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Regulatory Mechanisms- Lipid Metabolism (summary Chart)
- March 12, 2020
- Posted by: Namrata Chhabra
- Category: Learning resources Library Metabolism of lipids Quick Revision Series Quick revisions
 
						
| Enzyme and pathway | Effect of substrate concentration | Allosteric Modification/ Feedback Inhibition/Covalent modification | Induction/ Repression | Clinical Significance | 
| Acetyl CoA Carboxylase (Fatty acid synthesis) | Activity increases during the well-fed state Activity decreases during fasting | Activator- Citrate, ATP Acetyl CoA Insulin- activates the enzyme by covalent modification of the enzyme (dephosphorylation through stimulating protein phosphatase enzyme) 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 and beta-oxidation of fatty acids | Activity is low in the fed state and high during fasting | Activated by Glucagon through lipolysis and provision of fatty acids for oxidation  Inhibited by insulin and malonyl CoA |  | 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 is low in the fasting state, | Activated by Insulin, Thyroid hormone  Inhibited by Glucagon, Glucocorticoids,(by reversible phosphorylation) Dietary cholesterol (Hepatic synthesis) Mevalonate and cholesterol, the products of the pathway  | Expression of HMG COA reductase is regulated by sterol regulatory element-binding protein. Also induced by Insulin | Activity high in Diabetes mellitus due to the availability of excess Acetyl co A. 
 Activity is inhibited by Statins that are used as cholesterol-lowering drugs. | 
Author:Namrata Chhabra
 
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