Carbohydrate metabolism in renal failure.
Hyperglycemia and impaired glucose tolerance are well known phenomena occurring in patients with renal failure. In contrast to true diabetic subjects, an elevated ratio of insulin to glucose during the glucose tolerance test is consistently observed indicating a peripheral insulin insensitivity. Among the possible reasons, a disturbance at the cellular level seems to be most likely. There is some evidence of reduced peripheral glucose utilization on the one hand and increased hepatic glucose output--probably by stimulation of gluconeogenesis--on the other. Agents that have been suggested to be involved in these alterations of carbohydrate metabolism in uremia are hormones, electrolytes, pH, and "toxic" metabolic intermediates or end-products. Of these, an increase in insulin antagonistic hormones; among them growth hormone, catecholamines, and glucagon, seems to be of most significance. Although for the individual hormones no equivocal correlation with glucose intolerance has been proved, the interaction of all of them may result in a preponderance of insulin antagonism thus leading to an apparent insulin resistance.
D000311:Adrenal Glands / Q000502:physiology; D000818:Animals; D050260:Carbohydrate Metabolism; D004573:Electrolytes; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006943:Hyperglycemia / Q000150:complications; D007329:Insulin Antagonists; D007333:Insulin Resistance; D007674:Kidney Diseases / Q000150:complications / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008954:Models, Biological; D014511:Uremia / Q000150:complications / Q000378:metabolism
D004573:Electrolytes; D007329:Insulin Antagonists; D005947:Glucose