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Biochemistry General 45bbbb10

Regulation of lipid metabolism by insulin lacks which of the following feature:

A
Reduced activity of HMG CoA synthetase
B
Increased release of fatty acids from stored fat in adipose tissue
C
Increased availability of glycerol-3-phosphate
D
Increased Acetyl CoA carboxylase activity
High-Yield Explanation
The net effect of insulin on lipid metabolism is to reduce the release of fatty acids from the stored fat.Among the tissues, adipose tissue is the most sensitive to the action of the insulinLipogenesisIt is the process by which acetyl-CoA is conveed to fats.The former is an intermediate stage in metabolism of simple sugars, such as glucose.Through lipogenesis, the energy can be efficiently stored in the form of fats.Lipogenesis encompasses the processes of fatty acid synthesis and subsequent triglyceride synthesis (when fatty acids are esterified with glycerol to form fats).The products are secreted from the liver in the form of very-low-density lipoproteins (VLDL)Fatty acids synthesis stas with acetyl-CoA and builds up by the addition of two carbon units.The synthesis occurs in the cytoplasm in contrast to the degradation (oxidation), which occurs in the mitochondria.Many of the enzymes for the fatty acid synthesis are organized into a multienzyme complex called fatty acid synthetase.Control and regulationInsulin is an indicator of the blood sugar level of the body, as its concentration increases propoionally with blood sugar levels.Thus, a large insulin level is associated with the fed state.As one might expect, therefore, it increases the rate of storage pathways, such as lipogenesis.Insulin stimulates lipogenesis in two main ways:The enzymes pyruvate dehydrogenase (PDH), which forms acetyl-CoA, and acetyl-CoA carboxylase (ACC), which forms malonyl-CoA, are obvious control points.These are activated by insulin.So a high insulin level leads to an overall increase in the levels of malonyl-CoA, which is the substrate required for fatty acids synthesis.PDH dephosphorylation

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