کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5949822 | 1172392 | 2011 | 7 صفحه PDF | دانلود رایگان |
ObjectivesTo determine the effects of glucosamine-supplementation on endoplasmic reticulum (ER) stress levels and atherogenesis, and to investigate the potential role of glucosamine in hyperglycemia-associated accelerated atherosclerosis.MethodsFive week old apolipoprotein E-deficient (apoEâ/â) mice were provided with normal drinking water or water supplemented with 5% glucosamine (w/v) or 5% mannitol (w/v). To induce hyperglycemia, a separate group of apoEâ/â mice received multiple low dose injections of streptozotocin (STZ). All mice were provided with a standard chow diet and were euthanized at 15 weeks of age. Hepatic and vascular ER stress levels and atherosclerotic lesion area at the aortic root were determined.ResultsSTZ-induced hyperglycemic and glucosamine-supplemented mice had significantly larger and more advanced atherosclerotic lesions than control mice. Indications of ER stress were increased in the livers and atherosclerotic lesions of hyperglycemic and glucosamine-supplemented mice but not in the controls. In glucosamine-supplemented mice accelerated atherosclerosis was independent of detectable changes in blood glucose concentration, glucose tolerance, plasma insulin, or plasma lipid levels.ConclusionSimilar to hyperglycemia, glucosamine-supplementation promotes ER stress, hepatic steatosis and accelerated atherosclerosis. These findings support a model by which hyperglycemia promotes hepatic and vascular complications via a glucosamine intermediate.
Journal: Atherosclerosis - Volume 219, Issue 1, November 2011, Pages 134-140