases glucose formation from glycogen as well as non-carbohydrates &
indirectly enhances carbohydrate storage in tissues.
 It increases glucose uptake from extracellular fluid by muscles, adipocytes,
mammary glands, lens & many other extra hepatic tissues. It increases
hepatic glucose uptake by inducing synthesis of glucokinase.
 In enhances glycolysis in muscles, liver & other tissues by inducing
synthesis of phosphofructokinase & pyruvate kinase. It also enhances
transcription of genes of pyruvate kinase pathway.
 NADPH formation is stimulated by insulin inducing synthesis of G-6-P
Dehydrogenases (G6PD). In liver it stimulates glycogenesis by promoting
dephosphorylation & activation of glycogen synthase.
Glucagon:
 Glucagon is stimulated by a fall in blood sugar level; it is antagonistic to insulin & increases blood sugar,
lowers liver glycogen.
 It increases glycogenolysis in liver by activating glycogen phosphorylase.
 It prevents dephosphorylation & inactivation of glycogen phosphorylase & induces synthesis of glucose-6-
phosphatase.
 It decreases hepatic glycogenesis & thus reduces the removal of blood glucose by liver.
Adrenalin:
 Adrenaline or epinephrine has glycogenolytic action as it increases blood glucose by enhancing hepatic
glycogenolysis through its binding to β2 & α2 receptors.
 It has gluconeogenic action as it increases hepatic gluconeogenesis (β2- effect), stimulating synthesis of key
enzymes for gluconeogenesis.
 It reduces the utilization of blood glucose by increasing adipose tissue lipolysis.
Glucocorticoids:
 Adrenal Glucocorticoids tend to raise blood sugar. They help to maintain hepatic glycogen during fasting &
Glucocorticoids act as antagonists to insulin.
 It increases gluconeogenesis in liver by inducing synthesis of key gluconeogenesis enzymes. They also
made more gluconeogenic metabolites available.
 They decrease amino acid incorporation into protein by increasing protein catabolism in extra hepatic
tissues.
 They increase hepatic glycogen store by enhancing gluconeogenesis from amino acids, induces gene
transcription for glycogen synthase & activates protein phosphatase.
Growth hormones:
 Growth hormone (GH) is antagonistic to insulin in most of its affects on carbohydrate metabolism.
 It increase hepatic gluconeogenesis & mobilizes fatty acids from adipocytes for utilization.
 GH has diabetogenic effect, i.e. hyperglycemia & glucosauria by inhibiting glucose transport to muscles &
adipose cells.
 GH reduces insulin sensitivity & thereby decreasing the hypoglycemic effects of insulin (anti-insulin effect).
 It can also increase muscle & cardiac glycogen level probably by reducing glycolysis.
Prolactin:
 It has diabetogenic & anti-insulin effects like growth hormones.
Thyroid hormones:
 Thyroid hormones raise blood sugar; reduce glucose tolerance & increases glucose utilization.
 Hyperthyroidism produces hyperglycemia & glucosauria & thyroid hormones are antagonistic to insulin.
 They enhance intestinal absorption rate of glucose.
 Increases hepatic glycogenolysis by enhancing activity of G-6-phosphate & also potentiate the glycogenolytic
affect of adrenaline by up-regulating β-adrenergic receptors.
 They increase glucose oxidation by enhancing the activities of some mitochondrial Oxidoreductases.
 - See more at: http://www.dna2life.com/biochemistry/7-hormones-regulate-carbohydrate-
metabolism#sthash.mfAHSweB.dpuf
LIPIDS
Contents
Lipids
Fatty acids
Sources
Biological Significance of Fatty acids
Biological Synthesis of Fatty acids
Metabolism of Lipids
β-Oxidation
Kitogenesis
Kitolysis
Factor affecting the lipid metabolism (Hormonal)
Cholesterol Metabolism
Clinical Significance of Fatty acids (Disorders)
Lipid metabolism: Oxidation of saturated (oxidation): Ketogenesis and
ketolysis, biosynthesis of fatty acids, lipids, Synthesis & metabolism of
cholesterol, Hormonal regulation of lipid metabolism. Defective metabolism
of lipids (Atherosclerosis, fatty liver, hypercholesterolemia).
LIPID
 Defination:
It may regarded as organic substances relatively insoluble in
water, soluble in organic solvents(alcohol, ether etc.) or potentially
related to fatty acids and utilized by the living cells.
 Classification
I. Simple lipids
● Triacylglycerols TAG (fats)
● Waxes
II. Complex lipids
● Phospholipids
● Sphingopholipidsosph
● Glycolipids
III. Isoprenoids and steroids
Isoprenoids: vitamins A, D, E, K
Steroids: sterols, bile acids, steroid hormones
Function
Essential fatty acids (EFAs) are essential for survival of humans and
other mammals and they cannot be synthesized in the body and
hence, have to be obtained in our diet and thus, are essential.
