2. • Process by which large molecules are
hydrolyzed into smaller molecules , which can
be easily absorbed by the body.
• Digestion & absorption of individual foods
like carbohydrates, lipids, proteins & nucleic
acid occur in the GIT and also involving the
organs.
• Cooking & mastication of food makes the
digestion process easier.
• Process is starts in mouth but it occur for
limited time. Because gastric HCL will inhibits
the action of amylase .
3. • Main sites are:-
- Mouth:
- Small intestine
Dietary carbohydrate consists of :-
- Polysaccharides:- starch, glycogen & cellulose
- Disaccharides:- sucrose & lactose
- monosaccharides:- mainly glucose & fructose
monosaccharides need no digestion prior to
absorption, whereas disaccharides &
polysaccharides must be hydrolyzed to simple
sugars before their absorption.
5. Digestion in mouth
• Starch digestion begins in the mouth with
enzyme, amylase .
• During mastication amylase acts on starch &
glycogen that breaks it down into disaccharides –
continues in storage section of the stomach.
• Amylase is active at neutral pH & requires
chloride ions for its activity.
Plays only a small role in breakdown because of
the short time food is in the mouth.
Small intestine – amylase from the pancreas
continues starch digestion.
6. IN THE MOUTH
G
G
G
G
G
G
G
Ga 1-4 link
G
G
G
G a 1-6 link
G
G
G
GG
G G G G
G
G
G
G G
G
maltose
G
G
G
isomaltose
amylase
maltotriose
G
G
G
G
a Limit dextrins
• Pre-stomach – Salivary amylase : a 1-4
endoglycosidase
7. Digestion In Stomach
• Carbohydrate digestion stop in the
stomach.
• Because of high acidity inactivates
the salivary amylase.
8. • Further digestion occurs in the small intestine
by pancreatic enzymes , intestinal juice.
• When acidic stomach content reach in the
small intestine , they stimulate mucosal cells
of the duodenum to release secretin &
cholecystokinin (CCK) .
• Secretin the release of bicarbonate whose
function is to neutralize the acidic contents.
Digestion In Small Intestine
9. • CCK stimulate the release of digestive
enzymes including pancreatic alpha amylase.
• There are two phases of intestinal digestion:-
1) .digestion due to alpha amylase.
2). due to intestinal brush border membrane
enzymes.
10. Pancreatic amylase
Hydrolyzes alpha 1-4 linkages
Produces monosaccharides from disaccharides,
and polysaccharides.
Major importance in hydrolyzing starch and
glycogen to maltose
Amylase
Polysaccharides Disaccharides
11.
12. IN THE SMALL INTESTINE
• Pancreatic enzymes
a-amylase
G G GG G
G
G G G
G G GG
GG G
amylose
amylopectin
G G G G G
a amylase
+
G
G G
G G
maltotriose maltose
a Limit dextrins
G
13. Brush border membrane enzymes
G
G G
G G
G
G
G
G G
G
G
Glucoamylase (maltase)
or
a-dextrinase
G G
G
G
G
a-dextrinase
G GG
G
G G
Gmaltase
sucrase
a Limit dextrins G
14. • Location Enzymes Form of Dietary CHO
• Mouth Salivary Amylase Starch Maltose Sucrose Lactose
• Stomach (amylase from saliva) Dextrin→Maltose
• Small Intestine Pancreatic Amylase Maltose
Brush Border Enzymes Glucose Fructose Galactose
+ + +
Glucose Glucose Glucose
• Large Intestine None Bacterial Microflora Ferment
Cellulose
15. Carbohydrate absorption
• Monosaccharides are absorbed in small intestine
and enter the blood stream of the portal venous
system. All monosaccharides are absorbed to
some extent by simple diffusion process.
There are two mechanisms:-
• 1). Active transport:- uphill process i.e from low
glucose conc. Outside the cell to a higher conc.
With in the cell.
• 2). Facilitative transport:- down hill process, i.e
from higher conc. to lower one. It is mediated by
transport proteins is K/a glucose transporters
16.
17. Active transport
• Transport of glucose & galactose occur by
active transport.
• Its energy requiring process that require
specific transport protein which are
transmembrane protein.
• Process is mediated by Na dependent glucose
transporter(SGLT-1) binds both glucose & Na
at separate site & transport them through the
intestinal membrane.
