期刊
EMBO REPORTS
卷 14, 期 9, 页码 795-803出版社
WILEY
DOI: 10.1038/embor.2013.111
关键词
Autophagy; Myf5+progenitors; brown fat
资金
- Ellison Medical Foundation
- National Institutes of Health [5T32GM728837]
- [DK087776]
- [AG043517]
- [DK81412]
- [DK033823]
- [DK020541]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK026687, P60DK020541, R01DK081412, R01DK033823, K01DK087776, R37DK033823, P30DK020541] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007288] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG043517] Funding Source: NIH RePORTER
Macroautophagy (MA) regulates cellular quality control and energy balance. For example, loss of MA in aP2-positive adipocytes converts white adipose tissue (WAT) into brown adipose tissue (BAT)-like, enhancing BAT function and thereby insulin sensitivity. However, whether MA regulates early BAT development is unknown. We report that deleting Atg7 in myogenic Myf5+ progenitors inhibits MA in Myf5-cell-derived BAT and muscle. Knock out (KO) mice have defective BAT differentiation and function. Surprisingly, their body temperature is higher due to WAT lipolysis-driven increases in fatty acid oxidation in 'Beige' cells in inguinal WAT, BAT and muscle. KO mice also present impaired muscle differentiation, reduced muscle mass and glucose intolerance. Our studies show that ATG7 in Myf5+ progenitors is required to maintain energy and glucose homeostasis through effects on BAT and muscle development. Decreased MA in myogenic progenitors with age and/or overnutrition might contribute to the metabolic defects and sarcopenia observed in these conditions.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据