Tapeshwar Yadav, profile picture
Uploaded byTapeshwar Yadav
PPT, PDF79,176 views

Carbohydrate metabolism

The document provides a comprehensive overview of carbohydrate metabolism, detailing the definitions, significance, digestion, and various metabolic pathways involving carbohydrates. Key processes such as glycolysis, aerobic oxidation, the tricarboxylic acid cycle, and the pentose phosphate pathway are explained along with their enzymes and regulation mechanisms. Additionally, the document discusses the significance of glycogen synthesis and catabolism.

Embed presentation

Downloaded 1,219 times
1 / 108
2 / 108
3 / 108
4 / 108
5 / 108
6 / 108
7 / 108
8 / 108
9 / 108
10 / 108
11 / 108
12 / 108
13 / 108
14 / 108
15 / 108
16 / 108
17 / 108
18 / 108
19 / 108
20 / 108
21 / 108
22 / 108
23 / 108
24 / 108
25 / 108
26 / 108
27 / 108
28 / 108
29 / 108
30 / 108
31 / 108
32 / 108
33 / 108
34 / 108
35 / 108
36 / 108
37 / 108
38 / 108
39 / 108
40 / 108
41 / 108
42 / 108
43 / 108
44 / 108
45 / 108
46 / 108
47 / 108
48 / 108
49 / 108
50 / 108
51 / 108
52 / 108
53 / 108
54 / 108
55 / 108
56 / 108
57 / 108
58 / 108
59 / 108
60 / 108
61 / 108
62 / 108
63 / 108
64 / 108
65 / 108
66 / 108
67 / 108
68 / 108
69 / 108
70 / 108
71 / 108
72 / 108
73 / 108
74 / 108
75 / 108
76 / 108
77 / 108
78 / 108
79 / 108
80 / 108
81 / 108
82 / 108
83 / 108
84 / 108
85 / 108
86 / 108
87 / 108
88 / 108
89 / 108
Most read
90 / 108
91 / 108
92 / 108
93 / 108
94 / 108
95 / 108
96 / 108
97 / 108
Most read
98 / 108
99 / 108
100 / 108
101 / 108
102 / 108
Most read
103 / 108
104 / 108
105 / 108
106 / 108
107 / 108
108 / 108
Carbohydrate Metabolism Mr.Tapeshwar Yadav. II year M.Sc. Biochemistry Mamata Medical College Khammam
Carbohydrates Definition : Carbohydrates are polyhydroxy aldehydes or ketones.
Biological significance of Carbohydrates •These are major source of energy for living organisms. •Supplying a huge array of metabolic intermediates for biosynthetic reactions. •The structural elements in cell coat or connective tissues.
Digestion : • Partly digested in mouth by salivary amylase. • In stomach there is no digestion takes place. • Complete digestion and absorption will be taken place at small intestine
Glucose transporters (GLUT) • There are 5 types GLUT –GLUT1: RBC –GLUT4: Adipose tissue, Muscle
The metabolism of glucose •Aerobic oxidation •Glycolysis •Gluconeogenesis •Pentose phosphate pathway •Glycogenesis •Glycogenolysis •Uronic acid pathway
Glycogen Glycogenesis Glycogenolysis Pentose phosphate pathway Ribose, NADPH Glycolysis Pyruvate/ Lactate H2O+CO2 Aerobicoxidation Digestion absorption Starch Lactate, Amino acids, Glycerol Glucose Gluconeo -genesis
Aerobic oxidation • C6H12O6 6H2O+6CO2 + Energy (in the form of heat)
Glycolysis
•The anaerobic catabolic pathway by which a molecule of glucose is broken down into two molecules of lactate. Glucose → 2 Lactic acid (lack of O2) •All of the enzymes of glycolysis locate in cytosol.
Glycolysis overview Glucose Pyruvate Lactic acid Glycolysis If O2 is not available
1) Glycolytic pathway : Glucose → Pyruvate including 10 reactions.
•Phosphorylated Glucose cannot get out from cell. •Hexokinase (having 4 Isoenzymes). •Glucokinase, GK in liver. •Irreversible. (1) Glucose is phosphorylated to Glucose 6-phosphate OH OH H OH H OHH OH CH2 H HO OH OH H OH H OHH OH CH2 H OP ATP ADP Hexokinase Mg2+ G G-6-P
Particulars Hexokinase Glucokinase Occurrence in all tissues only in liver Km value 0.1mmol/L 10mmol/L Substrate Glucose, Fructose, Mannose Glucose Regulation G-6-P Insulin Comparison of Hexokinase and Glucokinase
(2) G-6-P is isomerised to Fructose 6-P OH OH H OH H OHH OH CH2 H OP G-6-P isomerase OH CH2OH H CH2 OH H H OH O OP F-6-P
(3) F-6-P is phosphorylated Fructose 1,6-bisphosphate •The second phosphorylation •Phosphofructokinase-1, PFK-1 OH CH2OH H CH2 OH H H OH O OP F-1,6-BP OH CH2 H CH2 OH H H OH O OP O P ATP ADP Mg2+ F-6-P PFK-1
(4) F-1,6-BP cleaved to 2 Triose phosphates •Reversible F-1,6-BP CH2 C O C HHO C OHH C OHH CH2 O P O P CH2 C O O P CHO CHOH CH2 O PCH2OH + aldolase dihydroxyacetone phosphate, DHAP glyceraldehyde 3-phosphate, GAP
(5) Triose phosphate isomerization G→2 molecule glyceraldehyde-3- phosphate, consume 2 ATP . CH2 C O O P CHO CHOH CH2 O PCH2OH DHAP GAP phosphotriose isomerase
(6) Glyceraldehyde 3-phosphate oxidised 1,3-bisphospho glycerate CHO CHOH CH2 O P NAD+ NADH+H + Pi glyceraldehyde 3-phosphate dehydrogenase, GAPDH C CHOH CH2 O P O O~ P glycerate 1,3-bisphosphate, 1,3-BPG glyceraldehyde 3-phosphate
(7) 1,3-BPG dephosphorylated to 3- phospho glycerate • Substrate level phosphorylation COO- CHOH CH2 O P C CHOH CH2 O P O O~ P ADP ATP glycerate 1,3-bisphosphate glycerate 3-phosphate Phosphoglycerate kinase
(8) Glycerate 3-phosphate mutated glycerate 2-phosphate COO- CHOH CH2 O P COO- CH CH2OH O P glycerate 3-phosphate glycerate 2-phosphate Mutase
(9) Glycerate 2-phosphate → phosphoenol pyruvate COO- CH CH2OH O P COO- C CH2 O PEP ~ P + H2O enolase glycerate 2-phosphate
(10) PEP →pyruvate • Second substrate level phosphorylation • irreversible COO- C CH3 ADP ATP COO- C CH2 O PEP ~ P pyruvate kinase O Pyruvate
2) Pyruvate → lactate COO C CH3 NAD+NADH + H+ O Pyr COO CHOH CH3 Lactate dehydrogenase, LDH Lactic acid
Summary of Glycolysis ATP ADP Mg2+ PFK-1 GAP DHAP glycerate 1,3-bisphosphate NADH+H+ glyceraldehyde 3-phosphate dehydrogenase H3PO4 NADH+H+ NAD+ ADP ATP glycerate 3-phosphate glycerate 2-phosphate H2O PEP ATP ADP pyruvate kinase lactate pyruvate G G-6-P F- 6-P F- 1,6-BP NAD+ Phosphoglycerate kinase Isomerase Aldolase Mutase Enolase LDH HK ATP ADP Mg2+
Total reaction: C6H12O6 + 2ADP + 2Pi 2CH3CHOHCOOH + 2ATP + 2H2O Formation of ATP: The net yield is 2 ~P or 2 molecules of ATP per glucose.
2. Regulation of Glycolysis • Three key enzymes catalyze irreversible reactions : Hexokinase, Phosphofructokinase & Pyruvate Kinase.
1) PFK-1 The reaction catalyzed by PFK-1 is usually the rate-limiting step of the Glycolysis pathway. This enzyme is regulated by covalent modification, allosteric regulation.
bifunctional enzyme
