Roles of a novel lepin-induced transcript in the regulation of obesity and leptin resistance.

新型瘦素诱导转录物在肥胖和瘦素抵抗调节中的作用。

• 批准号: 23791042
• 负责人: KOMORI Tadasuke
• 金额: $ 2.75万
• 依托单位: Wakayama Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791042/
• 关键词: レプチン; 視床下部; 摂食調節; 肥満; 糖尿病; レプチン; 視床下部; 摂食調節; 肥満; 糖尿病

In both normal and high-fat diet conditions, the body weights were decreased in LIT2-deficient mice compared to those in WT mice, although there were no changes in food intake between WT and LIT2-deficient mice. In addition, glucose tolerance and insulin sensitivity were increased in LIT2-deficient mice compared to those in WT mice. These results suggest that LIT2 regulates the actions of leptin such as energy expenditure and glucose metabolism rather than food intake in the hypothalamus.

在正常和高脂饮食条件下，与WT小鼠相比，LIT2缺陷小鼠的体重降低，尽管WT和LIT2缺陷型小鼠之间的食物摄入量没有变化。另外，与WT小鼠相比，LIT2缺陷小鼠的葡萄糖耐量和胰岛素敏感性增加。这些结果表明，LIT2调节瘦素的作用，例如能量消耗和葡萄糖代谢，而不是下丘脑中的食物摄入量。