Short-term treatment with metformin reduces hepatic lipid accumulation but induces liver inflammation in obese mice

Autor(es):Mostrar menos -

de Souza Teixeira, Alexandre Abilio ^[1] ; Souza, Camila O. ^[1] ; Biondo, Luana A. ^[1] ; Silveira, Loreana Sanches ^[2] ; Lima, Edson A. ^[1] ; Batatinha, Helena A. ^[1] ; Araujo, Adriane Pereira ^[1] ; Alves, Michele Joana ^[1] ; Hirabara, Sandro Massao ^[3] ; Curi, Rui ^{[4, 3]} ; Rosa Neto, Jose Cesar ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Cell Biol & Dev, Immunometab Res Grp, Sao Paulo, SP - Brazil

^[2] UNESP, Dept Phys Educ, Exercise & Immunometab Res Grp, Presidente Prudente - Brazil

^[3] Univ Cruzeiro Sul, Sao Paulo, SP - Brazil

^[4] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Sao Paulo, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: INFLAMMOPHARMACOLOGY; v. 26, n. 4, p. 1103-1115, AUG 2018.
• Citações Web of Science: 4

Resumo

The study aimed to evaluate the metabolic and inflammatory effects of short-term treatments (10 days) with metformin (MET) on the NAFLD caused by a high-fat diet (HFD) in C57BL/6 mice. After the treatment, histological liver slices were obtained, hepatocytes and macrophages were extracted and cultured with phosphate buffered saline, LPS (2.5 A mu g/mL) and MET (1 A mu M) for 24 h. Cytokine levels were determined by ELISA. NAFLD caused by the HFD was partially reduced by MET. The lipid accumulation induced by the HFD was not associated with liver inflammation; however, MET seemed to promote pro-inflammatory effects in liver, since it increased hepatic concentration of IL-1 beta, TNF-alpha, IL-6, MCP-1 and IFN-gamma. Similarly, MET increased the concentration of IL-1 beta, IL-6 in hepatocyte cultures. However, in macrophages culture, MET lowered levels of IL-1 beta, IL-6 and TNF-alpha stimulated by LPS. Overall, MET reduced liver NAFLD but promoted hepatocyte increase in pro-inflammatory cytokines, thus, leading to liver inflammation. (AU)

• Processo FAPESP: 15/16777-0 - Exercício físico como um sincronizador dos ritmos circadianos no câncer
• Beneficiário: Alexandre Abilio de Souza Teixeira
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 13/09367-4 - Efeitos metabólicos da doxorrubicina no músculo esquelético e tecido adiposo: possível papel adjuvante do treinamento físico e metformina
• Beneficiário: José Cesar Rosa Neto
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 16/01409-8 - Caracterização do efeito antiinflamatório da suplementação com ácido palmitoleico na inflamação hepática; o papel dos ppars.
• Beneficiário: José Cesar Rosa Neto
• Modalidade de apoio: Auxílio à Pesquisa - Regular