2) Pyruvate kinase • Allosteric regulation: F-1,6-BP acts as allosteric activator ； ATP and Ala in liver act as allosteric inhibitors;
• Covalent modification: phosphorylated by Glucagon through cAMP and PKA and inhibited. ATP ADP PKA Glucagon Pyruvate Kinase (active) Pyruvate Kinase- P (inactive) cAMP
3) Hexokinase and glucokinase • This enzyme is regulated by covalent modification, allosteric regulation and isoenzyme regulation. • Inhibited by its product G-6-P. • Insulin induces synthesis of glucokinase.
3. Significance of glycolysis 1) Glycolysis is the emergency energy- yielding pathway. 2) Glycolysis is the main way to produce ATP in some tissues, even though the oxygen supply is sufficient, such as red blood cells, retina, testis, skin, medulla of kidney. • In glycolysis, 1mol G produces 2mol lactic acid and 2mol ATP.
§ 3 Aerobic Oxidation of Glucose
• The process of complete oxidation of glucose to CO2 and water with liberation of energy as the form of ATP is named aerobic oxidation. • The main pathway of G oxidation.
1. Process of aerobic oxidation G Pyr cytosol Mitochodria glycolytic pathway second stage third stage CO2 + H2O+ATPPyr CH3CO~SCoA first stage TAC
1) Oxidative decarboxylation of Pyruvate to Acetyl CoA • irreversible; • in mitochodria. COO- C CH3 NAD+ NADH + H + O pyruvate CH3C Pyruvate dehydrogenase complex Acetyl CoA O ~SCoA+ HSCoA + CO2
Pyruvate dehydrogenase complex: E1 pyruvate dehydrogenase Es E2 dihydrolipoyl transacetylase E3 dihydrolipoyl dehydrogenase thiamine pyrophosphate, TPP (VB1 ) HSCoA (pantothenic acid) cofactors lipoic Acid NAD+ (Vpp) FAD (VB2 )
HSCoA NAD+ Pyruvate dehydrogenase complex:
The structure of pyruvate dehydrogenase complex
S S CH H2 C H2C (CH2)4 COOH SH SH CH H2 C H2C (CH2)4 COOH +2H - 2H lipoic acid dihydrolipoic acid C C NH2 HC N C H2 S C C N C N C H CH3 CH2CH2H3C O P O O- O P O O- O- + TPP
HSCoA HS CH2 CH2 NH C CH2 O CH2 NH C C O OH H C CH2 CH3 CH3 O P O OH O P OH O O 3'AMP ¦Â-alanine pantoic acid pyrophosphate pantothenic acid 4'-phosphopantotheine ¦Â-mercapto- ethylamine
CO2 CoASH NAD+ NADH +H+
2) Tricarboxylic acid cycle, TCAC • The cycle comprises the combination of a molecule of acetyl-CoA with oxaloacetate, resulting in the formation of a six-carbon tricarboxylic acid, citrate. There follows a series of reactions in the course of which two molecules of CO2 are released and oxaloacetate is regenerated. • Also called citrate cycle or Krebs cycle.
(1) Process of reactions
Citrate cycle CO CH2 COO COO CH3CO~SCoA C CH2 COO COO CH2 HO COO C CH COO COO CH2 COO CH CH COO COO CH2 COO H2O H2O HO CO2 CH2 CH2 COCOO COOCH2 CH2 COO CO~ SCoA CO2 NAD+NADH+H+ CH2 CH2 COO COO GDP+PiGTP CH CH2 COO COO OOC CH C COOH HO NAD+ NADH+H+ FAD FADH2 H2O acetyl CoA H2O oxaloacetate citrate synthase citrate aconitase cis-aconitate aconitase isocitrate NAD+ NADH+H+ isocitrate dehydrogenase ¦Á-keto- glutarate ¦Á-ketoglutarate dehydrogenase complex succinyl-CoA ADP ATP CoASH succinyl CoA syntetase succinate dehydrogenase fumarate succinate fumarase malate malate dehydrogenase HSCoA HSCoA
Summary of Krebs Cycle ① Reducing equivalents
② The net reaction of the TCAC: acetylCoA+3NAD+ +FAD+GDP+Pi+2H2O →2CO2+3NADH+3H+ +FADH2+GTP+ HSCoA ③ Irreversible and aerobic reaction ④ The enzymes are located in the mitochondrial matrix.
⑤ Anaplerotic reaction of oxaloacetate pyruvate carboxylase Biotin ATP ADP + Pi + CO2C CH3 COOH O C C COOH COOH O H2 NAD+ NADH+H+ malic acid DH + CO2 malic enzyme C CH3 COOH O NADPH+H+ NADP+ CHOH C COOH COOH C C COOH COOH O H2H2
(2) Bio-significance of TCAC ① Acts as the final common pathway for the oxidation of carbohydrates, lipids, and proteins. ② Serves as the crossroad for the interconversion among carbohydrates, lipids, and non-essential amino acids, and as a source of biosynthetic intermediates.
Krebs Cycle is at the hinge of metabolism.
2. ATP produced in the aerobic oxidation • acetyl CoA → TCAC : 3 (NADH+H+ ) + FADH2 + 1GTP → 12 ATP. • pyruvate →acetyl CoA: NADH+H+ →3 ATP • 1 G → 2 pyruvate : 2(NADH+H+ ) → 6 or 8ATP 1mol G ： 36 or 38mol ATP （ 12 ＋ 3 ） ×2 ＋ 6 （ 8 ）＝ 36 （ 38 ）
3. The regulation of aerobic oxidation • The Key Enzymes of aerobic oxidation The Key Enzymes of glycolysis Pyruvate Dehydrogenase Complex Citrate synthase Isocitrate dehydrogenase (rate-limiting ) α-Ketoglutarate dehydrogenase
(1) Pyruvate dehydrogenase complex Pyruvate dehydrogenase (active form) allosteric inhibitors: ATP, acetyl CoA, NADH, FA allosteric activators: AMP, CoA, NAD+ ,Ca2+ pyruvate dehydrogenase (inactive form) P pyruvate dehydrogenase kinase pyruvate dehydrogenase phosphatase ATP ADPH2O Pi Ca2+ ,insulin acetyl CoA, NADH ADP, NAD+
(2) Citrate synthase • Allosteric activator: ADP • Allosteric inhibitor: NADH, succinyl CoA, citrate, ATP (3) Isocitrate dehydrogenase • Allosteric activator: ADP, Ca2+ • Allosteric inhibitor: ATP (4) α-Ketoglutarate dehydrogenase • Similar with Pyruvate dehydrogenase complex
Oxidative phosphorylation→TCAC↑ •ATP/ADP↑ inhibit TCAC, Oxidative phosphorylation ↓ •ATP/ADP↓ ， promote TCAC ， Oxidative phosphorylation ↑
4. Pasteur Effect • Under aerobic conditions, glycolysis is inhibited and this inhibitory effect of oxygen on glycolysis is known as Pasteur effect. • The key point is NADH ： NADH mitochondria Pyr TCAC CO2 ＋ H2O Pyr can’t produce to lactate.
§4 Pentose Phosphate Pathway
1. The procedure of pentose phosphate pathway/shunt  In cytosol
1) Oxidative Phase NADP+ NADPH+H+ H2O CO2 G-6-P Xylulose 5-P Ribulose 5-P Ribose 5-P G-6-P dehydrogenase 6-Phosphogluconate 6-phosphogluconate dehydrogenase 6-Phospho gluconolactonase 6-phosphogluco- nolactone Epimerase Isomerase NADP+ NADPH+H+
2) Non-Oxidative Phase Ribose 5-p Xylulose 5-p Xylulose 5-p Fructose 6-p Glyceraldehyde 3-p Fructose 6-p • Transketolase: requires TPP • Transaldolase Glycolysis
The net reation: 3G-6-P + 6NADP+ → 2F-6-P + GAP + 6NADPH + H+ + 3CO2 2. Regulation of pentose phosphate pathway  Glucose-6-phosphate Dehydrogenase is the rate-limiting enzyme. NADPH/NADP+ ↑, inhibit; NADPH/NADP+ ↓, activate.