18. Sodium dependent glucose transporter (SGluT). Sodium
and glucose co transport system at luminal side; sodium is
then pumped out. Energy is used indirectly
19. • Na ions is transported from higher conc. to
lower conc. & at same time glucose is
transported against its conc. Gradient ,
process is known as co-transport mechanism.
• Free energy is obtained from hydrolysis of ATP
linked to sodium pump.
• Active transport is inhibited by cardiac
glycosides .
20.
21. • Sugar are actively transported have some
chemical features in common. Sugar must
have:-
- Six membered ring .
- One or more C-atom attached at the
site of C-5.
- Attached –OH gp at C-2.
22.
23. Facilitative transport
• Fructose & mannose are transported across
the brush border by Na ion independent
diffusion process.
• Involve glucose transporters, GLUTs ( 12 no.)
• Movement of sugar in this process is downhill,
going higher conc. to lower conc. until it
reaches an equilibrium.
24. • Blood carries monosaccharides to the liver.
–All are converted to glucose.
–Glucose travels to other cells via the blood.
–Extra glucose is stored as glycogen in the
liver and skeletal muscles.
25. • In most tissues the internal glucose
concentration is quite low; transport can only
proceed from the extracellular area into the
cell.
• In gluconeogenetic tissues (liver and kidney),
intracellular glucose concentration can exceed
blood glucose concentration in the post-
absorptive or fasting states.
26. Glucose Transporters
• Glucose is hydrophilic
• Two types
- GLUT
- SGLUT
- GLUTs :- 12 different types
- Sodium and ATP independent
- Ubiquitous
27. • SGLUT:-
- Sodium dependent
- Require ATP
- Located in :-
Intestine
Renal tubules
Blood brain barrier
28. Intestinal absorption of glucose. At the intestinal lumen,
absorption is by sodium dependent glucose transporter
(SGluT) and at the blood vessel side, absorption is by
glucose transporter 2 (GluT2).
29. • Common treatment for diarrhea is oral
rehydration fluid. It contains glucose and
sodium. Presence of glucose in oral
rehydration fluid allows uptake of sodium to
replenish body sodium chloride.
30. GLUT
• GLUT 2
• GLUT 3
Location
• Brain,
blood ,
heart
• Liver,
pancreas ,
small
intestine
Function
• low Km,
insulin
independent
• High Km
31. Glucose Transporter Type 2 (GluT2)
This transporter is not dependent on sodium, but it is a uniport,
facilitated diffusion system
32. • Large protein with 12 transmembrane
domians.
• Exists in two conformations-T1 T2.
• In T1 the glucose binding site is exposed on to
the outside.
• Then , change into T2 conformation & bound
glucose exposed onto inner side into the RBCs
• Different GLUTs have different Km values.
Glucose transporters (GLuT)
33. Glucose transporters (GLuT)
• These are GLuT 1to12 in no. GLuT-2 & 4 are
important among them.
• GLuT-1:- RBCs brain , kidney, colon, placanta &
erythrocyte, low Km
• Function :- uptake of glucose.
• GLuT-2:- liver, kidney, intestine & pancreatic beta
cell , high Km
• Function :- operates as co-transport system.
• Uniport, not dependent on sodium.
34. • Glucose is held on the GluT -2 with weak
hydrogen bonds. GluT -2 first open up on the
outerside & imbibes the glucose molecule.
After fixing the glucose molecule it changes
the configuration & opens out at the inner
side releasing the glucose. This process is
known as ping pong mechanism.
• rapid uptake & release of glucose.
35. • GluT2 transports glucose into cells when
blood sugar level is high. So in the well-fed
state, glucose is taken up by liver and
deposited as glycogen.
This mechanism also enables the pancreas to monitor
the glucose level and adjust the rate of insulin
secretion. The GluT4 is under control of insulin.
Other glucose transporters are not under the control of
insulin.
Insulin induces intracellular GluT4 molecules to move
to the cell membrane and thus increases glucose
uptake.
37. • GLuT-3:- brain , kidney, & placanta , low Km
• Function :- uptake of glucose
• GLuT-4:- heart & skeletal muscle, adipose
tissue, intermediate Km
• Function :- under control of insulin
• insulin stimulated uptake of glucose.
• GLuT-5:- small intestine, low Km
• Function :- absorption of glucose.
