Journal
CELL METABOLISM
Volume 13, Issue 3, Pages 283-293Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2011.01.019
Keywords
-
Categories
Funding
- NIAMS [AR053803-03]
- Human Frontier Science Program
- Netherlands Organization for Scientific Research
- Howard Hughes Medical Institute
- Hillblom Foundation
- Nuclear Receptor Signaling Atlas [U19DK62434-01]
- Helmsley Trust
- NIH [HD027183, DK057978]
- Muscular Dystrophy Association [174408]
Ask authors/readers for more resources
How type I skeletal muscle inherently maintains high oxidative and vascular capacity in the absence of exercise is unclear. We show that nuclear receptor ERR gamma is highly expressed in type I muscle and, when transgenically expressed in anaerobic type II muscles (ERRGO mice), dually induces metabolic and vascular transformation in the absence of exercise. ERRGO mice show increased expression of genes promoting fat metabolism, mitochondrial respiration, and type I fiber specification. Muscles in ERRGO mice also display an activated angiogenic program marked by myofibrillar induction and secretion of proangiogenic factors, neovascularization, and a 100% increase in running endurance. Surprisingly, the induction of type I muscle properties by ERR gamma does not involve PGC-1 alpha. Instead, ERR gamma genetically activates the energy sensor AMPK in mediating the metabovascular changes in ERRGO mice. Therefore, ERR gamma represents a previously unrecognized determinant that specifies intrinsic vascular and oxidative metabolic features that distinguish type I from type II muscle.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available