3. Significance of pentose Phosphate pathway 1) To supply ribose 5-phosphate for bio- synthesis of nucleic acid; 2) To supply NADPH as H-donor in metabolism;  NADPH is very important “reducing power” for the synthesis of fatty acids and cholesterol, and amino acids, etc.
 NADPH is the coenzyme of glutathione reductase to keep the normal level of reduced glutathione; So, NADPH, glutathione and glutathione reductase together will preserved the integrity of RBC membrane. 2GSH G-S-S-G NADPH + H+ glutathione reductase NADP+H2O2 2H2O
Deficiency of glucose 6-phosphate dehydrogenase results in hemolytic anemia. favism  NADPH serves as the coenzyme of mixed function oxidases (mono- oxygenases). In liver this enzyme participates in biotransformation.
§5 Glycogen synthesis and catabolism
Glycogen is a polymer of glucose residues linked by  α (1→4) glycosidic bonds, mainly  α (1→6) glycosidic bonds, at branch points.
• The process of glycogenesis occurs in cytosol of liver and skeletal muscle mainly. 1. Glycogen synthesis (Glycogenesis)
• UDPG: G active pattern, G active donor. • In glycogen anabolism, 1 G consumes 2~P. • Glycogen synthase: key E. G HK or GK G-6-P ATP ADP G-1-P UDPG pyrophosphorylase UDPG UTP PPi Gn UDP Gn+1 glycogen synthase
O O OHOH HH H CH2 H HN N O O OP O O− P O O− H O OH H OHH OH CH2OH H O H UDPG
Branching enzyme
Phosphorylase: key E; The end products: 85% of G-1-P and 15% of free G; There is no the activity of glucose 6- phosphatase (G-6-Pase) in skeletal muscle. Gn Pi Gn-1 G-1-P G-6-P G-6-Pase H2O Pi G Phosphorylase 2. Glycogen catabolism (glycogenolysis)
Debranching enzyme: glucan transferase α-1,6-glucosidase
Nonreducing ends (α1→6) linkage Glycogen phosphorylase (α1→6) glucosidase activity of debranching enzyme Glucose Transferase activity of debranching enzyme
3. Regulation of glycogenesis and glycogenolysis 1) Allosteric regulation In liver: G phosphorylase glycogenolysis In muscle:AMP phosphorylase-b ATP G-6-P phosphorylase-a glycogenolysis Ca2+
2) Covalent modification Glucagon epinephrine Adenylyl cyclase cAMP G proteinreceptor PKA glycogenolysis Phosphorylase Glycogen synthase glycogenesis Blood sugar
glucagon, epinephrine inactive adenylate cyclase active adenylate cyclase ATP cAMP inactive PKA active PKA phosphorylase b kinase phosphorylase b kinase P ATP ADP H2O Pi phosphorylase b P P ATP ADP Pi H2O ATP ADP glycogen synthase glycogen synthase P H2OPi protein phosphatase-1 (active) (inactive) inhibitor-1 (active) inhibitor-1 (inactive) phosphorylase a ATP
§6 Gluconeogenesis
• Concept: The process of transformation of non- carbohydrates to glucose or glycogen is termed as gluconeogenesis. • Materials: lactate, glycerol, pyruvate and glucogenic amino acid. • Site: mainly liver, kidney.
1. Gluconeogenic pathway • The main pathway for gluconeogenesis is essentially a reversal of glycolysis, but there are three energy barriers obstructing a simple reversal of glycolysis.
1) The shunt of carboxylation of Pyr PEP ADP ATP oxaloacetic acid Pyr carboxylase ADP+Pi ATP CO2 Biotin GTP GDP CO2 PEP carboxykinase Pyr kinase COO - C CH3 COO - CH CH2 O~ P O pyruvate COO - C CH2 O COOH £¨ Mt.£© £¨ 1/3Mt. 2/3cytosal£©.
2) F-1, 6-BP →F-6-P F-6-P F-1,6-BP ATP ADP Pi H2O PFK-1 Fructose- bisphosphatase
3) G-6-P →G • 2 lactic acid G consume ATP? G G-6-P ATP ADP Pi H2O Glucose-6- phosphatase HK
gluconeogenesis glucose G-6-P glycogen F-1,6BP glyceral- dehyde 3-P glycerol 1.3-bisphospho- glycerate glycerate 3-P glycerate 2-P lactate G-1-P malic acid phosphoenol pyruvate pyruvate GTP GDP CO2 2/3 malic acid pyruvate phosphoenol pyruvate GTP GDP CO2 1/3 CO2 CYTOSOL MITOCHONDRIA NAD+ NADH+H+ NAD+ NADH+H+ NAD+ NADH+H+ glutamate ¦Á-ketoglutarate ¦Á-ketoglutarate glutamate OAAAspAspOAADHAP ATP ADP ATP ADP PK ADP ATP F-6-P
2. Regulation of gluconeogenesis • Substrate cycle: The interconversion of two substrates catalyzed by different enzymes for singly direction reactions is called “substrate cycle”. • The substrate cycle produces net hydrolysis of ATP or GTP.------futile cycle
Key enzymes of gluconeogenesis PEP carboxykinase Pyr carboxylase Fructose-bisphosphatase Glucose-6-phosphatase
F-1,6-BP ATP ADP Pi H2O PFK-1FBPase-1 F-6-P F-2,6-BP AMP glycolysis gluconeogenesis:
F-1,6-BP ATP ADP F-2,6-BP PEP Pyr acetyl CoA glucagon insulin glucagon Ala in liver OAA
3. Significance of gluconeogenesis (1) Replenishment of Glucose by Gluconeogenesis and Maintaining Normal Blood Sugar Level. (2) Replenishment of Liver Glycogen. (3) Regulation of Acid-base Balance.
First stages (cytosol) Second stages (Mt.) Third stages (Mt.)
Lactic acid (Cori) cycle • Lactate, formed by the oxidation of glucose in skeletal muscle and by blood, is transported to the liver where it re-forms glucose, which again becomes available via the circulation for oxidation in the tissues. This process is known as the lactic acid cycle or Cori cycle. • prevent acidosis ； reused lactate
muscle glucose pyruvate lactate glucose blood pyruvate lactate glycolytic pathway glucose liver lactate NAD+ NADH+H+ NADH+H+ NAD+ gluconeo- genesis Lactic acid cycle
§6 Blood Sugar and Its Regulation
1. The source and fate of blood sugar blood sugar 3.89¡« 6.11mmol/L dietary supply liver glycogen (gluconeogenesis) other saccharides CO2 + H2O + energy glycogen other saccharides non-carbohydrates >8.89¡«10.00mmol/L (threshold of kidney) non-carbohydrate (lipids and some amino acids) urine glucose origin (income) fate (outcome)
Blood sugar level must be maintained within a limited range to ensure the supply of glucose to brain. The blood glucose concentration is 3.89 ～ 6.11mmol/L normally.
2. Regulation of blood sugar level 1 ） insulin ： for decreasing blood sugar levels. 2 ） glucagon ： for increasing blood sugar levels. 3 ） glucocorticoid: for increasing blood sugar levels. 4 ） adrenaline ： for increasing blood sugar levels.
3. Abnormal Blood Sugar Level • Hyperglycemia: > 7.22 ～ 7.78 mmol/L • The renal threshold for glucose: 8.89 ～ 10.00mmol/L • Hypoglycemia: < 3.33 ～ 3.89mmol/L
Pyruvate as a junction point
Carbohydrate metabolism
Carbohydrate metabolism

