Obesity in humans and rodents is characterized by mitochondrial dysfunction, but what connects obesity and mitochondrial damage? The small GTPase RalA, according to a report in Nature Metabolism.

The report’s authors observed increased RalA expression and activity in inguinal white adipose tissue (iWAT) during the development of obesity in mice fed a high-fat diet (HFD), prompting them to create adipocyte-specific Rala knockout (Rala^AKO) mice for further studies. These mice, when fed a HFD, were protected against weight gain, glucose intolerance and hepatic steatosis. A closer look revealed an increase in energy expenditure alongside increased mitochondrial oxidative phosphorylation, reflected by increased fatty acid oxidation, in primary adipocytes from Rala^AKO mice compared with wild-type primary adipocytes.

人类和啮齿动物肥胖的特点是线粒体功能障碍，但肥胖和线粒体损伤之间有何联系呢？根据Nature Metabolism的一篇报告，小 GTP 酶 RalA。

该报告的作者观察到，在喂食高脂饮食 (HFD) 的小鼠肥胖过程中，腹股沟白色脂肪组织 (iWAT) 中 RalA 的表达和活性增加，促使他们创建脂肪细胞特异性Rala敲除 ( Rala ^AKO ) 小鼠，以进一步研究研究。这些小鼠在喂食高脂饮食后，体重增加、葡萄糖不耐症和肝脂肪变性得到了保护。仔细观察发现，与野生型原代脂肪细胞相比， Rala ^AKO小鼠的原代脂肪细胞中能量消耗增加，同时线粒体氧化磷酸化增加（通过脂肪酸氧化增加反映出来）。