38. Glucose transporters
Present in Properties
GluT1 RBC, brain, kidney, Glucose uptake in colon, retina, most of
cells placenta
GluT2 Serosal surface of intestinal cells,
liver, beta cells of pancreas
Glucose uptake in liver; glucose sensor in
beta cells
GluT3 Neurons, brain Glucose into brain cells
GluT4 Skeletal, heart Insulin mediated muscle, adipose tissue
glucose uptake
GluT5 Small intestine, testis, sperms,
kidney
Fructose transporter; poor ability to
transport glucose
SGluT Intestine, kidney Cotransport; from lumen into cell
39. Clinical importance of GLUT4
• Type 2 Diabetes mellitus , due to insulin
deficiency the no. GLUT 4 decreased on cell
surfaces of heart , muscles & adipose tissues .
• This decrease the transport of glucose into the
cells by 50% and leads to cellular hypoglycemia .
• Then enter into the blood & leads hyperglycemia
• Antidiabetic drugs used for treatment of DM :-
sulphonylureas occur up regulation of GLUT4
40.
41. • These promote insulin secretion by inhibiting
the K channels and increasing intracellular Ca
levels. this decrease blood glucose levels
through glut 4 up regulation .
• In Type 2 diabetes mellitus, insulin
resistance is seen in muscle and fat cells.
• In diabetes, entry of glucose into muscle is
only half of normal cells.
42.
43. Regulation of Glucose Transport
• Glucose enters cells by facilitated diffusion.
• GLUT transporters are thought to be involved
in Na+-independent facilitated diffusion of
glucose (co-transport system) into cells.
• Insulin stimulates glucose transport by
promoting translocation of intracellular
vesicles that contain the GLUT4 and GLUT1
glucose transporters to the plasma
membrane.• This effect is reversible.
45. Disorders
• Impaired ability of digestion & absorption of
CHO is due to bacterial fermentation in the
large intestine.
• Abdominal cramps & flatulence occur due to
the accumulation of gases , which lead
diarrhoea & dehydration.
• Genetic deficiency occur most of the
disaccharides.
46. • Lactose intolerance – lack of the enzyme lactase
causes inability to digest lactose in milk
products.
• signs & Symptoms :-
• Diarrhoea & flatulence;- lactose accumulated in
the intestinal tract ,which is osmotically active &
hold water ,leads diarrhoea.
• Abdominal cramps & Distension :- lactose also
fermented by intestinal bacteria which produce
gas & leads cramps , distension.
47. –Some people are really allergic to milk. This
allergy seems to be increasing in infants.
–Big Problem – calcium deficiency.
Sucrase deficiency
Disacchariduria :- disaccharides appear in the
urine.
Monosaccharides malabsorption:
monosaccharides are deficient in the body.
Causes:- due to absence of transport protein.
48. Objective
• Explain the digestion of carbohydrates
• Describe the absorption of glucose and
glucose transporters.
• Note on lactose intolerance
49. Metabolism
Sum of all chemical reactions in the
body . The chemical changes that take
place in a cell that produce energy and
basic materials needed for important
life processes
• Creates energy (ATP)
50. Types of Metabolic Reactions
• Catabolic reactions
The chemical reactions that break larger molecules
into smaller molecules. It is usually an exergonic
process.
• Chemical breakdown releases energy
• Anabolic reactions
– the chemical reactions that form larger molecules
from smaller molecules. It is usually an endergonic
process.
– Building macromolecules in the body.
51. Amphibolic reactions
• Occur at the crossroads of anabolic &
catabolic reactions.
• Can operate in both ways depending upon the
body’s requirement.
• Eg;- acetyl COA catabolism through TCA cycle
to produce energy.
• Acetyl COA also produce cholesterol.
• Act at junction points b/w catabolism &
anabolism.
52. Metabolism is regulated
• Regulation is necessary because of needs of the
body change acc. To different factors.
• Divide into two parts :-
- Active regulation :- by substrate conc.
- Passive regulation :- by enzyme .
Regulatory step:- enzyme activity is slow.
Committed step:- whose product is committed to
undergo that specific pathway leading to final
product formation.
54. • Substrate level Phosphorylation:-Formation
of ATP through the conversion of substrates
to products is called substrate level
Phosphorylation.
• Oxidative Phosphorylation:- it requires
oxygen. This production of ATP is called
oxidative phosphorylation. It does not
directly involve substrates.
55.
