Insulin action in uremia.
The evidence appears overwhelming that insulin resistance is the major cause of the carbohydrate intolerance observed in chronically uremic subjects and that the primary site of this insulin resistance resides in peripheral tissues, muscle. Diminished lipoprotein lipase activity, perhaps related to decreased insulin sensitivity, is in large part responsible for the hypertriglyceridemia. However, there is some evidence that increased VLDL synthesis also contributes to the disturbance in lipid metabolism. This latter abnormality may be related to the high circulating insulin levels that result from the insulin resistance. In contrast to glucose and lipid metabolism, the plasma amino acid and potassium lowering effects of insulin are normal in uremic individuals. Whether there is an impaired ability of insulin to stimulate protein synthesis and inhibit protein degradation remains to be delineated.
D000328:Adult; D000596:Amino Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology; D007328:Insulin / Q000378:metabolism / Q000502:physiology*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D011188:Potassium / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism; D013997:Time Factors; D014511:Uremia / Q000503:physiopathology*
D000596:Amino Acids; D007328:Insulin; D011972:Receptor, Insulin; D005947:Glucose; D011188:Potassium