Wu Gengshu, Zhang Liyan, Li Tete, Lopaschuk Gary, Vance Dennis E, Jacobs René L
Group on the Molecular and Cell Biology of Lipids and Department of Biochemistry, University of Alberta, Edmonton, AB, Canada T6G 2S2.
J Obes. 2012;2012:319172. doi: 10.1155/2012/319172. Epub 2012 Jun 18.
Previous studies demonstrated that choline supply is directly linked to high-fat-diet-induced obesity and insulin resistance in mice. The aim of this study was to evaluate if choline supply could also modulate obesity and insulin resistance caused by a genetic defect. Eight-week-old male ob/ob mice were fed for two months with either choline-deficient or choline-supplemented diet. Tissue weight including fat mass and lean mass was assessed. Intracellular signaling, plasma glucagon and insulin, and glucose and insulin tolerance tests were also investigated. The choline-deficient diet slowed body weight gain and decreased fat mass. Choline deficiency also decreased plasma glucose level and improved glucose and insulin tolerance although fatty liver was exacerbated. Increased adipose lipolytic activity, decreased plasma glucagon and reduced expression of hepatic glucagon receptor were also observed with the choline-deficient diet. Our results demonstrate that a choline-deficient diet can decrease fat mass and improve glucose tolerance in obese and diabetic mice caused by a genetic defect.
先前的研究表明，胆碱供应与小鼠高脂饮食诱导的肥胖和胰岛素抵抗直接相关。本研究的目的是评估胆碱供应是否也能调节由基因缺陷引起的肥胖和胰岛素抵抗。给8周龄的雄性ob/ob小鼠喂食胆碱缺乏或补充胆碱的饮食两个月。评估包括脂肪量和瘦体重在内的组织重量。还研究了细胞内信号传导、血浆胰高血糖素和胰岛素，以及葡萄糖和胰岛素耐量试验。胆碱缺乏饮食减缓了体重增加并减少了脂肪量。胆碱缺乏还降低了血浆葡萄糖水平，改善了葡萄糖和胰岛素耐量，尽管脂肪肝加剧。胆碱缺乏饮食还观察到脂肪组织脂解活性增加、血浆胰高血糖素降低以及肝脏胰高血糖素受体表达减少。我们的结果表明，胆碱缺乏饮食可以减少肥胖和由基因缺陷引起的糖尿病小鼠的脂肪量并改善葡萄糖耐量。
