From the preceeding discussion, it is evident that derangements in glucose, insulin, and glucagon metabolism may be harmful to the uremic patient in a variety of ways. Hyperglycemia per se may contribute to the increased incidence of atherosclerosis and to the alteration of structural protein in several tissues, including the kidney. This latter phenomenon may play a role in the progression of renal disease in such individuals. Hyperinsulinemia also presents a risk factor to the uremic patient. Increased circulating insulin levels have been shown to stimulate arterial smooth muscle cell proliferation, enhance lipid transport into arterial smooth muscle cells, and enchance triglyceride synthesis. All of these effects are potentially atherogenic. Additionally, if the insulin resistance involves lipid metabolism, diminished activity of lipoprotein lipase will contribute further to the hyperlipidemia and enchance lipid synthesis. Last, insulin resistance may extend to protein synthesis and, in part, be responsible for the muscle wasting and negative nitrogen balance observed so commonly in patients with advanced renal insufficiency. Hyperglucagonemia, by stimulating gluconeogenesis, would be expected to exacerbate further the abnormalities in amino acid metabolism.
|Original language||English (US)|
|Issue number||SUPPL. 17|
|State||Published - 1985|
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