Visceral adiposity confers significant risk for developing metabolic disease in obesity whereas preferential expansion of subcutaneous white adipose tissue (WAT) appears protective. Unlike subcutaneous WAT, visceral WAT is resistant to adopting a protective thermogenic phenotype characterized by the accumulation of Ucp1 beige/BRITE adipocytes (termed 'browning'). In this study, we investigated the physiological consequences of browning murine visceral WAT by selective genetic ablation of , a transcriptional suppressor of the adipocyte thermogenic program. deletion in fetal visceral adipose precursors (; ), or adult visceral white adipose precursors (; ), results in the accumulation of beige-like thermogenic adipocytes within multiple visceral adipose depots. Thermogenic visceral WAT improves cold tolerance and prevents and reverses insulin resistance in obesity. These data indicate that beneficial visceral WAT browning can be engineered by directing visceral white adipocyte precursors to a thermogenic adipocyte fate, and suggest a novel strategy to combat insulin resistance in obesity.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5552276 | PMC |
| http://dx.doi.org/10.7554/eLife.27669 | DOI Listing |
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Article Synopsis
- Activation of Fas in adipocytes inhibits the browning process, potentially leading to increased body weight gain in mice, and its expression correlates with higher BMI in humans.
- The study found that Fas activation decreases energy expenditure through reduced protein levels of p53, a tumor suppressor, in adipocytes.
- In humans, higher p53 levels in subcutaneous and visceral white adipose tissue were linked to increased BMI, while higher levels in visceral fat were associated with lower insulin sensitivity.
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