EFAs form an important constituent of all cell membranes, and
membranes properties of fluidity and thus, determine and influence
the behaviour of membrane-bound enzymes and receptors.
The body can synthesize most of the fats it needs from the diet.
However, two essential fatty acids, linolenic and linoleic acid, cannot be
synthesized in the body and must be obtained from food.
These basic fats, found in plant foods, are used to build specialized fats
called omega-3 and omega-6 fatty acids.
Fatty Acid Synthesis
• Occurs mainly in liver and adipocytes, in mammary glands
during lactation
• Occurs in cytoplasm
• FA synthesis and degradation occur by two completely separate
pathways
• When glucose is plentiful, large amounts of acetyl CoA are
produced by glycolysis and can be used for fatty acid synthesis
Bio-synthesis of
FATTY ACID
1. Production of Acetyl-coA & NADPH
2. Conversion of Acetyl-coA Malonyl CoA
3. Reaction of fatty acid synthase complex----
Five separate stages:
(1) Loading of precursors via thioester derivatives
(2) Condensation of the precursors
(3) Reduction
(4) Dehydration
(5) Reduction
Sources of NADPH for Fatty Acid Synthesis
1. One molecule of NADPH is generated for each molecule of
acetyl CoA that is transferred from mitochondria to the cytosol
(malic enzyme).
2. NADPH molecules come from the pentose phosphate
pathway.
The CO2 group in carboxybiotin is transferred to acetyl CoA to form malonylCoA.
Acetyl CoA carboxylase is the regulatory enzyme.
Five separate stages:
(1) Loading of precursors via thioester
derivatives
(2) Condensation of the precursors
(3) Reduction
(4) Dehydration
(5) Reduction
During the fatty acid synthesis all intermediates are linked to the protein called acyl
carrier protein (ACP-SH), which is the component of fatty acyl synthase complex.
(1) Loading of precursors via thioester derivatives
The elongation phase of fatty acid synthesis starts with
the formation of acetyl ACP and malonyl ACP.
Acetyl transacylase and malonyl transacylase catalyze
these reactions.
Acetyl CoA + ACP  acetyl ACP + CoA
Malonyl CoA + ACP  malonyl ACP + CoA
(2)Condensation reaction.
Acetyl ACP and malonyl ACP react to form
acetoacetyl ACP.
Enzyme - acyl-malonyl ACP
condensing enzyme.
(3)Reduction.
Acetoacetyl ACP is reduced to
D-3-hydroxybutyryl ACP.
NADPH is the reducing agent
Enzyme: -ketoacyl ACP reductase
(4)Dehydration.
D-3-hydroxybutyryl ACP is
dehydrated to form
crotonyl ACP
(trans-2-enoyl ACP).
Enzyme: 3-hydroxyacyl ACP
dehydratase
(trans-2-enoyl ACP).
(5) Reduction.
The final step in the cycle reduces
crotonyl ACP to butyryl ACP.
NADPH is reductant.
Enzyme - enoyl ACP reductase.
This is the end of first
elongation cycle (first round).
(trans-2-enoyl ACP).
In the second round butyryl ACP
condenses with malonyl ACP to
form a C6--ketoacyl ACP.
Reduction, dehydration, and a
second reduction convert the C6--
ketoacyl ACP into a C6-acyl ACP,
which is ready for a third round of
elongation.
(trans-2-enoyl ACP).
• Rounds of synthesis continue until a C16 palmitoyl
group is formed
• Palmitoyl-ACP is hydrolyzed by a thioesterase
Final reaction of FA synthesis
Acetyl CoA + 7 Malonyl CoA + 14 NADPH + 14 H+
Palmitate + 7 CO2 + 14 NADP+ + 8 HS-CoA + 6 H2O
Overall reaction of palmitate synthesis from acetyl
CoA and malonyl CoA
β - Oxidation of
FATTY ACID (Metabolism)
i. Activation of fatty acids occuring in the cytosol
ii. Transport of fatty acids into mitochondria
iii. β – Oxidation proper in the mitochondrial matrix
Beta Oxidation of Fatty Acids
 Process by which fatty acids are degraded by removal of 2-C
units.
 ß-oxidation occurs in the mitochondria matrix
 The 2-C units are released as acetylCoA,not free acetate
 The process begins with oxidation of the carbon that is "beta" to
the carboxyl carbon, so the process is called"betaoxidation"
Fatty acid
ATP (Thio-kinase)
Acyl-adenylate
CoASH
Acyl-COA
• ß-oxidation occurs in the mitochondria, requires import of long chain
acylCoAs
• Acyl-CoAs are converted to acyl-carnitines by carnitine
acyltransferase.