56. Glycolysis
• Sequence of reactions that oxidize of glucose to
pyruvate in aerobic condition or lactate in
anaerobic with the generation of ATP and NADH.
• Also called as the Embden-Meyerhof Pathway.
(EM). It is unique pathway since it can utilize
oxygen if available, or it can function in the total
absence of oxygen.
• Glycolysis is a universal pathway; present in all
organisms: from yeast to mammals.
57. LOCATION
• In eukaryotes, glycolysis takes place in the
cytosol.
• Glycolysis is anaerobic; it does not require
oxygen & pyruvate can be fermented to
lactate.
• In the presence of O2, pyruvate is further
oxidized to CO2.
58. Significance of the Glycolysis Pathway
• Glycolysis is the only pathway that is taking place in
all the cells of the body.
• Glycolysis is the only source of energy in
erythrocytes.
• In strenuous exercise, when muscle tissue lacks
enough oxygen, anaerobic glycolysis forms the major
source of energy for muscles.
• It provides carbon skeletons for synthesis of non-
essential amino acids as well as glycerol part of fat.
• Most of the reactions of the glycolytic pathway are
reversible, which are also used for gluconeogenesis.
59. Stages of Glycolysis
The 3 stages of Glycolysis
• Stage 1 is the investment stage.
2 mols. of ATP are consumed
• stage 2 Splitting phase:-fructose-1,6-
bisphosphate is cleaved into 2 3-carbon units of
glycerladehyde-3-phosphate & Dihydroxy-
acetone-phosphate .
• Stage 3 Energy generating stage:- 4 mols. of ATP
and 2 mols. of NADH
60.
61. Step-wise reactions of glycolysis
• Reaction 1: Phosphorylation of glucose to
glucose-6 phosphate.
• This reaction requires energy and so it is
coupled to the hydrolysis of ATP to ADP and Pi.
• Enzyme:- hexokinase. It has a low Km for
glucose, once glucose enters the cell, it gets
phosphorylated. Hexokinase is inhibited by its
product glucose-6-P.( Regulatory step) .
• This step is irreversible. So the glucose gets
trapped inside the cell.
64. Hexokinase v/s glucokinase
• Site:- all tissues
• Low km value
• Acts on glucose ,fructose &
mannose
• Non inducible
• Acts at low blood glucose
level, remains staurated
• Inhibited by product i.e G-6-p
• Function
• Even when blood glucose
level is low, glucose is
utilised by body cells
• Only liver
• High Km
• Acts on glucose only
• Induced by insulin
• Acts only when high glucose
level as after meals
• Not inhibited.
• Acts only when blood glucose
level is more than 100 mg/dl;
then glucose is taken up by liver
cells for glycogen synthesis
65. • Reaction 2: Isomerization of glucose-6-
phosphate to fructose 6-phosphate. The
aldose sugar is converted into the keto form.
• Enzyme: phosphogluco-isomerase.
• This is a reversible reaction. The fructose-6-
phosphate is quickly consumed and the
forward reaction is favored. ( committed step)
66.
67. • Reaction 3: is another kinase reaction.
Phosphorylation of the hydroxyl group on C1
forming fructose-1,6- bisphosphate.
•Enzyme:phosphofructokinase. This allosteric
enzyme regulates the glycolysis.
• Reaction is coupled to the hydrolysis of an ATP
to ADP and Pi.
• This is the second irreversible reaction of the
glycolytic pathway.
68.
69. • Reaction 4: fructose-1,6-bisphosphate is split
into 2 3-carbon molecules, one aldehyde and
one ketone:- dihyroxyacetone phosphate
(DHAP) and glyceraldehyde 3-phosphate
(GAP).
• The enzyme is aldolase.
70.
71.
72. Arsenate bind the inorganic phosphate gp. &
inhibit the reaction in result no production of
ATP.
73.
74. Enolase requires Mg++. Fluoride will remove magnesium
ions and inhibit this enzyme.
So when taking blood for sugar estimation, fluoride is
added to blood.
If not, glucose is metabolised by the blood cells, so that
lower blood glucose values are obtained.
76. Pyruvate kinase deficiency causes
hemolytic anemia
• RBCs depend on glycolysis for ATP. The net ATP
production by glycolysis is zero in RBCs .
• ATP deficiency affects the Na/K ATPase pump
which maintains the shape of RBCs.