More Related Content

PPT
Carbohydrate metabolism
byHaseeb Quadri
 
PPTX
Carbohydrate metabolism
byDr.Priyanka Sharma
 
PPTX
Carbohydrate Metabolism - Biochemistry
byCU Dentistry 2019
 
PPT
carbohydrate metabolism new.ppt
byNiranjanShakya1
 
PPT
Carbohydrate metabolism, part 1
byenamifat
 
PPTX
Metabolism of Carbohydrate Part -I.pptx
byABHIJIT BHOYAR
 
PPT
Gluconeogenesis
bySathish Rajamani
 
PPTX
Carbohydrate metabolism
bySHIVANEE VYAS
 
Carbohydrate metabolism
byHaseeb Quadri
 
Carbohydrate metabolism
byDr.Priyanka Sharma
 
Carbohydrate Metabolism - Biochemistry
byCU Dentistry 2019
 
carbohydrate metabolism new.ppt
byNiranjanShakya1
 
Carbohydrate metabolism, part 1
byenamifat
 
Metabolism of Carbohydrate Part -I.pptx
byABHIJIT BHOYAR
 
Gluconeogenesis
bySathish Rajamani
 
Carbohydrate metabolism
bySHIVANEE VYAS
 

What's hot

PPTX
Fatty acid oxidation
byNamrata Chhabra
 
PPTX
Overview of lipid metabolism
bysubramaniam sethupathy
 
PPTX
GLUCONEOGENESIS & ITS REGULATION
byYESANNA
 
PPSX
Citric Acid Cycle
byAshok Katta
 
PPTX
GLYCOGENOLYSIS & REGULATION OF GLYCOGEN METABOLISM
byYESANNA
 
PPTX
Beta-oxidation of fatty acids
byYESANNA
 
PPTX
TCA CYCLE & ITS REGULATION
byYESANNA
 
PPSX
De novo synthesis of fatty acids (Biosynthesis of fatty acids)
byAshok Katta
 
PPTX
Ketone bodies
byKamlesh Yadav
 
PPSX
Glycolysis (with animated pathway)
byAshok Katta
 
PPTX
Glycolysis
byRAJENDRA SINGH
 
PPSX
Hexose Monophosphate Shunt
byAshok Katta
 
PPTX
Protein digestion and absorption
byDr. Aamir Ali Khan
 
PPT
TCA cycle- steps, regulation and significance
byNamrata Chhabra
 
PPTX
Gluconeogenesis
byFarhana Atia
 
PPTX
GLYCINE METABOLISM
byYESANNA
 
PDF
Transamination & deamination
byrohini sane
 
PPTX
BIOSYNTHESIS OF FATTY ACIDS
byYESANNA
 
PDF
Amino acid metabolism
byYash Institute of Pharmacy, Aurangabad. Maharashtra.
 
PPTX
Carbohydrate metabolism
byDevipriya Viswambharan
 
Fatty acid oxidation
byNamrata Chhabra
 
Overview of lipid metabolism
bysubramaniam sethupathy
 
GLUCONEOGENESIS & ITS REGULATION
byYESANNA
 
Citric Acid Cycle
byAshok Katta
 
GLYCOGENOLYSIS & REGULATION OF GLYCOGEN METABOLISM
byYESANNA
 
Beta-oxidation of fatty acids
byYESANNA
 
TCA CYCLE & ITS REGULATION
byYESANNA
 
De novo synthesis of fatty acids (Biosynthesis of fatty acids)
byAshok Katta
 
Ketone bodies
byKamlesh Yadav
 
Glycolysis (with animated pathway)
byAshok Katta
 
Glycolysis
byRAJENDRA SINGH
 
Hexose Monophosphate Shunt
byAshok Katta
 
Protein digestion and absorption
byDr. Aamir Ali Khan
 
TCA cycle- steps, regulation and significance
byNamrata Chhabra
 
Gluconeogenesis
byFarhana Atia
 
GLYCINE METABOLISM
byYESANNA
 
Transamination & deamination
byrohini sane
 
BIOSYNTHESIS OF FATTY ACIDS
byYESANNA
 
Amino acid metabolism
byYash Institute of Pharmacy, Aurangabad. Maharashtra.
 
Carbohydrate metabolism
byDevipriya Viswambharan
 

Viewers also liked

PPT
Carbohydrate metabolism
bySANA DANISH
 
PPT
Carbohydrate Metabolism
bydluetgens
 
PPTX
Carbohydrate presentation
byChristy Grissom Cheshire
 
PPT
synthesis writing
byPrince Anwar Ali
 
PPT
Carbohydrate metabolism
byDentist(Umar Ali )
 
PPTX
Renal function tests
byTapeshwar Yadav
 
PPT
Enzymology
bykuldip sodhi
 
PPT
Flow cytometry
byTapeshwar Yadav
 
PPT
Krebscycle 100410033222-phpapp01
byPrince Anwar Ali
 
PPT
Metabolism of Carbohydrates
byPave Medicine
 
PPTX
Class 2 glycolysis
byDhiraj Trivedi
 
PPT
Enzymology
byPave Medicine
 
PPT
Presentation glucose transporters
bykiro94
 
PPTX
Glycolysis and Cori's cycle Dr. Ashok Kumar Jeppu
byInternational Medical School Malaysia
 
PPT
Cell transport
byDr.M.Prasad Naidu
 
PPT
Clinical laboratory total quality management (TQM) system
byTapeshwar Yadav
 
PPT
Urea creatinine
byTapeshwar Yadav
 
PPTX
RAPAPORT-LEUBERING CYCLE
byYESANNA
 
PPT
Vitamins
byAnisul Mazumder
 
PPTX
Carbohydrate metabolism
bySachith Gamage
 
Carbohydrate metabolism
bySANA DANISH
 
Carbohydrate Metabolism
bydluetgens
 
Carbohydrate presentation
byChristy Grissom Cheshire
 
synthesis writing
byPrince Anwar Ali
 
Carbohydrate metabolism
byDentist(Umar Ali )
 
Renal function tests
byTapeshwar Yadav
 
Enzymology
bykuldip sodhi
 
Flow cytometry
byTapeshwar Yadav
 
Krebscycle 100410033222-phpapp01
byPrince Anwar Ali
 
Metabolism of Carbohydrates
byPave Medicine
 
Class 2 glycolysis
byDhiraj Trivedi
 
Enzymology
byPave Medicine
 
Presentation glucose transporters
bykiro94
 
Glycolysis and Cori's cycle Dr. Ashok Kumar Jeppu
byInternational Medical School Malaysia
 
Cell transport
byDr.M.Prasad Naidu
 
Clinical laboratory total quality management (TQM) system
byTapeshwar Yadav
 
Urea creatinine
byTapeshwar Yadav
 
RAPAPORT-LEUBERING CYCLE
byYESANNA
 
Vitamins
byAnisul Mazumder
 
Carbohydrate metabolism
bySachith Gamage
 

Similar to Carbohydrate metabolism

PPT
Carbohydrate metabolism
byMalik Abdulwadood
 
PPT
Carbohydrate Mechanism
byMalik Abdulwadood
 
PPTX
Carbohydrates Biochemistry .pptx CARBOHYDRATE METABOLISM
byameela006
 
PPT
CHO metabolism
byMD. ASIFUR RAHMAN
 
PPT
Central Metabolism
byMinistry of Education, Ethiopia
 
PDF
CARBOHYDRATE METABOLISM BY BISWANATH PRUSTY
byCollege of pharmaceutical sciences
 