• A translocator then imports Acyl carnitine into the matrix while
simultaneously exporting free carnitine to the cytosol
• Acyl-carnitine is then converted back to acylCoA in the matrix
Deficiencies of carnitine or carnitine transferase or translocator activity
are related to disease state
i. Symptons include muscle cramping during exercise, severe
weakness and death.
ii. Affects muscles, kidney, and heart tissues.
iii. Muscle weakness related to importance of fatty acids as long
term energy source
iv. People with this disease supplement diet with medium chain
fatty acids that do not require carnitine shuttle to enter
mitochondria.
Fatty acid
ATP (Thio-kinase)
Acyl-adenylate
CoASH
Acyl-COA
Activiation
Transport
Oxidation 1
Hydration
Oxidation 2
Thiolysis
Oxidation Synthesis
Localization mitochondria/ cytosol
peroxisomes
Transport Carnitine shuttle Citrate Shuttle
Acyl carrier CoenzymeA AcylCarrierProtein
Carbon units C2 C2
Acceptor/donor AcetylCoA, C2 MalonylCoA, C3
Redox Cofactors FAD, NAD+ NADPH
The Differences Between Fatty Acid
Biosynthesis and Fatty Acid Breakdown
The Differences Between Fatty Acid
Biosynthesis and Fatty Acid Breakdown
The Differences Between
Fatty Acid Biosynthesis and Fatty Acid Breakdown
KETO-GENESIS
&
KETO-LYSIS
The ketone bodies are
 acetoacetate
 β-hydroxybutyrate
 acetone
Ketone Bodies
• A special source of fuel and energy for certain tissues
• Some of the acetyl-CoA produced by fatty acid oxidation in liver
mitochondria is converted to acetone, acetoacetate and
ß-hydroxybutyrate.
• These are called "ketone bodies“
• Source of fuel for brain, heart and muscle
• Major energy source for brain during starvation
• They are transportable forms of fatty acids!
Three are distributed to peripheral tissues (muscle, brain) to be
used for ATP production.
Ketogenesis is the process by which ketone
bodies are produced as a result of fatty acid
breakdown
Water soluble
Easily transportable
Synthesis in liver
Acetoacetate
3-Hydroxybutyrate
Acetone
Ketogensis:
1. In Step 1, two acetyl-CoA molecules combine in a reversible
reaction catalyzed by thiolase to produce acetoacetyl-CoA.
2. In Step 2, a third acetyl-CoA and a water molecule react with
acetoacetyl-CoA to give 3-hydroxy-3-methylglutaryl-CoA
(HMGCoA) in a reaction catalyzed by HMGCoA synthase.
HMGCoA synthase is the regulatory enzyme of
ketone bodies synthesis, it is induced by high fats in blood and
inhibited by synthesis, it is induced by high fats in blood and
inhibited by COASH.
3. In Step 3: 3-hydroxy-3-methylglutaryl-CoA lyase catalyzes the
cleavage of HMGCoA removal of acetyl-CoA produces the
first of the ketone bodies,acetoacetate, the precursor of the other two
ketone bodies produced by ketogenesis, 3-hydroxybutyrate and
acetone.
4. In Step 4: the acetoacetate produced in Step 3 is reduced to
3-hydroxybutyrate by ß-hydroxy butyrate dehydrogenase.
Note that 3-hydroxybutyrate and acetoacetate
are connected by a reversible and NADH-dependant reaction.
Both 3-hydroxybutyrate and acetoacetate can be transported
across the mitochondrial membrane of liver cells blood
stream used as fuel by other body cells used as fuel by
other body cells.
NOTE
 Acetone is a spontaneous breakdown product
of
(a small amount)acetoacetate (decarboxylation)
in the bloodstream, and is excreted primarily
by exhalation, or it is formed by enzymatic
cleavage of acetoacetate by the enzyme
acetoacetate decarboxylase acetone formation
is minimal under normal conditions, while in
severe diabetes acetone odor may be detected
in breath or urinesevere diabetes acetone odor
may be detected in breath or urine
Utilization of ketone bodies at extrahepatic tissues
( Ketolysis):
Under well-fed, healthy conditions, skeletal muscles derive a small
portion of their daily energy needs from acetoacetate, and heart
muscles use it in preference to glucose.
During the early stages of starvation, heart and muscle tissues burn
larger quantities of acetoacetate, thereby preserving glucose for use larger quantities of
acetoacetate, thereby preserving glucose for use in the brain.
In prolonged starvation, even the brain can switch to ketone bodies to meet up to 75% of its
energy needs.
 Ketolysis (utilization of ketone bodies) does not occur in liver because liver does
not contain the enzymes responsible for this
process
ß-hydroxybutyrate is reconverted to
acetoacetate by ß-hydroxybutyrate
Dehyrogenase.