• So, the RBCs in ATP deficiency , swell, loose
their shape undergo lysis leading to hemolytic
anemia .
77. LDH has 4 subunits and 5 iso-enzymes. The cardiac iso-
enzyme of LDH (H4) will Increase in myocardial
infarction
83. Lactic acidosis
• Lactic acidosis is the accumulation of lactic
acid in the blood which affect the blood pH.
• Normal blood lactate levels are less than
1.2mM.
• High conc. Of lactate results in lowered blood
pH & bicarbonate levels.
• If oxygen supply is inadequate (hypoxia), the
mitochondria are unable to continue ATP
synthesis at a rate sufficient to supply the cell
with the required ATP.
84. • In this situation, glycolysis is increased to
provide additional ATP, and the excess
pyruvate produced is converted into lactate
and released from the cell into the blood
stream, where it accumulates over time.
• Increased glycolysis helps compensate for less
ATP from oxidative phosphorylation, it cannot
bind the protons resulting from ATP
hydrolysis. Therefore, proton concentration
rises and causes acidosis.
85. • The signs of lactic acidosis are deep and rapid
breathing, vomiting, and abdominal pain—
symptoms.
• Lactic acidosis may be caused by diabetic
ketoacidosis , liver, kidney disease, shock,
alcohol abuse.
• Heavy metal toxicity, including arsenic
poisoning can raise lactate levels and lead to
metabolic acidosis.
86. • Clinical importance of blood lactate:-
- measurement of blood lactate is useful
to assess the presence of shock & to
monitor the patients recovery.
Treatment :- giving bicarbonate I.V.
87. Aerobic :-With the present of oxygen in cells
pyruvate is oxidized to acetyl-CoA, which then
enters the citric acid cycle. The NADH molecules
are reoxidized through the mitochondrial
electron transport chain with electrons
transferred to the O2 molecules.
• Anaerobic :- in the absence of oxygen
–Need to oxidize NADH to regenerate NAD+
–Pyruvate converted to lactate by lactate
dehydrogenase.
Aerobic and anaerobic glycolysis
88. • Tissues that function under hypoxic conditions
produce lactate.
• It is emergency source of energy.
• The reoxidation of NADH via lactate formation
allows glycolysis to proceed in the absence of
oxygen by regenerating sufficient NAD for
another cycle of the reaction catalyzed by
glyceraldehye 3-p dehydrogenase.
• In RBCs , there is no mitochondria. RBCs take
energy only through glycolysis , where the end
product is lactic acid. Net production of ATP is
only 2.
91. Areobic glycolysis
• ATP consumed
- Hexokinase = 1 ATP
- Phosphofructokinase = 1 ATP
Total ATP = 2
ATP produced
Glyceraldehyde 3 P dehydrogenase = 1NADH = 2.5ATP
Bisphosphoglycerate kinase = 1ATP
Pyruvate kinase = 1ATP
Total ATP = 4.5
1 glucose = 2 pyruvate = 4.5x 2= 9 ATP
Total No. of ATP in glycolysis : ATP consumed- ATP produced
= 2- 9 = 7 ATP
92. Anaerobic glycolysis
• ATP produced
- Bisphosphoglycerate kinase = 1 ATP
Pyruvate kinase = 1 ATP
Total ATP = 2 ATP
1 glucose = 2 pyruvate = 2x 2= 4 ATP
Total No. of ATP in glycolysis : ATP produced -ATP consumed
4 – 2= 2 ATP
93. ATP produced from one mole. Of
glucose in glycolysis
• Anaerobic glycolysis :- anoxia condition ( absent
of O2 ) no NADPH production occur .
• ATP produced - ATP utilization = Total ATP
4 - 2 = 2
• AEROBIC :-
• ATP produced - ATP utilization = Total ATP
9 - 2 = 7
95. • Hexokinase catalyzed phosphorylation of glucose
is the first irreversible step of glycolysis regulated
by excess glucose-6-phosphate. If G6P
accumulates in the cell, there is feedback
inhibition of hexokinase till the G-6-P is
consumed.
Hexokinase
-allosteric feedback inhibition
glucose-6-p
Regulation of Hexokinase
96. high CHO diet insulin inducer
(+) (+)
glucokinase
(-) (-)
starvation, glucagon
diabetes
97. Regulation of Phosphofructokinase
• high CHO diet insulin inducer
(+) (+)
• fructose,2-6bp,
• (+) AMP
Phosphofructokinase
(-) (-)
• (-)
starvation, glucagon
diabetes citrate, ATP, c-AMP
98.
