Key result
Western diet drives opposing inflammatory responses in mouse fat depots via RORα.
RORα appears to play an anti-inflammatory role in inguinal adipose tissue in response to a Western diet, potentially contributing to healthy fat expansion.
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RORα modulation merits targeted investigation in obesity; leaves open translation from murine fat depots to human therapy.
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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Kadiri et al. (2017) studied Diet-induced inflammation and obesity. Western diet and RORα loss-of-function vs. Standard diet and wild-type mice was evaluated on Inflammatory status and insulin sensitivity of epididymal and inguinal adipose tissue. Western diet increased inflammation in epididymal fat but reduced it in inguinal fat in wild-type mice, an effect lost in RORα-deficient mice, suggesting an anti-inflammatory role for RORα.
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