Reactivation of acetoacetate by
mitochondrial enzyme ß-ketoacylCoA
transferase(thiophorase),
CoA transferase(thiophorase),
present in non hepatic tissues, that uses
succinylCoA as source of CoA
Then, acetoacetylCoA is cleaved into
2 acetyl-CoA molecules by thiolase
Enter Kreb’s cycle with production of
energy
THANKYOU

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Carbohydrate & lipid (biochemistry)

  • 2. 1. Introduction to biochemistry: Cell and its biochemical organization, transport process across the cell membranes. Energy rich compounds: ATP, Cyclic AMP and their biological significance. 2. Biological oxidation: Coenzyme system involved in Biological oxidation. Electron transport chain (its mechanism in energy capture: regulation and inhibition): Uncouplers of ETC: Oxidative phosphorylation. 3. Enzymes: Definition: Nomenclature, IUB classification, Factor affecting enzyme activity, Enzyme action, enzyme inhibition. Isoenzymes and their therapeutic and diagnostic applications, Coenzymes and their biochemical role and deficiency diseases. 4. Carbohydrate metabolism: Glycolysis, Citric acid cycle (TCA cycle), HMP shunt, Glycogenolysis, gluconeogenesis, glycogenesis. Metabolic disorders of carbohydrate metabolism (diabetes mellitus and glycogen storage diseases): Glucose, Galactose tolerance test and their significance, hormonal regulation of carbohydrate metabolism. 5. Lipid metabolism: Oxidation of saturated ( -oxidation): Ketogenesis and ketolysis, biosynthesis of fatty acids, lipids, metabolism of cholesterol, Hormonal regulation of lipid metabolism. Defective metabolism of lipids (Atherosclerosis, fatty liver, hypercholesterolemia).
  • 3. 6. Protein and amino acid metabolism: protein turn over, nitrogen balance, Catabolism of Amino acids (Transamination, deamination & decarboxylation).Urea cycle and its metabolic disorders, production of bile pigments, hyperbilirubinemia, porphoria, jaundice. Metabolic disorder of Amino acids. 7. Nucleic acid metabolism: Metabolism of purine and pyrimidine nucleotides, Protein synthesis, inhibition of protein synthesis 8. Introduction to clinical chemistry: a) Urine analysis (macroscopic and physical examination, quantitative and semi quantitative tests). b) Test for NPN constituents. (Creatinine /urea clearance, determination of blood and urine creatinine, urea and uric acid). c) Test for hepatic dysfunction-Bile pigments metabolism. d) Test for hepatic function: test- Serum bilirubin, urine bilirubin and urine urobilinogen. e) Lipid profile tests: Lipoproteins, composition, functions. Determination of serum lipids, total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides.
  • 5. Carbohydrate metabolism: Glycolysis, Citric acid cycle (TCA cycle), HMP shunt, Glycogenolysis, gluconeogenesis, glycogenesis. Metabolic disorders of carbohydrate metabolism (diabetes mellitus and glycogen storage diseases): Glucose, Galactose tolerance test and their significance, hormonal regulation of carbohydrate metabolism.
  • 7.  DEFINATION  CLASSIFICATION  GLYCO-LYSIS = (glucose+ -lysis degradation) {glucose to pyruvate}  GLYCO-NEO-GENESIS= Generation of glucose from non- carbohydrate carbon substrate such pyruvate,lactate,glycerol,etc {glucose to pyruvate}  CITRIC ACID (TCA) Tri-carboxylic-acid cycle or Krebs cycle {From pyruvate}  HMP SHUNT (Hexose-mono-phosphate) or(Phospho-gluconate-pathway) Is an alternative route for the metabolism of glucose.it does not lead to formation of ATP but has two major function : 1. formation of NADPH for synthesis of fatty acid and steroid 2. synthesis of ribose for nucleotide and nuclic acid formation  GLYCO-GENESIS = Process of glycogen synthesis, in which glucose molecule are added to chains of glycogen for storage. {glucose to glycogen}  GLYCO-GENO-LYSIS= Break down of glycogen(n) to glucose-1-phosphate & glycoge( n-1) {glycogen to glucose} Metabolicdisorders-  Dibetic mellitus.  Glycogen storage  Glucose & galactose tolerance test. and significance  Hormonal regulation of Carb. Meta
  • 8.
  • 9.  A reducing sugar is any sugar that either has an aldehyde group or is capable of forming one in solution through isomerism  A reducing sugar is any sugar that either has an aldehyde group or is capable of forming one in solution through isomerism.  The aldehyde functional group allows the sugar to act as a reducing agent, for example in the Tollens' test or Benedict's reagent, or the Maillard reaction, important in the browning of many foods.  The cyclic hemiacetal forms of aldoses can open to reveal an aldehyde and certain ketoses can undergo tautomerization to become aldoses. However, acetals, including those found in polysaccharide linkages, cannot easily become free aldehydes.  Monosaccharides which contain an aldehyde group are known as aldoses, and those with a ketone group are known as ketoses. The aldehyde can be oxidized via a redox reaction in which another compound is reduced. Thus, a reducing sugar is one that reduces certain chemicals. Nonreducing sugar A sugar that cannot donate electrons to other molecules and therefore cannot act as a reducing agent. Sucrose is the most common nonreducing sugar. The linkage between the glucose and fructose units in sucrose, which involves aldehyde and ketone groups, is responsible for the inability of sucrose to act as a reducing sugar. reducing sugar (elctron accept & change to alde & keto) Non-reducingsugar
  • 10. GLYCO-LYSIS (glucose+ -lysis degradation) 01
  • 11.
  • 12. KINASE is a type of enzyme that catalyzes the transfer of phosphate groups from high-energy, phosphate-donating molecules to specific substrates ISOMERASES are a general class of enzymes which convert a molecule from one isomer to another. Isomerases can either facilitate intramolecular rearrangements in which bonds are broken and formed or they can catalyze conformational changes. The general form of such a reaction is as follows: A–B → B–A ALDOLASE is an enzyme that catalyses a reversible aldol reaction: The substrate, fructose 1,6-bisphosphate (F-1,6-BP) is broken down into glyceraldehyde 3- phosphate and dihydroxyacetone phosphate (DHAP). This reaction is a part of glycolysis. MUTASE is an enzyme of the isomerase class that catalyzes the shifting of a functional group from one position to another within the same molecule.
  • 13.
  • 15. GLUCONEOGENESIS  DEFINITION The literal meaning of Gluconeogenesis is GLUCO – glucose; NEO – new; GENESIS – creation. Thus Gluconeogenesis is a biochemical term that describes the synthesis of glucose or glycogen from substances which are not carbohydrates. Gluconeogenesis is the procedure that generates the energy giving fuel ’ glucose’ from substances other than carbohydrates, which are stored in the body , when the carbohydrate substrates are not sufficiently available as in starvation or when they are of great demand as in intense physical exertion. 02
  • 17.
  • 19. Oxidative phase In this phase, two molecules of NADP+ are reduced to NADPH, utilizing the energy from the conversion of glucose- 6-phosphate into ribulose 5-phosphate. Oxidative phase of pentose phosphate pathway. Glucose-6-phosphate (1), 6-phosphoglucono-δ-lactone (2), 6-phosphogluconate (3), ribulose 5-phosphate (4) 2-PATHWAY
  • 20.
  • 21. GLYCO-GENESIS = Process of glycogen synthesis, in which glucose molecule are added to chains of glycogen for storage.(glucose to glycogen) Definition  Glycogenesis is the biosynthesis of glycogen, the major storage form of carbohydrate in animals similar to starch in plants. Glucose is the major source of energy to the cells.  Glucose and its precursors like starch are supplied through the food we eat and are not reliable and continuous sources.  Therefore our body has a built in mechanism which stores the excess carbohydrates we consume, in the form of glycogen which could be broken down to glucose when needed. 05
  • 22.  Glycogen comes to rescue when the blood glucose drops down, a situation which prevails between our daily meals.  The major sites of storage of glycogen are liver and muscle.  Although the glycogen content of liver is greater than that of muscle, three quarter of total glycogen is stored in muscles due to their mass. What is Glycogen ? Glycogen is a homopolymer made up of repeated units of α D glucose and each molecule is linked to each other by 1→4 glycosidic bond which is a link connecting the 1st C atom of the active glucose residue to the 6th C atom of the approaching glucose molecule. Once there is a chain consisting of 8 to 10 glycosidic residues in the glycogen fragment, branching begins by 1→6 linkages. Liver glycogen is synthesized in well fed states. Muscle glycogen is synthesized when the muscle glucose get depleted in intense physical exercise.
  • 23.  Glycogenenesis pathway is made up of series of steps resulting in the formation of complex glycogen molecule from α D glucose in the cytoplasm of liver and muscle cells. PATHWAY
  • 24. GLYCO-GENO-LYSIS= Break down of glycogen(n) to glucose-1- phosphate {glycogen to glucose} & glycogen( n-1)  Glycogenolysis is the process of degradation of glycogen to glucose 1 phosphate and glucose in liver and muscle.  Glycogen serves as the storage form of carbohydrate in our body corresponding to starch in plants.  When there is more supply of glucose to our body, immediately after meals, it gets stored in the form of glycogen in liver and muscles.  The stored Glycogen comes to rescue when the blood glucose drops down, a situation which prevails between our daily meals. Glycogenolysis Pathway 1. Glycogenolysis happens in the major storage organs of glycogen – liver and muscle, when the body is need of more energy or when the blood glucose is low. 2. Glycogenolysis is not the reversal of Glycogenesis. It is catalyzed by different set of enzymes. In this process, the linkages between the glucose residues are broken down, forming glucose 6 phosphate or free glucose so that it could be used for producing energy. 06
  • 26. Role of different hormones in carbohydrate metabolism:  The carbohydrate metabolism is regulated & the normal blood sugar level maintained by a balance between the actions of insulin, Glucocorticoids, growth hormones, adrenalin & thyroid hormones. Insulin:  Insulin increases utilization of glucose in energy production & lipogenesis, decreases glucose formation from glycogen as well as non-carbohydrates & indirectly enhances carbohydrate storage in tissues.  It increases glucose uptake from extracellular fluid by muscles, adipocytes, mammary glands, lens & many other extra hepatic tissues. It increases hepatic glucose uptake by inducing synthesis of glucokinase.  In enhances glycolysis in muscles, liver & other tissues by inducing synthesis of phosphofructokinase & pyruvate kinase. It also enhances transcription of genes of pyruvate kinase pathway.  NADPH formation is stimulated by insulin inducing synthesis of G-6-P Dehydrogenases (G6PD). In liver it stimulates glycogenesis by promoting dephosphorylation & activation of glycogen synthase.
  • 27. Glucagon:  Glucagon is stimulated by a fall in blood sugar level; it is antagonistic to insulin & increases blood sugar, lowers liver glycogen.  It increases glycogenolysis in liver by activating glycogen phosphorylase.  It prevents dephosphorylation & inactivation of glycogen phosphorylase & induces synthesis of glucose-6- phosphatase.  It decreases hepatic glycogenesis & thus reduces the removal of blood glucose by liver. Adrenalin:  Adrenaline or epinephrine has glycogenolytic action as it increases blood glucose by enhancing hepatic glycogenolysis through its binding to β2 & α2 receptors.  It has gluconeogenic action as it increases hepatic gluconeogenesis (β2- effect), stimulating synthesis of key enzymes for gluconeogenesis.  It reduces the utilization of blood glucose by increasing adipose tissue lipolysis. Glucocorticoids:  Adrenal Glucocorticoids tend to raise blood sugar. They help to maintain hepatic glycogen during fasting & Glucocorticoids act as antagonists to insulin.  It increases gluconeogenesis in liver by inducing synthesis of key gluconeogenesis enzymes. They also made more gluconeogenic metabolites available.  They decrease amino acid incorporation into protein by increasing protein catabolism in extra hepatic tissues.  They increase hepatic glycogen store by enhancing gluconeogenesis from amino acids, induces gene transcription for glycogen synthase & activates protein phosphatase.
  • 28. Growth hormones:  Growth hormone (GH) is antagonistic to insulin in most of its affects on carbohydrate metabolism.  It increase hepatic gluconeogenesis & mobilizes fatty acids from adipocytes for utilization.  GH has diabetogenic effect, i.e. hyperglycemia & glucosauria by inhibiting glucose transport to muscles & adipose cells.  GH reduces insulin sensitivity & thereby decreasing the hypoglycemic effects of insulin (anti-insulin effect).  It can also increase muscle & cardiac glycogen level probably by reducing glycolysis. Prolactin:  It has diabetogenic & anti-insulin effects like growth hormones. Thyroid hormones:  Thyroid hormones raise blood sugar; reduce glucose tolerance & increases glucose utilization.  Hyperthyroidism produces hyperglycemia & glucosauria & thyroid hormones are antagonistic to insulin.  They enhance intestinal absorption rate of glucose.  Increases hepatic glycogenolysis by enhancing activity of G-6-phosphate & also potentiate the glycogenolytic affect of adrenaline by up-regulating β-adrenergic receptors.  They increase glucose oxidation by enhancing the activities of some mitochondrial Oxidoreductases.  - See more at: http://www.dna2life.com/biochemistry/7-hormones-regulate-carbohydrate- metabolism#sthash.mfAHSweB.dpuf
  • 30. Contents Lipids Fatty acids Sources Biological Significance of Fatty acids Biological Synthesis of Fatty acids Metabolism of Lipids β-Oxidation Kitogenesis Kitolysis Factor affecting the lipid metabolism (Hormonal) Cholesterol Metabolism Clinical Significance of Fatty acids (Disorders)
  • 31. Lipid metabolism: Oxidation of saturated (oxidation): Ketogenesis and ketolysis, biosynthesis of fatty acids, lipids, Synthesis & metabolism of cholesterol, Hormonal regulation of lipid metabolism. Defective metabolism of lipids (Atherosclerosis, fatty liver, hypercholesterolemia).
  • 32. LIPID  Defination: It may regarded as organic substances relatively insoluble in water, soluble in organic solvents(alcohol, ether etc.) or potentially related to fatty acids and utilized by the living cells.  Classification I. Simple lipids ● Triacylglycerols TAG (fats) ● Waxes II. Complex lipids ● Phospholipids ● Sphingopholipidsosph ● Glycolipids III. Isoprenoids and steroids Isoprenoids: vitamins A, D, E, K Steroids: sterols, bile acids, steroid hormones
  • 33.
