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Depot‐Specific Response of Adipose Tissue to Diet‐Induced Inflammation: The Retinoid‐Related Orphan Receptor α (RORα) Involved?
Author(s) -
Kadiri Sarah,
Auclair Martine,
Capeau Jacqueline,
Antoine Bénédicte
Publication year - 2017
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.22006
Subject(s) - adipose tissue , endocrinology , inflammation , medicine , obesity , insulin resistance , orphan receptor , stroma , receptor , depot , biology , gene , immunohistochemistry , biochemistry , transcription factor , history , archaeology
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.