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

Autor(es):Mostrar menos -

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]

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: MOLECULAR NUTRITION & FOOD RESEARCH; v. 59, n. 5, p. 957-967, MAY 2015.
• Citações Web of Science: 25

Resumo

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)

• Processo FAPESP: 11/14172-2 - Envolvimento dos PPARgamma no desenvolvimento da inflamação crônica de baixa intensidade e resistência a insulina associada à obesidade. Participação nas ações dos ácidos graxos ômega-3.
• Beneficiário: Thiago Belchior de Oliveira
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 10/52191-6 - Envolvimento dos sensores de nutrientes mTOR e PPARgama no início, manutenção e término da inflamação associada à obesidade e resistência à insulina
• Beneficiário: William Tadeu Lara Festuccia
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 09/15354-7 - Envolvimento do tecido adiposo no desenvolvimento da obesidade e patologias associadas: investigação dos mecanismos moleculares e busca de novas alternativas terapêuticas
• Beneficiário: William Tadeu Lara Festuccia
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores