Mind Maps in Biochemistry - (Metabolism of Carbohydrates)

64 Mind Maps in Biochemistry, 2021, 64-86
CHAPTER 4
Metabolism of Carbohydrates
LEARNING OBJECTIVES: Keywords:
 Explain different anabolic and catabolic pathways of Diabetes, Digestion and

carbohydrate metabolism. assimilation of
 Describe the role of different enzymes and hormones carbohydrates, Enzymes of
involved in carbohydrate metabolism. carbohydrate metabolism,
 Identify the metabolic diseases related to carbohydrates. glycolysis, Glycogen
metabolism,
Gluconeogenesis, Glucose
homeostasis, Regulation of
glucose metabolism,
Tricarboxylic acid cycle.
CARBOHYDRATE STORAGE Starch Glycogen
Storage form of carbohydrates: Stored in plants Stored in animals
Both amylose and amylopectin Liver and muscle cells
DIGESTION AND ASSIMILATION OF CARBOHYDRATES: Pathway for digestion of

carbohydrates:
Substrate Site Enzyme Products
Starch Fructose Mouth Salivary amylase 1-4 Maltose

glycosides
Lactose Glucose  Maltotriose
Copyright © 2021. Bentham Science Publishers. All rights reserved.
Sucrose Limit dextrin

Stomach NO DIGESTION

Starch Intestine PANCREATIC AMYLASE Maltose
(1-4)
Simmi Kharb
All rights reserved-© 2021 Bentham Science Publishers
Kharb, Simmi. Mind Maps in Biochemistry, Bentham Science Publishers, 2021. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/otago/detail.action?docID=6512657.
Created from otago on 2022-11-28 08:21:48.
Chemistry of Carbohydrates Mind Maps in Biochemistry 65
Polysaccharides  Maltotriose
Limit dextrin
Epithelial brush OLIGOSACCHARIDASE
border & DISACCHARIDASES
Sucrose Sucrase (1-4) – Glucose
Maltotriose  Isomaltase (1-4) Fructose
Maltose
 - limit dextrins
Maltotriose Maltase (1-4) – Glucose
Maltose Glucoamylase (1-4)
Lactose Lactase (1-4) Glucose
Galactose
Portal vein

Liver (metabolism)

Circulation
(glucose)

Liver
Muscle
Adipose tissue
DEFECTS IN CARBOHYDRATE ABSORPTION
S. Disease Defect Clinical Feature

No.
1. Lactase deficiency Lactose intolerance Abdominal discomfort
Inherited lactase deficiency Cramps, diarrhea
66 Mind Maps in Biochemistry Simmi Kharb
Secondary lactase Intolerance to milk

deficiency
2. Inherited Sucrase Sucrase deficiency Same as lactase deficiency
deficiency
3. Disaccharidases Disacchariduria Fructose, sorbitol malabsorption
deficiency
4. Defect in SGLT-1 Monosaccharide Fructose, sorbitol malabsorption,
malabsorption watery diarrhea
Oral Hydration In cholera infection: NaCl absorption is inhibited, but not the facilitative
Therapy:
transport of Na & glucose
ORS (oral rehydration solution) provides: 110mM Glucose

SGLT-1 is not inhibited and in the presence 99 mM Na+
of glucose
74 mM Cl-
Na uptake takes place to replenish stores.
39 mM HCO-3
4 mM K+
Enzyme Site of Production/ Action Substrate Product
Salivary Amylase Salivary glands/ Oral cavity Starch Disaccharides (maltose),

oligosaccharides
Oligosaccharidases Lining of the intestine; Oligosaccharides Monosaccharides (e.g.,

brush border membrane/ Disaccharides glucose, fructose,
Small intestine galactose)
Pancreatic Pancreas/ Small intestine Starch Disaccharides (maltose),

