Details

Autor(en) / Beteiligte

• Gaspar, Rafael Calais
• Veiga, Camilla Bertuzzo
• Bessi, Mariana Pereira
• Dátilo, Marcella Neves
• Sant'Ana, Marcella Ramos
• Rodrigues, Patrícia Brito
• de Moura, Leandro Pereira
• da Silva, Adelino Sanchez Ramos
• Santos, Gustavo Aparecido
• Catharino, Rodrigo Ramos
• Ropelle, Eduardo Rochete
• Pauli, José Rodrigo
• Cintra, Dennys Esper

Titel

Unsaturated fatty acids from flaxseed oil and exercise modulate GPR120 but not GPR40 in the liver of obese mice: a new anti-inflammatory approach

Ist Teil von

• The Journal of nutritional biochemistry, 2019-04, Vol.66, p.52-62

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2019

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• GPR120 and GPR40 were recently reported as omega-3 (ω3) receptors with anti-inflammatory properties. Physical exercise could increase the expression of these receptors in the liver, improving hepatic metabolism in obesity and type 2 diabetes. Our aim was to investigate GPR120/40 in the liver of lean and obese mice after acute or chronic physical exercise, with or without the supplementation of ω3 rich flaxseed oil (FS), as well as assess the impact of exercise and FS on insulin signaling and inflammation. Mice were fed a high-fat diet (HF) for 4 weeks to induce obesity and subsequently subjected to exercise with or without FS, or FS alone. Insulin signaling, inflammatory markers and GPR120/40 and related cascades were measured. Chronic, but not acute, exercise and FS increased GPR120, but not GPR40, activating β-arrestin-2 and decreasing the inflammatory response, as well as reducing fat depots in liver and adipose tissue. Exercise or a source of ω3 led to a higher tolerance to fatigue and an increased running distance and speed. The combination of physical exercise and ω3 food sources could provide a new strategy against obesity through the modulation of hepatic GPR120 and an increase in exercise performance. (A) Proinflammatory cascades are induced by saturated fatty acids (SFA) or TNFα through the receptors TLR4 and TNF-R, respectively. (B) The insulin signaling cascade is blocked by cytokines. (C) Exercise increases GPR120 gene expression and subsequent protein levels, and upon their activation by alpha-linolenic fatty acids (C18:3), inflammatory signaling is disrupted via βarrestin2 (β-arr2). IR, insulin receptor; Y, tyrosine; IRS1/2, insulin receptor substrate 1 or 2; PI3K, phosphatidyl inositol 3 kinase; Akt, protein kinase B; DD, death domain; TNFα, tumoral necrosis factor alpha; Tradd, death domain associated to TNF receptor; RIP, receptor-interacting protein; TRAF2, factor 2 associated to TNFα receptor; TLR4, Toll-like receptor; Myd88, myeloid differentiation primary response 88; TAK1, TGFβ-activated kinase1; JNK, cJun N-terminal kinase; IκK, inhibitor kappa kinase; IκBα, NF-κB inhibitor alpha; P50/P65, protein 50/65; UB, ubiquitin; NF-κB, nuclear factor kappa B. [Display omitted]