The document discusses energy demand and supply as well as the integration of major metabolic pathways for energy metabolism. It outlines several key metabolic pathways including glycolysis, fatty acid oxidation, degradation of amino acids, the citric acid cycle, oxidative phosphorylation, the hexose monophosphate shunt, gluconeogenesis, and glycogen metabolism. It then describes how different organs specialize in carbohydrate, lipid, and protein metabolism both during fed and starved states to regulate energy supply and demand at the organism level.
14. ORGAN SPECIALIZATION AND METABOLIC INTEGRATION
• DURING WELL-FED STATE
ORGANS CARBOHYDRATE
METABOLISM
LIPID
METABOLISM
PROTEIN
METABOLISM
LIVER
(CENTRAL
METABOLIC
CLEARING
HOUSE)
GLYCOLYSIS
GLYCOGENESIS
HMP SHUNT
GLUCONEOGENESIS
SYNTHESIS OF
FATTY ACIDS
AND
TRIACYLGLYCEROL
DEGRADATION OF
Aas &
PROTEIN
SYNTHESIS
ADIPOSE
TISSUE
(ENERGY
STORAGE
TISSUE)
15KG TAG
STORED IN A
NORMAL
ADULT MAN
GLYCOLYSIS
HMP
SYNTHESIS OF
FATTY ACIDS
AND
TRIACYLGLYCEROL
17. •METABOLISM IN STARVATION
ORGANS CARBOHYDRATE
METABOLISM
LIPID METABOLISM PROTEIN
MET.
LIVER
(ACTS AS
BLOOD
GLUCOSE
BUFFERING
ORGAN)
GLUCONEOGENESIS
GLYCOGEN
DEGRADATION
FATTY ACID OXIDATION
KETONE BODIES
SYNTHESIS
ADIPOSE
TISSUE
GLUCOSE UPTAKE &
ITS METABOLISM
DEGRADATION OF
TAG
FATTY ACID GLYCEROL
18. METABOLISM IN STARVATION
ORGANS CARBOHYDRATE
METABOLISM
LIPID
METABOLISM
PROTEIN MET.
SKELETAL
MUSCLE
GLUCOSE UPTAKE
& ITS METABOLISM
FATTTY ACIDS & KETONE
BODIES UTILISED BY
SK MUSCLE AS A FUEL
SOURCES
STARVATION (>3WKS)
INCREASED KB IN Bd
CIRCULATION
EARLY PERIOD
STARVATION
MUSCLE PROTEINS
DEGRADED INTO AAs
UTILISED BY LIVER
PROLONGED
STARVATION
PROTEIN BREAK
DOWN REDUCED
BRAIN STARVATION FOR FIRST
2WKS BRAIN IS
MOSTLY DEPENDENT ON
GLUCOSE (SUPPLIED BY
LIVER
GLUCONEOGENESIS)
>3WKS INCREASED IN
PLASMA KETONE
BODIES BY THIS TIME
BRAIN DEPENDS ON KB
FOR ENERGY NEEDS