  • 34. Function Essential fatty acids (EFAs) are essential for survival of humans and other mammals and they cannot be synthesized in the body and hence, have to be obtained in our diet and thus, are essential. EFAs form an important constituent of all cell membranes, and membranes properties of fluidity and thus, determine and influence the behaviour of membrane-bound enzymes and receptors. The body can synthesize most of the fats it needs from the diet. However, two essential fatty acids, linolenic and linoleic acid, cannot be synthesized in the body and must be obtained from food. These basic fats, found in plant foods, are used to build specialized fats called omega-3 and omega-6 fatty acids.
  • 35. Fatty Acid Synthesis • Occurs mainly in liver and adipocytes, in mammary glands during lactation • Occurs in cytoplasm • FA synthesis and degradation occur by two completely separate pathways • When glucose is plentiful, large amounts of acetyl CoA are produced by glycolysis and can be used for fatty acid synthesis
  • 36. Bio-synthesis of FATTY ACID 1. Production of Acetyl-coA & NADPH 2. Conversion of Acetyl-coA Malonyl CoA 3. Reaction of fatty acid synthase complex---- Five separate stages: (1) Loading of precursors via thioester derivatives (2) Condensation of the precursors (3) Reduction (4) Dehydration (5) Reduction
  • 37.
  • 38. Sources of NADPH for Fatty Acid Synthesis 1. One molecule of NADPH is generated for each molecule of acetyl CoA that is transferred from mitochondria to the cytosol (malic enzyme). 2. NADPH molecules come from the pentose phosphate pathway.
  • 39. The CO2 group in carboxybiotin is transferred to acetyl CoA to form malonylCoA. Acetyl CoA carboxylase is the regulatory enzyme.
  • 40. Five separate stages: (1) Loading of precursors via thioester derivatives (2) Condensation of the precursors (3) Reduction (4) Dehydration (5) Reduction
  • 41. During the fatty acid synthesis all intermediates are linked to the protein called acyl carrier protein (ACP-SH), which is the component of fatty acyl synthase complex. (1) Loading of precursors via thioester derivatives
  • 42. The elongation phase of fatty acid synthesis starts with the formation of acetyl ACP and malonyl ACP. Acetyl transacylase and malonyl transacylase catalyze these reactions. Acetyl CoA + ACP  acetyl ACP + CoA Malonyl CoA + ACP  malonyl ACP + CoA
  • 43. (2)Condensation reaction. Acetyl ACP and malonyl ACP react to form acetoacetyl ACP. Enzyme - acyl-malonyl ACP condensing enzyme.
  • 44. (3)Reduction. Acetoacetyl ACP is reduced to D-3-hydroxybutyryl ACP. NADPH is the reducing agent Enzyme: -ketoacyl ACP reductase
  • 45. (4)Dehydration. D-3-hydroxybutyryl ACP is dehydrated to form crotonyl ACP (trans-2-enoyl ACP). Enzyme: 3-hydroxyacyl ACP dehydratase (trans-2-enoyl ACP).
  • 46. (5) Reduction. The final step in the cycle reduces crotonyl ACP to butyryl ACP. NADPH is reductant. Enzyme - enoyl ACP reductase. This is the end of first elongation cycle (first round). (trans-2-enoyl ACP).
  • 47. In the second round butyryl ACP condenses with malonyl ACP to form a C6--ketoacyl ACP. Reduction, dehydration, and a second reduction convert the C6-- ketoacyl ACP into a C6-acyl ACP, which is ready for a third round of elongation.
  • 49. • Rounds of synthesis continue until a C16 palmitoyl group is formed • Palmitoyl-ACP is hydrolyzed by a thioesterase Final reaction of FA synthesis Acetyl CoA + 7 Malonyl CoA + 14 NADPH + 14 H+ Palmitate + 7 CO2 + 14 NADP+ + 8 HS-CoA + 6 H2O Overall reaction of palmitate synthesis from acetyl CoA and malonyl CoA
  • 50. β - Oxidation of FATTY ACID (Metabolism) i. Activation of fatty acids occuring in the cytosol ii. Transport of fatty acids into mitochondria iii. β – Oxidation proper in the mitochondrial matrix
  • 51. Beta Oxidation of Fatty Acids  Process by which fatty acids are degraded by removal of 2-C units.  ß-oxidation occurs in the mitochondria matrix  The 2-C units are released as acetylCoA,not free acetate  The process begins with oxidation of the carbon that is "beta" to the carboxyl carbon, so the process is called"betaoxidation"
  • 53.
