Endocrine control of lipoprotein metabolism
All hormones exert an influence on lipoprotein metabolism. However, with respect to diet and the control of postprandial lipid metabolism, insulin has by far the greatest impact. Although classically associ-ated with carbohydrate metabolism and the uptake of glucose into cells, the actions of insulin are critical to the control of postprandial lipid metabolism. Insulin is secreted in response to the reception of food in the gut and it:
●stimulates LPL in adipose tissue
●suppresses the intracellular lipolysis of stored TAG in adipose tissue by inhibiting hormone-sensitive lipase
●suppresses the release of VLDL from the liver.
Insulin coordinates the lipolysis of dietary TAG and uptake of NEFA into adipose tissue. It achieves this by minimizing the release of NEFA from TAG stores in adipose tissue and TAGs produced in the liver by suppressing the secretion of VLDL. The sensitivity of the target tissues – liver, adipose tissue, and, perhaps to a lesser extent, skeletal muscle – to insulin is critical to the maintenance of these effects. Failure of insulin action, insulin resistance, in conditions such as obesity and diabetes results in dyslipidemia characterized by an impaired capacity to lipolyze TAG-rich lipopro-teins (TAG intolerance or enhanced postprandial lipemia). This effect is compounded by the failure of insulin to suppress the mobilization of NEFA from adipose tissue TAG, which increases the flux of NEFA to the liver and stimulates the overproduction of VLDL (‘portal hypothesis’). The suppression of VLDL secretion is also abolished so that VLDL is released into the postprandial circulation and is free to compete with chylomicrons, augmenting postprandial lipemia still further. This series of events gives rise to a dys-lipidemia or ALP, which is found frequently in insulin- resistant conditions. Insulin also stimulates the synthesis of cholesterol by activating HMG-CoA reductase and the activity of LDL receptors, although the overall effect on cholesterol homeostasis is small in relation to the control of the LDL pathway described above.
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