AI Article Synopsis
- Aging leads to metabolic issues like increased fat and lower energy use, but the exact transcriptional controls are unclear.
- Research shows that removing PPARγ in fat tissue of aging mice causes more fat, insulin resistance, and less heat production.
- The study highlights PPARγ's vital role in regulating energy use as we age, suggesting it could be a target for improving age-related metabolic problems.
Article Abstract
It is well established that aging is associated with metabolic dysfunction such as increased adiposity and impaired energy dissipation; however, the transcriptional mechanisms regulating energy balance during late life stages have not yet been fully elucidated. Here, we show that ablation of the nuclear receptor PPARγ specifically in inguinal fat tissue in aging mice is associated with increased fat tissue expansion and insulin resistance. These metabolic effects are accompanied by decreased thermogenesis, reduced levels of brown fat genes, and browning of subcutaneous adipose tissue. Comparative studies of the effects of PPARγ downregulation in young and mid-aged mice demonstrate a preferential regulation of brown fat gene programs in inguinal fat in an age-dependent manner. In conclusion, our study uncovers an essential role for PPARγ in maintaining energy expenditure during the aging process and suggests the possibility of targeting PPARγ to counteract age-associated metabolic dysfunction.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5847881 | PMC |
| http://dx.doi.org/10.1111/acel.12721 | DOI Listing |
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