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Mechanism of glucose intolerance induced by a low-carbohydrate diet

低碳水化合物饮食诱发葡萄糖不耐受的机制

基本信息

批准号：
11670365
负责人：
KANEKO Takashi
金额：
$ 2.37万
依托单位：
山梨医科大学
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2001
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11670365/
关键词：
Type2diabetesmellitus Carbohydrate Glucose-fattyacidcycle Rat Glucose tolerance Insulin secretion Insulin sensitivity

项目摘要

In this study, we clarified the mechanism of glucose intolerance induced by a low-carbohydrate (LC) diet. We examined how long a LC diet must be consumed in order to impair glucose tolerance in rats, and whether insulin secretion and insulin sensitivity are affected by the increased level of free fatty acids cFEA) induced by the diet. Intraperitoneal glucose tolerance tests were performed onmale Wistar rats that were fed a control diet (carbohydrate 6050 or aLC (carbohydrate 1050 diet for 1, 3, or 7 day(s) in a randomized crossover desiga Insulin release was measured in pancreatic islets isolated from rats fed control and LC diets for 3 days. Insulin secretion was also examined in islets exposed to palmitic acid (PA) during 244i culture. Whole body insulin sensitivity was measured by an intravenous insulin tolerance test in rats fed LC diet for 3 days or in rats intravenously in fused withPA for 24 h. Glucose tolerancewas impaired after 3 and 7 days of consuming a LC diet ; the impairment was more severe after 7 days. The glucose tolerance impairment was accompanied by a rise in the fasting plasma FFA level. Glucose-stimulated insulin secretion was significantly reduced in pancreatic islets from rats fed LC diet for 3 days. Exposure of control rat islets to PA impaired glucose-stimulated insulin secretion Rats fed LC diet for 3 days developed insulin resistance inviva Intravenous PA infusion into rats decreased thewhole body insulin sensitivity. Feeding rats a LC diet for 3 days impaired glucose tolerance The impairment may be induced by a decrease in both insulin secretion and insulin sensitivity, \rtiich may be caused by the increased plasma FFA level due to the LC diet.

在这项研究中，我们阐明了低碳水化合物（LC）饮食诱导的葡萄糖耐受不良的机制。我们检查了为了损害大鼠的葡萄糖耐量必须消耗LC饮食多长时间，以及胰岛素分泌和胰岛素敏感性是否受到饮食诱导的游离脂肪酸水平增加的影响。对雄性Wistar大鼠进行腹膜内葡萄糖耐量试验，所述大鼠在随机交叉设计中喂食对照饮食（碳水化合物6050或aLC（碳水化合物1050饮食）1、3或7天。在244i培养期间，还检查了暴露于棕榈酸（PA）的胰岛中的胰岛素分泌。用静脉胰岛素耐量试验测定LC饲料喂养3天或与PA静脉融合24小时的大鼠的全身胰岛素敏感性。糖耐量受损后3和7天的消费LC饮食，损害更严重后7天。糖耐量受损伴随着空腹血浆FFA水平的升高。在饲喂LC饲料3天的大鼠胰岛中，葡萄糖刺激的胰岛素分泌显著减少。对照组大鼠胰岛暴露于PA损害葡萄糖刺激的胰岛素分泌。LC饲料喂养大鼠3天后产生体内胰岛素抵抗。给大鼠喂食LC饮食3天损害葡萄糖耐量该损害可由胰岛素分泌和胰岛素敏感性的降低诱导，这可由LC饮食引起的血浆FFA水平增加引起。