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Omega‐3 fatty acids protect from diet‐induced obesity, glucose intolerance, and adipose tissue inflammation through PPARγ‐dependent and PPARγ‐independent actions
Author(s) -
Belchior Thiago,
Paschoal Vivian A.,
Magdalon Juliana,
Chimin Patricia,
Farias Talita M.,
ChavesFilho Adriano B.,
Gorjão Renata,
St.Pierre Philippe,
Miyamoto Sayuri,
Kang Jing X.,
Deshaies Yves,
Marette André,
Festuccia William
Publication year - 2015
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400914
Subject(s) - adipose tissue , endocrinology , medicine , inflammation , white adipose tissue , peroxisome proliferator activated receptor , biology , receptor
Scope We tested herein the hypothesis that peroxisome proliferator activated receptor γ (PPARγ) is a major mediator of omega‐3 ( n ‐3) protective actions against high‐fat diet (HFD) induced obesity, glucose intolerance, and adipose tissue inflammation. Methods and results C57BL6 wild‐type and fat‐1 transgenic ( fat‐1 ) mice were fed a low‐fat diet (LFD) or HFD, treated or not with PPARγ antagonist, and evaluated for energy balance, adiposity, glucose tolerance, and adipose tissue inflammation. Fat‐1 mice were protected from obesity, fasting hyperglycemia, glucose intolerance, and adipose tissue inflammation. PPARγ inhibition completely abolished fat‐1 protection against HFD‐induced glucose intolerance, but not obesity or adipose tissue inflammation. To investigate the role of myeloid cell as mediator of n ‐3 beneficial metabolic actions, mice with deletion (LyzM‐PPARγ KO ) or nondeletion (LyzM‐PPARγ WT ) of PPARγ in myeloid cells were fed either LFD or HFD (lard) or an HFD rich in n ‐3 (fish oil). Our findings indicate that myeloid cell associated PPARγ is not involved in the attenuation of HFD‐induced glucose intolerance and adipose tissue inflammation induced by n ‐3. Conclusion High endogenous n ‐3 fatty acid levels protect from HFD obesity, glucose intolerance, and adipose tissue inflammation. Among these, only protection against glucose intolerance is mediated by non‐myeloid cell PPARγ.