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Enzyme

Pathway

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

Activator-

Citrate,

ATP

Acetyl co A

Insulin-by causing de phosphorylation by stimulating protein phosphatase

Inhibitors

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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