PPTX
Metabolic pathways governing to catbohydrate.pptx
byPreetiBajpai14
 
PDF
263922643-Carbohydrate-Metabolism-1-ppt.pdf
byBinaKhan8
 
PDF
Metabolism
byShaliniBarad
 
PPTX
carbohydrate metabolism & its disorders.pptx
bySangeeta Khyalia
 
PPT
Carbohydrate-Metabolism-1sjdbfbdkdkd.ppt
byTEHJIBFREEFIRE
 
PPT
Carbohydrte metabolism
byhumaira noor
 
PDF
Glycolysis.pdf
byqahtanali2
 
PDF
Carbohydrate & lipid Metabolism_food Sci.pdf
byEmmanuelSimonMarino
 
PPTX
1. COH met1 .pptx
byMohammed669214
 
PPTX
First year Sem 2 Biochemistry (unit 2)B pharmacy
bypayalpilaji
 
PPTX
Class 2 3 glycolysis
byDhiraj Trivedi
 
PPT
Carbohydrate metabolism
byRavish Yadav
 
PDF
M.Carbohydrate Metabolism[2].pdf UNDERGRADUATE
bystudylap23
 
PPTX
Unit IV Biochemistry Carbohydratpptes.pptx
byfacultynursingtibri
 
Carbohydrate metabolism
byMalik Abdulwadood
 
Carbohydrate Mechanism
byMalik Abdulwadood
 
Carbohydrates Biochemistry .pptx CARBOHYDRATE METABOLISM
byameela006
 
CHO metabolism
byMD. ASIFUR RAHMAN
 
Central Metabolism
byMinistry of Education, Ethiopia
 
CARBOHYDRATE METABOLISM BY BISWANATH PRUSTY
byCollege of pharmaceutical sciences
 
Metabolic pathways governing to catbohydrate.pptx
byPreetiBajpai14
 
263922643-Carbohydrate-Metabolism-1-ppt.pdf
byBinaKhan8
 
Metabolism
byShaliniBarad
 
carbohydrate metabolism & its disorders.pptx
bySangeeta Khyalia
 
Carbohydrate-Metabolism-1sjdbfbdkdkd.ppt
byTEHJIBFREEFIRE
 
Carbohydrte metabolism
byhumaira noor
 
Glycolysis.pdf
byqahtanali2
 
Carbohydrate & lipid Metabolism_food Sci.pdf
byEmmanuelSimonMarino
 
1. COH met1 .pptx
byMohammed669214
 
First year Sem 2 Biochemistry (unit 2)B pharmacy
bypayalpilaji
 
Class 2 3 glycolysis
byDhiraj Trivedi
 
Carbohydrate metabolism
byRavish Yadav
 
M.Carbohydrate Metabolism[2].pdf UNDERGRADUATE
bystudylap23
 
Unit IV Biochemistry Carbohydratpptes.pptx
byfacultynursingtibri
 

More from Tapeshwar Yadav

PDF
Essential Textbook of Biochemistry For Nursing (B.Sc.Nursing & PBN)
byTapeshwar Yadav
 
PPT
Basics of Amino Acids & Plasma Proteins
byTapeshwar Yadav
 
PPT
Basics of Proteins Chemistry
byTapeshwar Yadav
 
PPTX
Medical Terminology of Endocrine System
byTapeshwar Yadav
 
PPT
Basics of Carbohydrates Chemistry
byTapeshwar Yadav
 
PPT
Introduction to biochemistry
byTapeshwar Yadav
 
PPTX
Medical Parasitology Laboratory
byTapeshwar Yadav
 
PPTX
Medical Microbiology Laboratory
byTapeshwar Yadav
 
PPTX
Clinical Hematology Laboratory
byTapeshwar Yadav
 
PPTX
Clinical Biochemistry Laboratory
byTapeshwar Yadav
 
PPT
Ion Specific Electrodes (ISE)
byTapeshwar Yadav
 
PPT
Biological Safety Cabinet
byTapeshwar Yadav
 
PPT
Clinical Laboratory Biosafety
byTapeshwar Yadav
 
PPT
Pipettes and Their Safely Use
byTapeshwar Yadav
 
PPT
Safe Use and Storage of Chemicals and Reagents
byTapeshwar Yadav
 
PPT
Laboratory Hazards, Accidents and Safety Rules
byTapeshwar Yadav
 
PDF
Guideline on-Health-Laboratory-Establishment-and-Operational by NPHL
byTapeshwar Yadav
 
PDF
Tapeshwar Yadav Updated CV, 2020
byTapeshwar Yadav
 
PDF
Revised Curriculum of Certificate in Medical Laboratory Technology(CMLT) by C...
byTapeshwar Yadav
 
PDF
Textbook of Clinical Pathology book cover
byTapeshwar Yadav
 
Essential Textbook of Biochemistry For Nursing (B.Sc.Nursing & PBN)
byTapeshwar Yadav
 
Basics of Amino Acids & Plasma Proteins
byTapeshwar Yadav
 
Basics of Proteins Chemistry
byTapeshwar Yadav
 
Medical Terminology of Endocrine System
byTapeshwar Yadav
 
Basics of Carbohydrates Chemistry
byTapeshwar Yadav
 
Introduction to biochemistry
byTapeshwar Yadav
 
Medical Parasitology Laboratory
byTapeshwar Yadav
 
Medical Microbiology Laboratory
byTapeshwar Yadav
 
Clinical Hematology Laboratory
byTapeshwar Yadav
 
Clinical Biochemistry Laboratory
byTapeshwar Yadav
 
Ion Specific Electrodes (ISE)
byTapeshwar Yadav
 
Biological Safety Cabinet
byTapeshwar Yadav
 
Clinical Laboratory Biosafety
byTapeshwar Yadav
 
Pipettes and Their Safely Use
byTapeshwar Yadav
 
Safe Use and Storage of Chemicals and Reagents
byTapeshwar Yadav
 
Laboratory Hazards, Accidents and Safety Rules
byTapeshwar Yadav
 
Guideline on-Health-Laboratory-Establishment-and-Operational by NPHL
byTapeshwar Yadav
 
Tapeshwar Yadav Updated CV, 2020
byTapeshwar Yadav
 
Revised Curriculum of Certificate in Medical Laboratory Technology(CMLT) by C...
byTapeshwar Yadav
 
Textbook of Clinical Pathology book cover
byTapeshwar Yadav
 

Recently uploaded

PPTX
MICROSPORIDIAL KERATITIS , CLINICAL FEATURES , TREATMENT
byDr Aarushi Choudhary
 
PPTX
Labour1.docx-flashcards.pptx..............
bySir Fad'hi
 
PPTX
B SCAN . TECHNIQUES , PROBE POSITIONS , INDICATIONS
byDr Aarushi Choudhary
 
PPTX
Basic overview and structural elucidation of Morphine
bySumitSharma743530
 
PPT
Forging New Paths With Earlier Use of ADCs in Breast Cancer: From Clinical Br...
byPVI, PeerView Institute for Medical Education
 
PDF
Anxiety and Antianxiety Drugs: Pathophysiology of Anxiety Disorders, Classifi...
byShagufta Farooqui
 
PPTX
Updated PALS slides 2025 guidelines.pptx
bydrabrehman121
 
PPTX
COGNITION IN DEPRESSION
byDr Hari Ram Sedai
 
PDF
Dyes/ Stain Used In Ophthalmology - Clinical uses, Indication & Side effects....
bySamikshaRai22
 
PDF
RETINAL VEIN OCCLUSION; CRVO & BRVO types, pathophysiology, diagnosis & manag...
bySamikshaRai22
 
PPTX
Pharmacology and Toxicology Multiple Choice Questions (MCQs) Part 3
byVanarajRabari
 
PPT
New Kids on the Block in mHSPC: Personalising Approaches Through Emerging Pre...
byPVI, PeerView Institute for Medical Education
 
PPTX
Unit- II (Bioavaliability & Bioequivalence).pptx
byUditiHanda
 
PPTX
Pressure ulcer Internal KPIs results for July,2024.pptx
byprofyasser95
 
PPTX
Seminar on Ebola virus , سیمینارێکی ئامادەکراو لەسەر Ebola virus
bydanaShalal2
 
PPTX
NEUROBIOLOGY OF AUTISM SPECTRUM DISORDER
byDr Hari Ram Sedai
 
PPTX
Drug Distribution Explained | Pharmacokinetics, Barriers, Vd & Redistribution...
byRGUHS
 
PPTX
HSV KERATITIS . CLINICAL FEATURES , TYPES , DIAGNOSIS , TREATMENT , HEDS TRIAL
byDr Aarushi Choudhary
 
PPTX
Types of Communication Disorders SLP lecture 3.pptx
byDr Zonera Khalid PT
 
PPTX
Imaging of benign focal lesions of the Liver
byDr. Aryan (Anish Dhakal)
 
