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Ethanol decreases basal insulin secretion from HIT-T15 cells

机译:乙醇减少HIT-T15细胞的基础胰岛素分泌

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摘要

Various epidemiological studies suggest that alcohol intake is one of the risk factors leading to type II or non-insulin-dependent diabetes mellitus (NIDDM), but the effect of alcohol on beta-cell function remains unexplored. To study the mechanism of the diabetogenic action of ethanol, we investigated the effect of ethanol on beta-cell functions using a single clonal beta-cell line, HIT-T15 cells. When HIT cells were treated with ethanol, the metabolic activity judged by MTT assay was inhibited in dose- and time dependent manners, but cytotoxicity was not observed. Ethanol also inhibited basal insulin secretion by 30% compared to the untreated control. However, glucose-stimulated insulin secretion was not impaired by ethanol although the basal insulin secretion was inhibited. These results imply that ethanol exert beta-cells to overwork in order to compensate inhibition of the basal secretion. This finding may at least in part explain the diabetogenic action of ethanol. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 19]
机译:各种流行病学研究表明,饮酒是导致II型或非胰岛素依赖型糖尿病(NIDDM)的危险因素之一,但酒精对β细胞功能的影响尚待探索。为了研究乙醇的致糖尿病作用机理,我们使用单一的克隆β细胞系HIT-T15细胞研究了乙醇对β细胞功能的影响。用乙醇处理HIT细胞后,MTT法判断的代谢活性呈剂量和时间依赖性,但未观察到细胞毒性。与未处理的对照组相比,乙醇还抑制了基础胰岛素分泌30%。然而,尽管基础胰岛素分泌被抑制,但乙醇不会损害葡萄糖刺激的胰岛素分泌。这些结果表明,乙醇会过度发挥β细胞的作用,以补偿对基础分泌的抑制。这一发现至少可以部分解释乙醇的致糖尿病作用。 (C)2002 Elsevier Science Inc.保留所有权利。 [参考:19]

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