Amylase monosaccharides (e.g.,
glucose, fructose,
galactose)
GLUCOSE METABOLISM
Involves the following steps: Glycolysis:  Importance:
Glycolysis A cytoplasmic pathway Only pathway taking place in

all the cells.
Krebs cycle Converts glucose into two
Oxidative phosphorylation moles of pyruvate Principal route for glucose
metabolism
Before glycolysis begins, glucose Releases energy captured in
must be transported into the cell by two substrate-level The main pathway for
different glucose transporters phosphorylation and one fructose, lactose and
(GLUT1-GLUT5). oxidation reaction. galactose metabolism.
Glycolysis:  Provides:
Requires 10 enzymes, 2 ATP molecules Pyruvate TCA via acetyl CoA
Liberates four ATP and two NADH+H+ and G-6-P fatty acids via acetyl CoA
pyruvate
G-6-P glycogen
 Supplies precursors for other pathways:
G-6-P PPP
Pyruvate for alanine formation
GA3P 3 carbon metabolisms
Dihydroxyacetone for triglyceride formation.
DHAP glycerol and TAG
 Energy source:
1,3 BPG  substrate level ATP
The only source of energy in erythrocytes. production
Provides ATP to skeletal muscle in the absence 2,3 BPG: Regulates O2 release in RBCs
of oxygen.
Lactate GNG to generate glucose
 Under anaerobic conditions:
Occurs in erythrocytes, exercising skeletal

muscle.
It recycles NADH by making lactate to produce

ATP.
 Reactions:
Reaction Input/ output Clinical correlation: basis
Preparatory phase: Energy investment
Phase I:
Glucose + ATP G-1-P + ADP. +ATP Frutose-1,6 BP + ADP
Reaction 1: Input: glucose, MODY: maturity-onset diabetes

1ATP, one enzyme of young.
Glucose +ATP-GK/ HK G-6-P+
ADP Output: one G-6P Autosomal dominant mutation in
glucokinase gene Presents as non-
HK inhibited by G6P progressive hyperglycemia.
Reaction 2: - -
 G-6-P --PHI  F – 6 – P
Reaction 3: Input: 1ATP Exercise intolerance

Committed step
F-6 – P + ATP -PFK F – 1, 6-BP
Inactive when cell

[ATP] is high
Inhibited by citrate
Activated by F2,6
BP
Phase II: Splitting Stage
Reaction 4: Yield: 2 GA3P Absence of Aldolase (in RBC,

muscle): presents with hemolytic
anemia
TPI: hemolytic anemia
Phase III: Yield Stage
Reaction 5: 2 NADH: 6ATP Arsenite, Mercuric ions:
-SH group of lipoic acid,
Arsenate used by GAPDH—> 1

arsenato-3-phosphoglycerate
(instead of 1,3 BPG): it
hydrolyzes and no ATP generated
by substrate level
phosphorylation.
Reaction 6: 1, 3 BPG <—PGK—> 3- - Exercise intolerance

PG
Reaction 7: 3 PG PGM 2 PG - Exercise intolerance
Reaction 8: PKG: substrate level 2, 3 BPG: Adaptation to high

phosphorylation: altitude:
Increased number of RBCs
2 ATP
Increases Hb concentration
Lowers affinity of Hb for O2

Increases ability of Hb to
unload O2 to tissues.
2PG—enolase—> PEP Enolase:

Exercise intolerance
Fluoride inhibits enolase:
used as preservative for
blood glucose estimation
Reaction 9: Substrate level ATP Hemolytic anemia
generation
PEP + ADP -- pyruvate kinase 
pyruvate + ATP Inhibited by high
[ATP]
Reaction 10: Consumption of Exercise intolerance
2NADH
Lactic acidosis
Cori Cycle: LDH enzyme oxidizes lactate to pyruvate that is used by heart as fuel.
ENERGETICS
Reaction Enzyme ATP gain/loss
GG6P GK, HK -1ATP
F6PF1,6BP PFK -1 ATP
GA3P 1, 3BPG GAPDH +2NADH = +6ADP
1,3 BPG  3BPG PGK +2 ATP
PEP  Pyruvate PK +2 ATP

