Niswender Kevin D, Magnuson Mark A
Tennessee Valley Healthcare System and Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
J Clin Invest. 2007 Oct;117(10):2753-6. doi: 10.1172/JCI33528.
In this issue of the JCI, Morioka et al. report on mice with a whole-pancreas knockout of the leptin receptor that exhibit improved glucose tolerance due to enhanced insulin secretion . At first glance, their findings are very different from those reported in another recent study in which beta cell-specific and hypothalamic knockout of the same gene caused obesity and impaired beta cell function. The differences, which are understandable when one considers the body weights of the animals studied, provide new insight into the links among insulin, leptin action, and beta cell function.
在本期《临床研究杂志》中,森冈等人报道了全胰腺敲除瘦素受体的小鼠,这些小鼠由于胰岛素分泌增强而表现出改善的葡萄糖耐量。乍一看,他们的发现与最近另一项研究报道的结果截然不同,在该研究中,同一基因的β细胞特异性敲除和下丘脑敲除导致了肥胖和β细胞功能受损。考虑到所研究动物的体重,这些差异是可以理解的,它们为胰岛素、瘦素作用和β细胞功能之间的联系提供了新的见解。