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）饮食引起的葡萄糖不耐受的机制。我们研究了必须消耗 LC 饮食多长时间才能损害大鼠的葡萄糖耐量，以及饮食引起的游离脂肪酸 cFEA) 水平增加是否会影响胰岛素分泌和胰岛素敏感性。对喂食对照饮食（碳水化合物 6050 或 aLC（在随机交叉设计中碳水化合物 1050 饮食 1、3 或 7 天）的雄性 Wistar 大鼠进行腹膜内葡萄糖耐量测试在从大鼠分离的胰岛中测量胰岛素释放还检查了在 244i 培养期间暴露于棕榈酸 (PA) 的胰岛中饲喂对照和 LC 饮食 3 天的胰岛素分泌。通过静脉注射胰岛素耐受性试验，对喂食 3 天的 LC 饮食的大鼠或静脉注射与 PA 混合 24 小时的大鼠进行全身胰岛素敏感性测定，摄入 LC 饮食 3 天和 7 天后，葡萄糖耐受性受损更为严重。 7天后，喂食LC饮食3天的大鼠的胰岛中，葡萄糖耐量受损伴随着空腹血浆FFA水平的升高。控制大鼠胰岛PA受损葡萄糖刺激的胰岛素分泌喂食LC饮食3天的大鼠体内出现胰岛素抵抗。给大鼠静脉注射PA降低了全身胰岛素敏感性。给大鼠喂食 LC 饮食 3 天，糖耐量受损该受损可能是由胰岛素分泌和胰岛素敏感性下降引起的，这可能是由于 LC 饮食导致血浆 FFA 水平增加所致。