Anaerobic glycolysis: Net ATP = 10-2 ATP = 8ATP
Pyruvate  Lactate (LDH)
2NADH = -6ATP
Comparison of Various Pathways of Carbohydrate Metabolism
Cycle/ Features Peculiarity

pathway
Glycolysis Site: cytoplasm 2, 3BPG Shunt:
Can occur both under aerobic and 2, 3BPG has a role in transport of O2 in
anaerobic conditions blood
Requirement: Rate of glycolysis is higher in tumor cells
10 enzymes, Defects:
2 ATP 1. Hemolytic anemia: Due to defect in

Aldolase A, Pyruvate kinase, Hexokinase
Liberates: enzymes.
four ATP and two NADH+H+ and 2. Exercise intolerance: Due to defect in
pyruvate muscle phosphofructokinase enzyme
Three key regulatory steps: HK, PFK Poisoning:

and PK
1. Arsenic, mercuric poisoning: They
Energetics: bind to –SH group of lipoic acid and
inhibit PDH enzyme
Aerobic:
Four ATP
Two NADH+H+
Net gain= 8 ATP

Anaerobic: 2ATP
PDH (Pyruvate dehydrogenase): Multi-enzyme complex

Site: inner mitochondrial membrane
5 cofactors:
PDH carries out oxidative TPP, Lipoamide, FAD, Coenzyme A,

decarboxylation of pyruvate to acetyl NAD+
CoA 3 enzymes:
Pyruvate dehydrogenase, Dihydrolipoyl
transacetylase, Dihydrolipoyl
dehydrogenase.
4 Vitamins:
Thiamin (TPP)
Riboflavin (FAD)
Nicotinamide (NAD+)
Pantothenic acid (coenzyme A)
Cycle/ Features Peculiarity Energetics

Pathway
TCA Location: Mitochondrial Common pathway for Generates NADH+, FADH2 and
matrix, liver final oxidation of all substrate level ATP
metabolic fuels
Strictly aerobic (carbohydrates, fats, One mole of glucose on
ketone bodies and complete oxidation produces 30
Function: production of amino acids). ATP
energy, biosynthesis of
glucose, FA amino acid Amphibolic:
and heme.
both oxidative
Eight enzymatic (catabolic: pyruvate
reactions: acetyl CoA;
TAG FFA+
four oxidations, glycerol;
two decarboxylation. AA acetyl CoA &

TCA intermediates)
and synthetic
(anabolic: Glucose,
non-essential amino
acids, porphyrin:
heme) process
Anaplerotic
reactions:
Replenish
intermediates of TCA
cycle that participate
in biosynthetic
reactions
Include:
PEP carboxykinase,
pyruvate carboxylase,
transaminases, malic
enzyme steps
Defects: Very rare

defects, usually
incompatible with
life.

Pathway
Glycogen Synthesis Readily available No ATP produced

metabolism source of glucose
Site: between meals and
during a 12-hr. fast
Liver and muscle in (in liver)
cytosolic fraction
Products of glycogen
REQUIREMENTS breakdown:
Five enzymes: HK, Limit dextrin
PGM, Uridyl transferase, (phosphorylase step)
glycogen synthase,
branching enzyme;
Glycogen primer, small G-1-P (-14

glycogen hydrolysis): 90%
Two moles of ATP G-6-P (-16

hydrolysis, branch
point)
G-1-P is then
converted to G-6-P by
PGM in muscle (***
defects)
Break down: Sequential removal of G-6-P serves as energy source

glucose units from for supporting muscle
Not reversal of non-reducing end of contraction
glycogenesis, but is a glycogen
separate pathway
Site: cytosol
- liver and muscle

Pathway
Gluconeo- Biosynthesis of new Situations where Does not generate ATP

Genesis glucose from various GNG occurs:
non-carbohydrate
sources Normal physiological
situation:
Location: Cytosolic
Between meals,
Liver: 85-95%; Not in during sleep,
muscle Exercise/work, after

heavy exercise or
During starvation: work
Kidney: 50% After protein- rich

diet Starvation
Epithelial tissue, small Metabolic acidosis,

intestine: 5%
Use of dietary
proteins in
carbohydrate
pathway.