MICROSPORIDIAL KERATITIS , CLINICAL FEATURES , TREATMENT
byDr Aarushi Choudhary
 
Labour1.docx-flashcards.pptx..............
bySir Fad'hi
 
B SCAN . TECHNIQUES , PROBE POSITIONS , INDICATIONS
byDr Aarushi Choudhary
 
Basic overview and structural elucidation of Morphine
bySumitSharma743530
 
Forging New Paths With Earlier Use of ADCs in Breast Cancer: From Clinical Br...
byPVI, PeerView Institute for Medical Education
 
Anxiety and Antianxiety Drugs: Pathophysiology of Anxiety Disorders, Classifi...
byShagufta Farooqui
 
Updated PALS slides 2025 guidelines.pptx
bydrabrehman121
 
COGNITION IN DEPRESSION
byDr Hari Ram Sedai
 
Dyes/ Stain Used In Ophthalmology - Clinical uses, Indication & Side effects....
bySamikshaRai22
 
RETINAL VEIN OCCLUSION; CRVO & BRVO types, pathophysiology, diagnosis & manag...
bySamikshaRai22
 
Pharmacology and Toxicology Multiple Choice Questions (MCQs) Part 3
byVanarajRabari
 
New Kids on the Block in mHSPC: Personalising Approaches Through Emerging Pre...
byPVI, PeerView Institute for Medical Education
 
Unit- II (Bioavaliability & Bioequivalence).pptx
byUditiHanda
 
Pressure ulcer Internal KPIs results for July,2024.pptx
byprofyasser95
 
Seminar on Ebola virus , سیمینارێکی ئامادەکراو لەسەر Ebola virus
bydanaShalal2
 
NEUROBIOLOGY OF AUTISM SPECTRUM DISORDER
byDr Hari Ram Sedai
 
Drug Distribution Explained | Pharmacokinetics, Barriers, Vd & Redistribution...
byRGUHS
 
HSV KERATITIS . CLINICAL FEATURES , TYPES , DIAGNOSIS , TREATMENT , HEDS TRIAL
byDr Aarushi Choudhary
 
Types of Communication Disorders SLP lecture 3.pptx
byDr Zonera Khalid PT
 
Imaging of benign focal lesions of the Liver
byDr. Aryan (Anish Dhakal)
 

