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Glycolysis:
The degradation of glucose to pyruvate or
lactate generates 8 ATP.
Pyruvate is converted to acetyl CoA.
Fatty acid oxidation:
Fatty acids undergo sequential degradation
with a release of acetyl CoA.
The energy is trapped in the form of NADH &
FADH2
Degradation of amino acids:
Amino acids, when consumed in excess than
required for protein synthesis, are degraded &
utilized to meet the fuel demands of the body.
The glucogenic amino acids can serve as
precursors for the synthesis of glucose
The ketogenic amino acids are the precursors
for acetyl CoA.
Citric acid cycle:
Acetyl CoA is the key & common metabolite,
produced from different fuel sources
(carbohydrates, lipids, amino acids).
Acetyl CoA enters TCA cycle & oxidized to CO2.
Most of the energy is trapped in the form of
NADH & FADH2.
Oxidative phosphorylation:
The NADH & FADH2, produced in different
metabolic pathways, are finally oxidized in
the electron transport chain (ETC).
The ETC is coupled with oxidative
phosphorylation to generate ATP.
Hexose monophosphate shunt:
It is primarily concerned with the liberation
of NADPH & ribose sugar.
NADPH is utilized for the biosynthesis of
several compounds, including fatty acids.
Ribose is an essential component of
nucleotides & nucleic acids.
Gluconeogenesis:
The synthesis of glucose from non-
carbohydrate sources constitutes
gluconeogenesis.
Several compounds (e.g. pyruvate, glycerol,
amino acids) can serve as precursors for
gluconeogenesis.
Glycogen metabolism:
Glycogen is the storage form of glucose,
mostly found in liver & muscle.
It is degraded (glycogenolysis) & synthesized
(glycogenesis) by independent pathways.
Glycogen effectively serves as a fuel reserve
to meet body needs.
The metabolic pathways are controlled by
four different mechanisms.
1. The availability of substrates
2. Covalent modification of enzymes
3. Allosteric regulation
4. Regulation of enzyme synthesis.
Liver: The body's central metabolic clearing house.
Carbohydrate metabolism:
Increased glycolysis, glycogenesis & HMP shunt &
decreased gluconeogenesis.
Lipid metabolism:
Increased synthesis of fatty acids & TAG.
Protein metabolism:
Increased degradation of amino acids & protein
synthesis.
Adipose tissue:
Adipose tissue is the energy storage tissue.
Carbohydrate metabolism:
The uptake of glucose is increased &
increase in glycolysis & HMP shunt.
Lipid metabolism:
The synthesis of fatty acids & TAGs is
increased.
The degradation of TAGs is inhibited.
Skeletal Muscle:
Carbohydrate metabolism:
The uptake of glucose is higher & glycogen
synthesis is increased.
Lipid metabolism:
Fatty acids are fuel sources for skeletal muscle.
Protein metabolism:
Incorporation of amino acids into proteins is
higher.
Brain:
Carbohydrate metabolism:
In an absorptive state, glucose is the only
fuel source to the brain.
About 120 g of glucose is utilized per day.
50% of the energy is utilized by plasma
membrane Na+ - K+ ATPase for nerve
impulse transmission.
Lipid metabolism:
The free fatty acids cannot cross the blood-
brain barrier, hence their contribution to the
brain is insignificant.
In a fed state, ketone bodies are almost
negligible as fuel source to the brain.
Brain predominantly depends on ketone
bodies during prolonged starvation.
Metabolic integration in well fed state
Liver in starvation:
Carbohydrate metabolism:
Liver is to act as a blood glucose buffering
organ.
During starvation, increased
gluconeogenesis & elevated glycogen
degradation furnish glucose to the needy
tissues (mostly brain).
Lipid metabolism:
Fatty acid oxidation is increased with an
elevated synthesis of ketone bodies.
This is due to TCA cycle cannot cope up with
the excess production of acetyl CoA & it is
diverted for ketone body synthesis.
The brain slowly adapts itself to use ketone
bodies.
Metabolic integration in Starvation
Adipose tissue in starvation:
Carbohydrate metabolism:
Glucose uptake & its metabolism are lowered.
Lipid metabolism:
The degradation of TAG is elevated &
increased release of fatty acids which serve as
fuel source (brain is an exception).
Glycerol is precursor for glucose.
Synthesis of fatty acids & TAG is stopped.
Skeletal muscle in starvation:
Carbohydrate metabolism:
Glucose uptake & its metabolism are depressed.
Lipid metabolism:
Fatty acids & ketone bodies are utilized by
muscle.
On prolonged starvation, muscle adapts to
exclusively utilize fatty acids.
This increases the ketone bodies in circulation.
Protein metabolism:
During the early period of starvation, muscle
proteins are degraded to liberate the amino
acids which are effectively utilized by the
liver for glucose synthesis (gluconeogenesis).
On prolonged starvation, however, protein
breakdown is reduced.
Brain in starvation:
The brain is mostly dependent on glucose.
This, in turn, is dependent on the amino acids
released from the muscle protein degradation.
Starvation beyond 3 weeks, results in increase
in ketone bodies.
The brain adapts itself to depend on ketone
bodies for the energy needs.
Textbook of Biochemistry-U Satyanarayana
Textbook of Biochemistry-DM Vasudevan
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