Insulin Synthesis

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3.4.2 INSULIN DEPENDENT PROTEIN SYNTHESIS There is considerable evidence that insulin plays a major role in the regulation of muscle protein metabolism. In healthy subjects, after an acute increase in insulin concentration, with amino acid levels maintained at normal or high levels, as occurs after a mixed meal, a net protein deposition in muscle may occur. This is primarily because of a stimulation of synthesis, with a possible inhibition of breakdown (26). It is also shown to decrease proteolytic activity of lysosomes. A number of studies, performed at the molecular level, have demonstrated insulin’s ability to promote several steps of the process of protein synthesis in skeletal muscle (28). The synthesis of new contractile units takes…show more content…
Therefore insulin generates a reduced response in target tissues like skeletal muscle, liver, and adipocytes when compared with subjects with normal glucose tolerance [NGT]. The most accurate way to measure insulin resistance is the euglycemic insulin clamp technique, in which insulin is infused to maintain a constant plasma insulin level. Glucose is then infused and, as the plasma level falls because of the action of insulin, more glucose is added to maintain a steady level. The amount of glucose infused over time provides a measure of insulin resistance. This and other similar methods are useful for research but are otherwise impractical…show more content…
The insulin secretory capacity of the β-cell is augmented in an attempt to overcome this disturbance. Thus, an individual with impaired glucose tolerance or early diabetes mellitus (FBS-120 mg/dl) can secrete up to twice as much insulin as a normal person (FBS- 80 mg/dl) would. When, however, the fasting glucose level increases further, the β-cell can no longer maintain increased secretion of insulin. Thus further increase in the plasma glucose concentration is associated with a progressive decline in insulin secretion. Hence a diabetic person (FBS - 150mg/dl or more) will secrete an amount of insulin similar to that in a nondiabetic individual (18). The increase in total insulin concentrations reflects an attempt of β cells to maintain glucose tolerance in the non-diabetic range, despite worsening insulin resistance. The decrease in insulin secretion is relative to insulin resistance and hyperglycemia and is a hallmark of the onset of type 2 diabetes. Thus there is absolute hyperinsulinemia, but relative deficiency of insulin in type 2 diabetic patients, implying reduced sensitivity to insulin

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