Carbohydrate metabolism

  • 1.
    Carbohydrate Metabolism Mr.Tapeshwar Yadav. IIyear M.Sc. Biochemistry Mamata Medical College Khammam
  • 2.
    Carbohydrates Definition : Carbohydratesare polyhydroxy aldehydes or ketones.
  • 3.
    Biological significance of Carbohydrates •Theseare major source of energy for living organisms. •Supplying a huge array of metabolic intermediates for biosynthetic reactions. •The structural elements in cell coat or connective tissues.
  • 4.
    Digestion : • Partlydigested in mouth by salivary amylase. • In stomach there is no digestion takes place. • Complete digestion and absorption will be taken place at small intestine
  • 5.
    Glucose transporters (GLUT) •There are 5 types GLUT –GLUT1: RBC –GLUT4: Adipose tissue, Muscle
  • 6.
    The metabolism ofglucose •Aerobic oxidation •Glycolysis •Gluconeogenesis •Pentose phosphate pathway •Glycogenesis •Glycogenolysis •Uronic acid pathway
  • 7.
    Glycogen Glycogenesis Glycogenolysis Pentose phosphate pathway Ribose,NADPH Glycolysis Pyruvate/ Lactate H2O+CO2 Aerobicoxidation Digestion absorption Starch Lactate, Amino acids, Glycerol Glucose Gluconeo -genesis
  • 8.
    Aerobic oxidation • C6H12O66H2O+6CO2 + Energy (in the form of heat)
  • 11.
  • 12.
    •The anaerobic catabolicpathway by which a molecule of glucose is broken down into two molecules of lactate. Glucose → 2 Lactic acid (lack of O2) •All of the enzymes of glycolysis locate in cytosol.
  • 13.
  • 14.
    1) Glycolytic pathway: Glucose → Pyruvate including 10 reactions.
  • 15.
    •Phosphorylated Glucose cannotget out from cell. •Hexokinase (having 4 Isoenzymes). •Glucokinase, GK in liver. •Irreversible. (1) Glucose is phosphorylated to Glucose 6-phosphate OH OH H OH H OHH OH CH2 H HO OH OH H OH H OHH OH CH2 H OP ATP ADP Hexokinase Mg2+ G G-6-P
  • 16.
    Particulars Hexokinase Glucokinase Occurrencein all tissues only in liver Km value 0.1mmol/L 10mmol/L Substrate Glucose, Fructose, Mannose Glucose Regulation G-6-P Insulin Comparison of Hexokinase and Glucokinase
  • 17.
    (2) G-6-P isisomerised to Fructose 6-P OH OH H OH H OHH OH CH2 H OP G-6-P isomerase OH CH2OH H CH2 OH H H OH O OP F-6-P
  • 18.
    (3) F-6-P isphosphorylated Fructose 1,6-bisphosphate •The second phosphorylation •Phosphofructokinase-1, PFK-1 OH CH2OH H CH2 OH H H OH O OP F-1,6-BP OH CH2 H CH2 OH H H OH O OP O P ATP ADP Mg2+ F-6-P PFK-1
  • 19.
    (4) F-1,6-BP cleavedto 2 Triose phosphates •Reversible F-1,6-BP CH2 C O C HHO C OHH C OHH CH2 O P O P CH2 C O O P CHO CHOH CH2 O PCH2OH + aldolase dihydroxyacetone phosphate, DHAP glyceraldehyde 3-phosphate, GAP
  • 20.
    (5) Triose phosphateisomerization G→2 molecule glyceraldehyde-3- phosphate, consume 2 ATP . CH2 C O O P CHO CHOH CH2 O PCH2OH DHAP GAP phosphotriose isomerase
  • 21.
    (6) Glyceraldehyde 3-phosphateoxidised 1,3-bisphospho glycerate CHO CHOH CH2 O P NAD+ NADH+H + Pi glyceraldehyde 3-phosphate dehydrogenase, GAPDH C CHOH CH2 O P O O~ P glycerate 1,3-bisphosphate, 1,3-BPG glyceraldehyde 3-phosphate
  • 22.
    (7) 1,3-BPG dephosphorylatedto 3- phospho glycerate • Substrate level phosphorylation COO- CHOH CH2 O P C CHOH CH2 O P O O~ P ADP ATP glycerate 1,3-bisphosphate glycerate 3-phosphate Phosphoglycerate kinase
  • 23.
    (8) Glycerate 3-phosphatemutated glycerate 2-phosphate COO- CHOH CH2 O P COO- CH CH2OH O P glycerate 3-phosphate glycerate 2-phosphate Mutase
  • 24.
    (9) Glycerate 2-phosphate→ phosphoenol pyruvate COO- CH CH2OH O P COO- C CH2 O PEP ~ P + H2O enolase glycerate 2-phosphate
  • 25.
    (10) PEP →pyruvate •Second substrate level phosphorylation • irreversible COO- C CH3 ADP ATP COO- C CH2 O PEP ~ P pyruvate kinase O Pyruvate
  • 26.
    2) Pyruvate →lactate COO C CH3 NAD+NADH + H+ O Pyr COO CHOH CH3 Lactate dehydrogenase, LDH Lactic acid
  • 27.
    Summary of Glycolysis ATP ADP Mg2+ PFK-1 GAPDHAP glycerate 1,3-bisphosphate NADH+H+ glyceraldehyde 3-phosphate dehydrogenase H3PO4 NADH+H+ NAD+ ADP ATP glycerate 3-phosphate glycerate 2-phosphate H2O PEP ATP ADP pyruvate kinase lactate pyruvate G G-6-P F- 6-P F- 1,6-BP NAD+ Phosphoglycerate kinase Isomerase Aldolase Mutase Enolase LDH HK ATP ADP Mg2+
  • 28.
    Total reaction: C6H12O6 +2ADP + 2Pi 2CH3CHOHCOOH + 2ATP + 2H2O Formation of ATP: The net yield is 2 ~P or 2 molecules of ATP per glucose.
  • 29.
    2. Regulation ofGlycolysis • Three key enzymes catalyze irreversible reactions : Hexokinase, Phosphofructokinase & Pyruvate Kinase.
  • 30.
    1) PFK-1 The reactioncatalyzed by PFK-1 is usually the rate-limiting step of the Glycolysis pathway. This enzyme is regulated by covalent modification, allosteric regulation.
  • 31.
  • 32.
    2) Pyruvate kinase •Allosteric regulation: F-1,6-BP acts as allosteric activator ； ATP and Ala in liver act as allosteric inhibitors;
  • 33.
    • Covalent modification: phosphorylatedby Glucagon through cAMP and PKA and inhibited. ATP ADP PKA Glucagon Pyruvate Kinase (active) Pyruvate Kinase- P (inactive) cAMP
  • 34.
    3) Hexokinase andglucokinase • This enzyme is regulated by covalent modification, allosteric regulation and isoenzyme regulation. • Inhibited by its product G-6-P. • Insulin induces synthesis of glucokinase.
  • 35.
    3. Significance ofglycolysis 1) Glycolysis is the emergency energy- yielding pathway. 2) Glycolysis is the main way to produce ATP in some tissues, even though the oxygen supply is sufficient, such as red blood cells, retina, testis, skin, medulla of kidney. • In glycolysis, 1mol G produces 2mol lactic acid and 2mol ATP.
  • 36.
    § 3 AerobicOxidation of Glucose
  • 37.
    • The processof complete oxidation of glucose to CO2 and water with liberation of energy as the form of ATP is named aerobic oxidation. • The main pathway of G oxidation.
  • 38.
    1. Process ofaerobic oxidation G Pyr cytosol Mitochodria glycolytic pathway second stage third stage CO2 + H2O+ATPPyr CH3CO~SCoA first stage TAC
  • 39.
    1) Oxidative decarboxylationof Pyruvate to Acetyl CoA • irreversible; • in mitochodria. COO- C CH3 NAD+ NADH + H + O pyruvate CH3C Pyruvate dehydrogenase complex Acetyl CoA O ~SCoA+ HSCoA + CO2
  • 40.
    Pyruvate dehydrogenase complex: E1pyruvate dehydrogenase Es E2 dihydrolipoyl transacetylase E3 dihydrolipoyl dehydrogenase thiamine pyrophosphate, TPP (VB1 ) HSCoA (pantothenic acid) cofactors lipoic Acid NAD+ (Vpp) FAD (VB2 )
  • 41.
  • 42.
    The structure of pyruvatedehydrogenase complex
  • 43.
    S S CH H2 C H2C (CH2)4COOH SH SH CH H2 C H2C (CH2)4 COOH +2H - 2H lipoic acid dihydrolipoic acid C C NH2 HC N C H2 S C C N C N C H CH3 CH2CH2H3C O P O O- O P O O- O- + TPP
  • 44.
    HSCoA HS CH2 CH2NH C CH2 O CH2 NH C C O OH H C CH2 CH3 CH3 O P O OH O P OH O O 3'AMP ¦Â-alanine pantoic acid pyrophosphate pantothenic acid 4'-phosphopantotheine ¦Â-mercapto- ethylamine
  • 45.
  • 46.
    2) Tricarboxylic acidcycle, TCAC • The cycle comprises the combination of a molecule of acetyl-CoA with oxaloacetate, resulting in the formation of a six-carbon tricarboxylic acid, citrate. There follows a series of reactions in the course of which two molecules of CO2 are released and oxaloacetate is regenerated. • Also called citrate cycle or Krebs cycle.
  • 47.
    (1) Process ofreactions
  • 51.
    Citrate cycle CO CH2 COO COO CH3CO~SCoA C CH2 COO COO CH2 HO COO C CH COO COO CH2 COO CH CH COO COO CH2COO H2O H2O HO CO2 CH2 CH2 COCOO COOCH2 CH2 COO CO~ SCoA CO2 NAD+NADH+H+ CH2 CH2 COO COO GDP+PiGTP CH CH2 COO COO OOC CH C COOH HO NAD+ NADH+H+ FAD FADH2 H2O acetyl CoA H2O oxaloacetate citrate synthase citrate aconitase cis-aconitate aconitase isocitrate NAD+ NADH+H+ isocitrate dehydrogenase ¦Á-keto- glutarate ¦Á-ketoglutarate dehydrogenase complex succinyl-CoA ADP ATP CoASH succinyl CoA syntetase succinate dehydrogenase fumarate succinate fumarase malate malate dehydrogenase HSCoA HSCoA
  • 52.
  • 53.
    ② The netreaction of the TCAC: acetylCoA+3NAD+ +FAD+GDP+Pi+2H2O →2CO2+3NADH+3H+ +FADH2+GTP+ HSCoA ③ Irreversible and aerobic reaction ④ The enzymes are located in the mitochondrial matrix.
  • 54.
    ⑤ Anaplerotic reactionof oxaloacetate pyruvate carboxylase Biotin ATP ADP + Pi + CO2C CH3 COOH O C C COOH COOH O H2 NAD+ NADH+H+ malic acid DH + CO2 malic enzyme C CH3 COOH O NADPH+H+ NADP+ CHOH C COOH COOH C C COOH COOH O H2H2
  • 55.