Pathway
Hmp Shunt Location: Maintains reduced Does not generate ATP

state of Hb:
Cytosolic Pathways requiring NADPH:
Provides NADPH to
Most active in RBC, RBCs for: Synthesis of FA, cholesterol,
liver, adipose tissue, neurotransmitter, nucleotide.
adrenal cortex and Reduction of
mammary glands. oxidized glutathione Detoxification:
(GSSG) to reduced
Does not generate ATP glutathione (GSH) by Reduction of GSH,
enzyme glutathione
Provides: Cyt P450, monooxygenases
reductase
NADPH Defects:
Pentose phosphates G6PD deficiency:
Hemolytic anemia*
Alternative route for
metabolism of glucose Defective
transketolase:
Wernicke Korsakoff
syndrome**

Pathway
Uronic Alternative oxidative Defects: No ATP is produced

Acid pathway for glucose
Pathway
Occurs in liver 1. Essential

cytoplasm pentosuria:
Starts with G-6-P G6PD deficiency
Ends with glucuronic 2. Diminished activity

acid, ascorbic acid and of UDP glucuronyl
pentoses transferase:
i. Neonatal jaundice:
ii. Criggler Najjar

syndrome
iii. Gilbert’s
syndrome

Pathway
Fructose, Fructose: Defects: ATP production via glycolysis

Galactose Essential fructosuria:
Metabolism Rapidly metabolized (Hepatic fructokinase)
after intake by entering
glycolysis at GA3P step Hereditary fructose
intolerance
This bypasses two major
(Aldolase B)
regulatory steps of
glycolysis (HK, FK) Fructose induced
hypoglycemia
Fructokinase and
(F1, 6 BPase)
aldolase B are not under
control of insulin Fructose and sorbitol
in lens cause cataract

Galactose: in diabetes by polyol
pathway
Galactose uptake by the
cells insulin – Galactose is required
independent for synthesis of
lactose, glycolipid,
glycogen, glucuronic
acid, glycoproteins
and proteoglycan
Defects:
Galactosemia
(Galactokinase)
Classical
galactosemia (4-
epimerase
uridyltransferase)
* In response to oxidants (such as aspirin, primaquin, sulfonamide and nitrofurans, flava beans),
reduced GSH is oxidized and impairment of generation of NADPH manifests as hemolysis.
** Weakness or paralysis and impaired mental function.
Defects in Glycogen Metabolism (***):
Disease Enzyme Defect
von Gierk's disease or Type І Glucose-6-phosphatase
Pompe's disease or Type ІІ Defective glycogen breakdown in lysosomes
Coris disease or Type ІІІ Deficiency of debranching enzyme
Anderson's disease or Type ІV Deficiency of branching enzyme
McArdle's syndrome or Type V Deficiency of muscle Phosphorylase
Her's disease or Type VІ Deficiency of liver phosphorylase
REGULATION OF PATHWAYS
Pathway Enzyme Inhibitors Activators
Glycolysis Hexokinase (HK) G-6-P -
Allosteric
PFK ATP, Citrate, ADP, AMP

NADH
Pyruvate kinase (PK) ATP, alanine F1, 6 BiP
TCA Citrate synthase Via feedback ADP

inhibition by
ICD ATP, Citrate,
NADH,
KGDH Succinyl CoA
PDH acetyl CoA, -

NADH
 NADH/NAD,
SDH
 Acetyl
CoA/CoA
OAA, 
ATP/ADP
Glycogen Phosphorylase Muscle:

Metabolism
Allosteric:
ATP, G-6-P AMP
Covalent: Glucagon, Epinephrine, cAMP,

Ca+2, AMP, Phosphorylation
Insulin, ATP,
Glucose
Liver: -
Allosteric:
Glucose
Glycogen Covalent:
phosphorylase
Glucagon, Insulin, G-6-P
Epinephrine,
cAMP, Ca+2,
AMP,
Phosphorylation
Gluconeogenesis Pyruvate carboxylase ADP, insulin Acetyl CoA, Glucocorticoids,

glucagon, epinephrine
Phosphoenolpyruvate ADP, insulin Acetyl CoA, Glucocorticoids,

glucagon, epinephrine
carboxykinase
Glucose 6- Insulin Glucocorticoids, glucagon,

phosphatase epinephrine
KREB’S CYCLE, CITRIC ACID CYCLE OR TRICARBOXYLIC ACID CYCLE (TCA)
Common pathway for final oxidation of all Reactions:

metabolic fuels (carbohydrates, fats,
ketone bodies and amino acids). Steps1&2: Conversion of acetyl CoA to citrate by
citrate synthase; latter further converted to isocitrate
Strictly aerobic via cis-aconitate intermediate.
Generates NADH, FADH2 and substrate Step 3: Oxidative decarboxylation of isocitrate to

level ATP. alpha ketoglutarate by enzyme ICD.
Amphibolic: Step 4: Oxidative decarboxylation of alpha KG to

succinyl CoA by enzyme alpha ketoglutarate
Both oxidative (catabolic) and synthetic
dehydrogenase.
(anabolic) process
Step 5: Substrate level phosphorylation: conversion
of succinyl CoA to succinate by succinyl CoA
synthase and generation of ATP.
Step 6-8: Dehydrogenation reaction: Succinate in IMM forms fumarate and NADH by
dehydrogenase. Addition of water to fumarate (at trans double bond) forms malate and finally
malate is converted to oxaloacetate by enzyme malate dehydrogenase. This completes one trip of
TCA cycle.
Energetics:
Enzyme ATP One mole of glucose on complete

oxidation produces:
ICDH  1 NADH 3ATP
2 x TCA cycle ATP = 24ATP; 2 x PDH
KGDH  1 NADH 3ATP = 6 ATP
Succinate thiokinase 1 ATP 1 ATP
SDH  1 FADH2 2ATP Total = 30 ATP
MDH  1 NAD 3ATP Net gain from glycolysis = 8 ATP
Net ATP 12 ATP
Anaplerotic Reactions: Isoleucine, valine, methionine and threonine to

succinyl CoA.
These reactions replenish intermediates of TCA
cycle that participate in biosynthetic reactions. Carboxylase
They include reactions catalyzed by PEP

carboxykinase, pyruvate carboxylase,
transaminases, malic enzyme.
PEPCK Malic Enzyme

Transaminase: GDH
GlutamateKG GlutamateKG
Importance of regulating blood glucose levels: Intake: glucose absorption from gut
Glucose is obligate fuel for CNS and RBC. Tissue utilization: glycolysis, PPP, TCA,
glycogenesis.
Glucose turnover in a fasting 70 kg individual: 22
mg/kg/min (200 g/24hr) Endogenous production: GNG,
glycogenolysis.
Plasma glucose concentration reflects balance
between intake and tissue utilization.
HORMONES REGULATING CARBOHYDRATE METABOLISM (Fig. 4.1)
Pathway/ Step Pathway / Step Inhibited

Stimulated
Insulin Glycogen Synthesis of enzymes of GNG

synthase
Glycolysis
Glucagon Induces GNG Pyruvate kinase
enzymes Glycogen synthesis
Glycogenolysis
Cortisol Induces all -
enzymes of
GNG
Amino acid
degradation
Insulin
E-cell pancreas
stimulated to
release insulin
Liver takes up more Body Cells

HIGH BLOOD glucose to store it as take up more
GLUCOSE Glycogen Glucose
LEVEL
STIMULUS:
rising blood
glucose after
meal
Homeostasis normal
blood glucose (90
mg/dL)
Stimulus: declining
blood glucose level
(after skipping meal)
Blood glucose levels rises D-cells of pancreas

to set point: glucagon stimulated to release
release diminishes glucagon into blood
Glucagon
Liver breakdown
glycogen releases
glucose in blood
Fig. (4.1). Glucose Homeostasis.
Diabetes Type 1 or Insulin – Dependent Type 2 or Non-Insulin