  • 54. • ß-oxidation occurs in the mitochondria, requires import of long chain acylCoAs • Acyl-CoAs are converted to acyl-carnitines by carnitine acyltransferase. • A translocator then imports Acyl carnitine into the matrix while simultaneously exporting free carnitine to the cytosol • Acyl-carnitine is then converted back to acylCoA in the matrix
  • 55. Deficiencies of carnitine or carnitine transferase or translocator activity are related to disease state i. Symptons include muscle cramping during exercise, severe weakness and death. ii. Affects muscles, kidney, and heart tissues. iii. Muscle weakness related to importance of fatty acids as long term energy source iv. People with this disease supplement diet with medium chain fatty acids that do not require carnitine shuttle to enter mitochondria.
  • 56.
  • 59. Oxidation Synthesis Localization mitochondria/ cytosol peroxisomes Transport Carnitine shuttle Citrate Shuttle Acyl carrier CoenzymeA AcylCarrierProtein Carbon units C2 C2 Acceptor/donor AcetylCoA, C2 MalonylCoA, C3 Redox Cofactors FAD, NAD+ NADPH The Differences Between Fatty Acid Biosynthesis and Fatty Acid Breakdown The Differences Between Fatty Acid Biosynthesis and Fatty Acid Breakdown The Differences Between Fatty Acid Biosynthesis and Fatty Acid Breakdown
  • 60. KETO-GENESIS & KETO-LYSIS The ketone bodies are  acetoacetate  β-hydroxybutyrate  acetone
  • 61.
  • 62. Ketone Bodies • A special source of fuel and energy for certain tissues • Some of the acetyl-CoA produced by fatty acid oxidation in liver mitochondria is converted to acetone, acetoacetate and ß-hydroxybutyrate. • These are called "ketone bodies“ • Source of fuel for brain, heart and muscle • Major energy source for brain during starvation • They are transportable forms of fatty acids! Three are distributed to peripheral tissues (muscle, brain) to be used for ATP production.
  • 63. Ketogenesis is the process by which ketone bodies are produced as a result of fatty acid breakdown
  • 64. Water soluble Easily transportable Synthesis in liver Acetoacetate 3-Hydroxybutyrate Acetone
  • 65.
  • 66. Ketogensis: 1. In Step 1, two acetyl-CoA molecules combine in a reversible reaction catalyzed by thiolase to produce acetoacetyl-CoA. 2. In Step 2, a third acetyl-CoA and a water molecule react with acetoacetyl-CoA to give 3-hydroxy-3-methylglutaryl-CoA (HMGCoA) in a reaction catalyzed by HMGCoA synthase. HMGCoA synthase is the regulatory enzyme of ketone bodies synthesis, it is induced by high fats in blood and inhibited by synthesis, it is induced by high fats in blood and inhibited by COASH.
  • 67. 3. In Step 3: 3-hydroxy-3-methylglutaryl-CoA lyase catalyzes the cleavage of HMGCoA removal of acetyl-CoA produces the first of the ketone bodies,acetoacetate, the precursor of the other two ketone bodies produced by ketogenesis, 3-hydroxybutyrate and acetone. 4. In Step 4: the acetoacetate produced in Step 3 is reduced to 3-hydroxybutyrate by ß-hydroxy butyrate dehydrogenase. Note that 3-hydroxybutyrate and acetoacetate are connected by a reversible and NADH-dependant reaction. Both 3-hydroxybutyrate and acetoacetate can be transported across the mitochondrial membrane of liver cells blood stream used as fuel by other body cells used as fuel by other body cells.
  • 68. NOTE  Acetone is a spontaneous breakdown product of (a small amount)acetoacetate (decarboxylation) in the bloodstream, and is excreted primarily by exhalation, or it is formed by enzymatic cleavage of acetoacetate by the enzyme acetoacetate decarboxylase acetone formation is minimal under normal conditions, while in severe diabetes acetone odor may be detected in breath or urinesevere diabetes acetone odor may be detected in breath or urine
  • 69. Utilization of ketone bodies at extrahepatic tissues ( Ketolysis): Under well-fed, healthy conditions, skeletal muscles derive a small portion of their daily energy needs from acetoacetate, and heart muscles use it in preference to glucose. During the early stages of starvation, heart and muscle tissues burn larger quantities of acetoacetate, thereby preserving glucose for use larger quantities of acetoacetate, thereby preserving glucose for use in the brain. In prolonged starvation, even the brain can switch to ketone bodies to meet up to 75% of its energy needs.  Ketolysis (utilization of ketone bodies) does not occur in liver because liver does not contain the enzymes responsible for this process
  • 70. ß-hydroxybutyrate is reconverted to acetoacetate by ß-hydroxybutyrate Dehyrogenase. Reactivation of acetoacetate by mitochondrial enzyme ß-ketoacylCoA transferase(thiophorase), CoA transferase(thiophorase), present in non hepatic tissues, that uses succinylCoA as source of CoA Then, acetoacetylCoA is cleaved into 2 acetyl-CoA molecules by thiolase Enter Kreb’s cycle with production of energy