    (2) Bio-significance ofTCAC ① Acts as the final common pathway for the oxidation of carbohydrates, lipids, and proteins. ② Serves as the crossroad for the interconversion among carbohydrates, lipids, and non-essential amino acids, and as a source of biosynthetic intermediates.
  • 56.
    Krebs Cycle isat the hinge of metabolism.
  • 57.
    2. ATP producedin the aerobic oxidation • acetyl CoA → TCAC : 3 (NADH+H+ ) + FADH2 + 1GTP → 12 ATP. • pyruvate →acetyl CoA: NADH+H+ →3 ATP • 1 G → 2 pyruvate : 2(NADH+H+ ) → 6 or 8ATP 1mol G ： 36 or 38mol ATP （ 12 ＋ 3 ） ×2 ＋ 6 （ 8 ）＝ 36 （ 38 ）
  • 58.
    3. The regulationof aerobic oxidation • The Key Enzymes of aerobic oxidation The Key Enzymes of glycolysis Pyruvate Dehydrogenase Complex Citrate synthase Isocitrate dehydrogenase (rate-limiting ) α-Ketoglutarate dehydrogenase
  • 59.
    (1) Pyruvate dehydrogenasecomplex Pyruvate dehydrogenase (active form) allosteric inhibitors: ATP, acetyl CoA, NADH, FA allosteric activators: AMP, CoA, NAD+ ,Ca2+ pyruvate dehydrogenase (inactive form) P pyruvate dehydrogenase kinase pyruvate dehydrogenase phosphatase ATP ADPH2O Pi Ca2+ ,insulin acetyl CoA, NADH ADP, NAD+
  • 60.
    (2) Citrate synthase •Allosteric activator: ADP • Allosteric inhibitor: NADH, succinyl CoA, citrate, ATP (3) Isocitrate dehydrogenase • Allosteric activator: ADP, Ca2+ • Allosteric inhibitor: ATP (4) α-Ketoglutarate dehydrogenase • Similar with Pyruvate dehydrogenase complex
  • 62.
    Oxidative phosphorylation→TCAC↑ •ATP/ADP↑ inhibit TCAC, Oxidativephosphorylation ↓ •ATP/ADP↓ ， promote TCAC ， Oxidative phosphorylation ↑
  • 63.
    4. Pasteur Effect •Under aerobic conditions, glycolysis is inhibited and this inhibitory effect of oxygen on glycolysis is known as Pasteur effect. • The key point is NADH ： NADH mitochondria Pyr TCAC CO2 ＋ H2O Pyr can’t produce to lactate.
  • 64.
  • 65.
    1. The procedureof pentose phosphate pathway/shunt  In cytosol
  • 66.
    1) Oxidative Phase NADP+ NADPH+H+ H2O CO2 G-6-P Xylulose5-P Ribulose 5-P Ribose 5-P G-6-P dehydrogenase 6-Phosphogluconate 6-phosphogluconate dehydrogenase 6-Phospho gluconolactonase 6-phosphogluco- nolactone Epimerase Isomerase NADP+ NADPH+H+
  • 67.
    2) Non-Oxidative Phase Ribose5-p Xylulose 5-p Xylulose 5-p Fructose 6-p Glyceraldehyde 3-p Fructose 6-p • Transketolase: requires TPP • Transaldolase Glycolysis
  • 68.
    The net reation: 3G-6-P+ 6NADP+ → 2F-6-P + GAP + 6NADPH + H+ + 3CO2 2. Regulation of pentose phosphate pathway  Glucose-6-phosphate Dehydrogenase is the rate-limiting enzyme. NADPH/NADP+ ↑, inhibit; NADPH/NADP+ ↓, activate.
  • 69.
    3. Significance ofpentose Phosphate pathway 1) To supply ribose 5-phosphate for bio- synthesis of nucleic acid; 2) To supply NADPH as H-donor in metabolism;  NADPH is very important “reducing power” for the synthesis of fatty acids and cholesterol, and amino acids, etc.
  • 70.
     NADPH isthe coenzyme of glutathione reductase to keep the normal level of reduced glutathione; So, NADPH, glutathione and glutathione reductase together will preserved the integrity of RBC membrane. 2GSH G-S-S-G NADPH + H+ glutathione reductase NADP+H2O2 2H2O
  • 71.
    Deficiency of glucose6-phosphate dehydrogenase results in hemolytic anemia. favism  NADPH serves as the coenzyme of mixed function oxidases (mono- oxygenases). In liver this enzyme participates in biotransformation.
  • 72.
    §5 Glycogen synthesisand catabolism
  • 73.
    Glycogen is apolymer of glucose residues linked by  α (1→4) glycosidic bonds, mainly  α (1→6) glycosidic bonds, at branch points.
  • 75.
    • The processof glycogenesis occurs in cytosol of liver and skeletal muscle mainly. 1. Glycogen synthesis (Glycogenesis)
  • 76.
    • UDPG: Gactive pattern, G active donor. • In glycogen anabolism, 1 G consumes 2~P. • Glycogen synthase: key E. G HK or GK G-6-P ATP ADP G-1-P UDPG pyrophosphorylase UDPG UTP PPi Gn UDP Gn+1 glycogen synthase
  • 77.
  • 79.
  • 80.
    Phosphorylase: key E; Theend products: 85% of G-1-P and 15% of free G; There is no the activity of glucose 6- phosphatase (G-6-Pase) in skeletal muscle. Gn Pi Gn-1 G-1-P G-6-P G-6-Pase H2O Pi G Phosphorylase 2. Glycogen catabolism (glycogenolysis)
  • 81.
  • 82.
    Nonreducing ends (α1→6) linkage Glycogen phosphorylase (α1→6)glucosidase activity of debranching enzyme Glucose Transferase activity of debranching enzyme
  • 83.
    3. Regulation ofglycogenesis and glycogenolysis 1) Allosteric regulation In liver: G phosphorylase glycogenolysis In muscle:AMP phosphorylase-b ATP G-6-P phosphorylase-a glycogenolysis Ca2+
  • 84.
    2) Covalent modification Glucagon epinephrine Adenylyl cyclase cAMP Gproteinreceptor PKA glycogenolysis Phosphorylase Glycogen synthase glycogenesis Blood sugar
  • 85.
    glucagon, epinephrine inactive adenylate cyclase active adenylatecyclase ATP cAMP inactive PKA active PKA phosphorylase b kinase phosphorylase b kinase P ATP ADP H2O Pi phosphorylase b P P ATP ADP Pi H2O ATP ADP glycogen synthase glycogen synthase P H2OPi protein phosphatase-1 (active) (inactive) inhibitor-1 (active) inhibitor-1 (inactive) phosphorylase a ATP
  • 86.
  • 87.
    • Concept: The processof transformation of non- carbohydrates to glucose or glycogen is termed as gluconeogenesis. • Materials: lactate, glycerol, pyruvate and glucogenic amino acid. • Site: mainly liver, kidney.
  • 88.
    1. Gluconeogenic pathway •The main pathway for gluconeogenesis is essentially a reversal of glycolysis, but there are three energy barriers obstructing a simple reversal of glycolysis.
  • 89.
    1) The shuntof carboxylation of Pyr PEP ADP ATP oxaloacetic acid Pyr carboxylase ADP+Pi ATP CO2 Biotin GTP GDP CO2 PEP carboxykinase Pyr kinase COO - C CH3 COO - CH CH2 O~ P O pyruvate COO - C CH2 O COOH £¨ Mt.£© £¨ 1/3Mt. 2/3cytosal£©.
  • 90.
    2) F-1, 6-BP→F-6-P F-6-P F-1,6-BP ATP ADP Pi H2O PFK-1 Fructose- bisphosphatase
  • 91.
    3) G-6-P →G •2 lactic acid G consume ATP? G G-6-P ATP ADP Pi H2O Glucose-6- phosphatase HK
  • 92.
    gluconeogenesis glucose G-6-P glycogen F-1,6BP glyceral- dehyde 3-P glycerol 1.3-bisphospho- glycerate glycerate 3-P glycerate2-P lactate G-1-P malic acid phosphoenol pyruvate pyruvate GTP GDP CO2 2/3 malic acid pyruvate phosphoenol pyruvate GTP GDP CO2 1/3 CO2 CYTOSOL MITOCHONDRIA NAD+ NADH+H+ NAD+ NADH+H+ NAD+ NADH+H+ glutamate ¦Á-ketoglutarate ¦Á-ketoglutarate glutamate OAAAspAspOAADHAP ATP ADP ATP ADP PK ADP ATP F-6-P
  • 93.
    2. Regulation ofgluconeogenesis • Substrate cycle: The interconversion of two substrates catalyzed by different enzymes for singly direction reactions is called “substrate cycle”. • The substrate cycle produces net hydrolysis of ATP or GTP.------futile cycle
  • 94.
    Key enzymes ofgluconeogenesis PEP carboxykinase Pyr carboxylase Fructose-bisphosphatase Glucose-6-phosphatase
  • 95.
  • 96.
  • 97.
    3. Significance ofgluconeogenesis (1) Replenishment of Glucose by Gluconeogenesis and Maintaining Normal Blood Sugar Level. (2) Replenishment of Liver Glycogen. (3) Regulation of Acid-base Balance.
  • 98.
  • 99.
    Lactic acid (Cori)cycle • Lactate, formed by the oxidation of glucose in skeletal muscle and by blood, is transported to the liver where it re-forms glucose, which again becomes available via the circulation for oxidation in the tissues. This process is known as the lactic acid cycle or Cori cycle. • prevent acidosis ； reused lactate
  • 100.
  • 101.
    §6 Blood Sugarand Its Regulation
  • 102.
    1. The sourceand fate of blood sugar blood sugar 3.89¡« 6.11mmol/L dietary supply liver glycogen (gluconeogenesis) other saccharides CO2 + H2O + energy glycogen other saccharides non-carbohydrates >8.89¡«10.00mmol/L (threshold of kidney) non-carbohydrate (lipids and some amino acids) urine glucose origin (income) fate (outcome)
  • 103.
    Blood sugar levelmust be maintained within a limited range to ensure the supply of glucose to brain. The blood glucose concentration is 3.89 ～ 6.11mmol/L normally.
  • 104.
    2. Regulation ofblood sugar level 1 ） insulin ： for decreasing blood sugar levels. 2 ） glucagon ： for increasing blood sugar levels. 3 ） glucocorticoid: for increasing blood sugar levels. 4 ） adrenaline ： for increasing blood sugar levels.
  • 105.
    3. Abnormal BloodSugar Level • Hyperglycemia: > 7.22 ～ 7.78 mmol/L • The renal threshold for glucose: 8.89 ～ 10.00mmol/L • Hypoglycemia: < 3.33 ～ 3.89mmol/L
  • 106.
    Pyruvate as ajunction point