Omega-3 fatty acids protect from diet-induced obesity, glucose intolerance, and adipose tissue inflammation through PPAR gamma-dependent and PPAR gamma-independent actions

Author(s):Show less -

Belchior, Thiago ^[1] ; Paschoal, Vivian A. ^[1] ; Magdalon, Juliana ^[1] ; Chimin, Patricia ^[1] ; Farias, Talita M. ^[1] ; Chaves-Filho, Adriano B. ^[2] ; Gorjao, Renata ^[3] ; St-Pierre, Philippe ^[4] ; Miyamoto, Sayuri ^[2] ; Kang, Jing X. ^[5] ; Deshaies, Yves ^[4] ; Marette, Andre ^[4] ; Festuccia, William ^[1]

Affiliation

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-05508000 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Inst Chem, Dept Biochem, BR-05508000 Sao Paulo - Brazil

^[3] Univ Cruzeiro Sul, Inst Phys Act & Sports, Sao Paulo - Brazil

^[4] Univ Laval, Dept Med, Fac Med, Quebec Heart & Lung Inst Res Ctr, Quebec City, PQ G1K 7P4 - Canada

^[5] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Lab Lipid Med & Technol, Boston, MA - USA

• Document type: Journal article
• Source: MOLECULAR NUTRITION & FOOD RESEARCH; v. 59, n. 5, p. 957-967, MAY 2015.
• Web of Science Citations: 25

Abstract

Scope: We tested herein the hypothesis that peroxisome proliferator activated receptor gamma (PPAR) 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 PPAR gamma 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. PPAR gamma 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 beneficialmetabolic actions, mice with deletion (LyzM-PPAR gamma(KO)) or nondeletion (LyzM-PPAR gamma(WT)) of PPAR gamma 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 PPAR gamma 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 PPAR gamma. (AU)

• FAPESP's process: 11/14172-2 - Involvement of PPARgamma in development of low-intensity chronic inflammation and insulin resistance associated with obesity. Participation in the actions of omega-3 fatty acids.
• Grantee: Thiago Belchior de Oliveira
• Support Opportunities: Scholarships in Brazil - Doctorate
• FAPESP's process: 09/15354-7 - Role of adipose tissue in the development of obesity and associated co-morbidities: investigation of molecular mechanism and search for alternative therapies
• Grantee: William Tadeu Lara Festuccia
• Support Opportunities: Research Grants - Young Investigators Grants