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Depot-Specific Response of Adipose Tissue to Diet-Induced Inflammation: The Retinoid-Related Orphan Receptor α (RORα) Involved? | LitMetric

AI Article Synopsis

  • The study investigates the role of the nuclear receptor RORα in managing inflammation and insulin sensitivity in different fat types, specifically epididymal adipose tissue (EAT) and inguinal adipose tissue (IAT).
  • In experiments using RORα loss-of-function mice and wild-type mice on different diets, results showed that RORα impacts inflammatory status and insulin sensitivity differently in EAT and IAT when exposed to a Western diet.
  • Findings indicate that RORα may have an anti-inflammatory effect in IAT, potentially leading to healthier fat expansion, while EAT becomes more inflammatory and insulin-resistant under the same dietary conditions.

Article Abstract

Objective: Epididymal adipose tissue (EAT), a visceral fat depot, is more closely associated with metabolic dysfunction than inguinal adipose tissue (IAT), a subcutaneous depot. This study evaluated whether the nuclear receptor RORα, which controls inflammatory processes, could be implicated.

Methods: EAT and IAT were compared in a RORα loss-of-function mouse (sg/sg) and in wild-type (WT) littermates, fed a standard diet (SD) or a Western diet (WD), to evaluate the impact of RORα expression on inflammatory status and on insulin sensitivity (IS) of each fat depot according to the diet.

Results: Sg/sg mice fed the SD exhibited a decreased inflammatory status and a higher IS in their fat depots than WT mice. WD-induced obesity had distinct effects on the two fat depots. In WT mice, EAT exhibited increased inflammation and insulin resistance while IAT showed reduced inflammation and improved IS, together with a depot-specific increase of RORα, and its target gene IκBα, in the stroma vascular fraction (SVF). Conversely, in sg/sg mice, WD increased inflammation and lowered IS of IAT but not of EAT.

Conclusions: These findings suggest an anti-inflammatory role for RORα in response to WD, which occurs at the level of SVF of IAT, thus possibly contributing to the "healthy" expansion of IAT.

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Source
http://dx.doi.org/10.1002/oby.22006DOI Listing

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