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Autophagy in Myf5+ progenitors regulates energy and glucose homeostasis through control of brown fat and skeletal muscle development
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Martinez-Lopez, Nuria, Athonvarangkul, Diana, Sahu, Srabani, Coletto, Luisa, Zong, Haihong, Bastie, Claire C., Pessin, Jeffrey E., Schwartz, Gary J. and Singh, Rajat (2013) Autophagy in Myf5+ progenitors regulates energy and glucose homeostasis through control of brown fat and skeletal muscle development. EMBO reports, 14 (9). pp. 795-803. doi:10.1038/embor.2013.111 ISSN 1469-221X.
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Official URL: http://dx.doi.org/10.1038/embor.2013.111
Abstract
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.
Item Type: | Journal Article | ||||||
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Subjects: | Q Science > QP Physiology | ||||||
Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School > Biomedical Sciences > Translational & Experimental Medicine Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School |
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Library of Congress Subject Headings (LCSH): | Fat cells, Brown adipose tissue, Insulin | ||||||
Journal or Publication Title: | EMBO reports | ||||||
Publisher: | Nature Publishing Group | ||||||
ISSN: | 1469-221X | ||||||
Official Date: | 14 September 2013 | ||||||
Dates: |
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Volume: | 14 | ||||||
Number: | 9 | ||||||
Page Range: | pp. 795-803 | ||||||
DOI: | 10.1038/embor.2013.111 | ||||||
Status: | Peer Reviewed | ||||||
Publication Status: | Published | ||||||
Access rights to Published version: | Open Access (Creative Commons) | ||||||
Date of first compliant deposit: | 14 October 2016 | ||||||
Date of first compliant Open Access: | 17 October 2016 | ||||||
Funder: | Ellison Medical Foundation, Einstein-Mount Sinai Diabetes Research Center, National Institutes of Health (U.S.) (NIH) | ||||||
Grant number: | DK087776, AG043517 (Ellison), DK81412, DK033823, DK020541 (Einstein), 5T32GM728837 (NIH) |
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