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Effect of substrate concentration

Allosteric Modification/ Fed back Inhibition

Induction/ Repression

Clinical Significance

Acetyl co A Carboxylase

Fatty acid synthesis

Activity increases during well fed state

Activity decrease during fasting




Acetyl co A

Insulin-by causing de phosphorylation by stimulating protein phosphatase


Long chain fatty acids, Epinephrine, Glucagon- via changes in phosphorylation state through c AMP mediated phosphorylation cascade

Induced by Insulin


Repressed by Glucagon

Activity decreases in diabetes Mellitus

Carnitine Acyl Transferase

Carnitine shuttle

Activity low in fed state, high during fasting

Activated by Glucagon through lipolysis and provision of fatty acids for oxidation


Inhibited by insulin and malonyl co A


Inherited CAT-I deficiency affects only the liver, resulting in reduced fatty acid oxidation and ketogenesis, with hypoglycemia.

HMG co A Reductase

Cholesterol synthesis

Activity low in fasting state,

Activated by Insulin, Thyroid hormone


Inhibited by – Glucagon, Glucocorticoids,(By reversible phosphorylation)

Dietary cholesterol (Hepatic synthesis)

Mevalonate and cholesterol ,the products of pathway


Expression of HMG COA reductase is regulated by sterol regulatory element binding protein

Also induced by Insulin

Activity high in Diabetes mellitus die to availability of excess Acetyl co A.


Activity inhibited by Statins used as cholesterol lowering drugs.



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