Department of Internal Medicine, University of Texas Southwestern Medical Center, Touchstone Center for Diabetes Research, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Trends Endocrinol Metab. 2010 Jun;21(6):345-52. doi: 10.1016/j.tem.2010.01.009. Epub 2010 Mar 10.
Once considered divine retribution for sins, comorbidities of obesity (metabolic syndrome) are today attributed to obesity-induced metabolic defects. Here, we propose that obesity and hyperleptinemia protect lipid-intolerant nonadipose organs against lipotoxic lipid spillover during sustained caloric surplus. Metabolic syndrome is ascribed to lipotoxicity caused by age-related resistance to antilipotoxic protection by leptin.
一度被认为是罪恶的天谴,肥胖(代谢综合征)的合并症如今归因于肥胖引起的代谢缺陷。在这里,我们提出肥胖和高瘦素血症可保护不耐脂的非脂肪组织免受持续热量过剩时的脂毒性脂质溢出。代谢综合征归因于与年龄相关的抗瘦素脂毒性保护作用的抵抗引起的脂毒性。