POSITIONAL CLONING OF THE MOUSE OBESE GENE AND ITS HUMAN HOMOLOG
POSITIONAL CLONING OF THE MOUSE OBESE GENE AND ITS HUMAN HOMOLOG
复制标题
DOI：
10.1038/372425a0
复制
发表时间：
1994-12-01
期刊：
影响因子：
64.8
通讯作者：
FRIEDMAN, JM
中科院分区：
文献类型：
--
作者：
ZHANG, YY;PROENCA, R;FRIEDMAN, JM
平衡食物摄入和能量消耗的机制决定了谁会肥胖，谁会瘦。其中一个调节老鼠体内能量平衡的分子是肥胖基因。ob突变导致严重肥胖和II型糖尿病，这是一种类似于人类病态肥胖的综合征的一部分。ob基因产物可以作为来自脂肪组织的信号传导途径的一部分起作用，该信号传导途径用于调节身体脂肪库的大小。
The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.