Diabetes Mellitus (1DDM) Dependent DM (NIDDM)
Features of diabetes Type 1 Type II

mellitus
Other names Juvenile onset Insulin dependent Maturity onset, Non-insulin

(IDDM) dependent (NIDDM)
Defect Autoimmune destruction of - Defective insulin secretion and

cells insulin resistance
Age of onset 6 months-25 years >40 years
Body physique Lean Obese
Prevalence Lower Higher
Treatment Insulin Diet, Drug, Insulin
Lab Features of Diabetes Symptoms
Normal blood glucose: 80-90mg/dL Hyperglycemia (high blood glucose)
Diabetic patient: 110-140 mg/dL Glycosuria (glucose in urine)
After Meals: Polyuria (passage of copious urine)
Normal 120-140 mg/dL Polydypsia (drinking large amount of water)
Diabetic patient >200mg/dL Polyphagia (increased appetite)
Weight loss
Acids and ketones in blood from lipid

breakdown
Coma, if ketones build up
Complications of Diabetes Diagnostic Tests Include
1. Reduction in blood flow to feet causes tissue Blood sugar, Self-monitoring of blood glucose
death, ulceration, infection, loss of toe or (SMBG), Fasting plasma glucose (FPG),
feet. Fasting blood sugar (FBS), Fasting blood
glucose (FBG), Glucose challenge test, Oral
2. Nephropathy – kidney damage. Glucose tolerance test (OGTT).
3. Retinopathy – damage to blood vessel of

retina cataract, skin infection, periodontitis,
and neuritis.
QUESTIONS
1. Describe digestion and absorption of carbohydrates
2. Discuss briefly:
a. Glucose transporters
b. Amylase
c. Lactose intolerance
3. Discuss glycolysis along with energetics.
4. Discuss importance of HMP shunt.
5. Describe citric acid cycle.
6. Compare glycolysis and gluconeogenesis.
7. What is gluconeogenesis? Give an account of conditions favoring gluconeogenesis.
8. Explain the process of glycogen synthesis.
9. Discuss difference in glycogen metabolism in muscle and liver.
10. Discuss briefly:
a. Glucose – alanine cycle
b. Von Gierke’s disease
c. Glycated haemoglobin
d. Glucose tolerance test

e. Insulin actions
f. Glucagon
g. Diabetic keto acidosis
h. Complications of diabetes
i. G6PD deficiency
j. Flavism
k. Galactoseomia
l. Fructose intolerance.
11. Discuss hormonal regulation of blood glucose levels.
12. Discuss diabetes mellitus.
13. What is the end product formed after action of salivary amylase on starch?
14. Name various disorder associated with defect in enzymes of carbohydrate digestion.
15. What is lactose intolerance? How will you diagnose it?
16. What are the conditions when glycolysis is altered?
17. Write short note on 2,3 BPG pathway.
18. Name disorders of glycolysis.
19. Write a brief note on regulation of glycolysis.
20. Differentiate between glycerol phosphate shuttle and malate aspartate shuttle.
21. How does the metabolism of RBC differ from other tissues?
22. What is Cori cycle?
23. What are the different components of PDH complex?

24. Give example of substrate level phosphorylation.
25. Describe the amphibolic nature of TCA cycle.
26. Why is glucose stored as glycogen?
27. What is the difference between glycogenesis and glycogenolysis?
28. What are the end products of glycogen breakdown?
BIBLIOGRAPHY
Denise R Ferrier. Lippincott illustrated reviews: biochemistry. 7th Edition. Philadelphia Wolters Kluwer; 2017
Donald Voet, Judith G Voet, Charlotte W Pratt. Fundamentals of Biochemistry. 5th Edition. New York: Wiley;
2016.
Lehninger A, Nelson D, Cox M. Lehninger principles of biochemistry. New York: Worth Publishers; 2000.
Victor W Rodwell, David A Bender, Kathleen M Botham, Peter J Kennelly, P Anthony Weil. Harper's illustrated
biochemistry. 31st edition. New York: Mcgraw-Hill Education; 2018.

