In:
Molecular Nutrition & Food Research, Wiley, Vol. 59, No. 5 ( 2015-05), p. 957-967
Kurzfassung:
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.
Materialart:
Online-Ressource
ISSN:
1613-4125
,
1613-4133
DOI:
10.1002/mnfr.201400914
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2015
ZDB Id:
2160372-8
SSG:
12
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