99.
100.
101. • Under normal physiological condition & anoxia :-
- End product is NADH , pyruvate & lactate
NADH:- enters into mitochondria & goes to ETC.
finally produced ATP.
Pyruvate:-
Converted into acetyl COA & then oxidized in TCA.
surplus glucose ------ fats & a.a.( alanine)
Under fasting :-
Pyruvate is produced from lactate& a.a.
Then undergo gluconeogensis to provide glucose.
102. Cori cycle ( fate of lactate)
• The Cori cycle is the flow of lactate and
glucose between the muscles and the liver.
• When anaerobic conditions occur in active
muscle, glycolysis produces lactate.
• lactate moves blood stream liver
oxidized back to pyruvate.
• pyruvate glucose via gluconeogensis
(which is carried back to the muscles).
• The Cori Cycle operates during exercise.
103.
104. Glucose-Alanine cycle
• Transport of amino acids from muscle to
liver, occur during starvation .
• The liver the alanine is converted back to
pyruvate by transaminase enzyme and
used as a gluconeogenic substrate or
oxidized in the TCA cycle. The amino
nitrogen is converted to urea in the urea
cycle and excreted by the kidneys.
107. Significance of 2-3 BPG
• The 2,3-BPG combines with hemoglobin , and reduces the
affinity towards oxygen. So, in presence of 2,3-
BPG,oxyhemoglobin will unload oxygen more easily in
tissues.
• Under hypoxic conditions the 2,3-BPG concentration in
the RBC increases, thus favouring the release of oxygen to
the tissues even when pO2 is low.
• The compensatory increase in 2,3-BPG in high altitudes
favors oxygen dissociation. BPG is increased in fetal
circulation.
• In this shunt pathway, no ATP is generated
113. Regulation of PDH
End product inhibition by
- acetyl CoA
- NADH
Co-valent modification of PDH enzyme
CLINICAL ASPECTS
1. Thiamine deficiency:
- PDH activity decreased
- pyruvate is converted to lactate
-lactic acidosis
2. Inherited deficiency of glycolytic enzymes
- Pyruvate kinase
- aldolase
114. • Pyruvate dehydrogenase (PDH): PDH
requires thiamine pyrophosphate (TPP); due
to thiamine deficiency beriberi occur. TPP
deficiency in alcoholism causes pyruvate
accumulation in tissues and resultant lactic
acidosis. Inherited PDH deficiency may also
lead to lactic acidosis.
115. citric acid cycle
Definition:-- Acetate in the form of acetyl-CoA,
is derived from pyruvate and other
metabolites, and is oxidized to CO2in the
citric acid cycle.
• Also called Krebs cycle or tricarboxylic acid
(TCA) cycle.
• All enzymes are in the mitochondrial matrix
or inner mitochondrial membrane
123. The 3 enzymes:
1. Citrate Synthase:- Inhibited by citrate; ATP
2. IsoCitrate Dehydrogenase:- Inhibited by NADH
3. α-KG Dehydrogenase:- Inhibited by succinyl Co-A and
NADH.
124. Significance of TCA
1. Complete oxidation of acetyl-CoA
2. ATP generation
3. Final common oxidative pathway
4. Integration of major metabolic pathways
5. Fat is burned on the wick of carbohydrates
6. Excess carbohydrates are converted as neutral fat
7. No net synthesis of carbohydrates from fat
8. Carbon skeletons of amino acids finally enter the citric acid
cycle
9. Amphibolic pathway
10. Anaplerotic role ( intermediate use as synthesis of new product)
125. Fat cannot be converted to glucose
Except ODD chain fatty acid ( end product propinyl
COA (3C) occur glucose synthesis
126.
127. Amphibolic pathways
•Intermediates of the TCA cycle serve as
precursors for biosynthesis of biomolecules.
•Many amino acids are synthesized starting with
transamination of α-ketoglutarate.
• Porphyrins and heme are synthesized from
succinyl CoA.
• Oxaloacetate is another α-keto acid and its
transamination leads to aspartate and other
amino acid biosynthesis.
128. • Oxaloacetate is also the precursor of purines
and pyrimidines via aspartate.
• Fatty acids and sterols are synthesized from
citrate.