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64 Mind Maps in Biochemistry, 2021, 64-86

 Explain different anabolic and catabolic pathways of Diabetes, Digestion and

CARBOHYDRATE STORAGE Starch Glycogen

Storage form of carbohydrates: Stored in plants Stored in animals

Both amylose and amylopectin Liver and muscle cells

DIGESTION AND ASSIMILATION OF CARBOHYDRATES: Pathway for digestion of

Substrate Site Enzyme Products

Starch Fructose Mouth Salivary amylase 1-4 Maltose

Sucrose Limit dextrin

S. Disease Defect Clinical Feature

Secondary lactase Intolerance to milk

Enzyme Site of Production/ Action Substrate Product

Salivary Amylase Salivary glands/ Oral cavity Starch Disaccharides (maltose),

Oligosaccharidases Lining of the intestine; Oligosaccharides Monosaccharides (e.g.,

Small intestine galactose)

Pancreatic Pancreas/ Small intestine Starch Disaccharides (maltose),

Involves the following steps: Glycolysis:  Importance:

Glycolysis A cytoplasmic pathway Only pathway taking place in

Requires 10 enzymes, 2 ATP molecules Pyruvate TCA via acetyl CoA

 Under anaerobic conditions:

Occurs in erythrocytes, exercising skeletal

It recycles NADH by making lactate to produce

Reaction Input/ output Clinical correlation: basis

Preparatory phase: Energy investment

Glucose + ATP G-1-P + ADP. +ATP Frutose-1,6 BP + ADP

Reaction 1: Input: glucose, MODY: maturity-onset diabetes

Reaction 3: Input: 1ATP Exercise intolerance

Inactive when cell

Phase II: Splitting Stage

Reaction 4: Yield: 2 GA3P Absence of Aldolase (in RBC,

TPI: hemolytic anemia

Phase III: Yield Stage

Reaction 5: 2 NADH: 6ATP Arsenite, Mercuric ions:

-SH group of lipoic acid,

Arsenate used by GAPDH—> 1

Reaction 6: 1, 3 BPG <—PGK—> 3- - Exercise intolerance

Reaction 7: 3 PG PGM 2 PG - Exercise intolerance

Reaction 8: PKG: substrate level 2, 3 BPG: Adaptation to high

Lowers affinity of Hb for O2

2PG—enolase—> PEP Enolase:

GG6P GK, HK -1ATP

F6PF1,6BP PFK -1 ATP

GA3P 1, 3BPG GAPDH +2NADH = +6ADP

1,3 BPG  3BPG PGK +2 ATP

PEP  Pyruvate PK +2 ATP

Anaerobic glycolysis: Net ATP = 10-2 ATP = 8ATP

Pyruvate  Lactate (LDH)

Comparison of Various Pathways of Carbohydrate Metabolism

Cycle/ Features Peculiarity

Glycolysis Site: cytoplasm 2, 3BPG Shunt:

Requirement: Rate of glycolysis is higher in tumor cells

2 ATP 1. Hemolytic anemia: Due to defect in

Three key regulatory steps: HK, PFK Poisoning:

Net gain= 8 ATP

PDH (Pyruvate dehydrogenase): Multi-enzyme complex

PDH carries out oxidative TPP, Lipoamide, FAD, Coenzyme A,

Cycle/ Features Peculiarity Energetics

two decarboxylation. AA acetyl CoA &

Defects: Very rare

Cycle/ Features Peculiarity Energetics

Glycogen Synthesis Readily available No ATP produced

Glycogen primer, small G-1-P (-14

Two moles of ATP G-6-P (-16