Reduced Slc2a4/GLUT4 expression in subcutaneous adipose tissue of monosodium glutamate obese mice is recovered after atorvastatin treatment

Autor(es)

Poletto, Ana Claudia ^[1] ; David-Silva, Aline ^[1] ; de Melo Yamamoto, Aline Pedro ^[1] ; Machado, Ubiratan Fabres ^[1] ; Furuya, Daniela Tomie ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-05508900 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: DIABETOLOGY & METABOLIC SYNDROME; v. 7, MAR 14 2015.
• Citações Web of Science: 12

Resumo

Background: Decreased expression of glucose transporter protein GLUT4, encoded by the solute carrier 2A4 (Slc2a4) gene, is involved in obesity-induced insulin resistance. Local tissue inflammation, by nuclear factor-kappa B (NF kappa B)-mediated pathway, has been related to Slc2a4 repression; a mechanism that could be modulated by statins. Using a model of obesity with insulin resistance, this study investigated whether (1) inflammatory markers and Slc2a4 expression are altered; (2) atorvastatin has beneficial effects on inflammation and Slc2a4 expression; and (3) inhibitor of NF kappa B (IKK)/NF kappa B pathway is involved in subcutaneous adipose tissue (SAT). Findings: Obese mice showed insulin resistance, decreased expression of Slc2a4 mRNA (66%, P < 0.01) and GLUT4 protein (30%, P < 0.05), and increased expression of interleukin 6 (Il6) mRNA (44%, P < 0.05) in SAT. Obese mice treated with atorvastatin had enhanced in vivo insulin sensitivity, besides increased Slc2a4/GLUT4 expression and reduced Il6 expression in SAT. No alterations of tumor necrosis factor-alpha, interleukin 1 beta and adiponectin expression or IKK alpha/beta activity in SAT of obese mice or obese mice treated with atorvastatin were observed. Conclusions: Atorvastatin has beneficial effect upon glycemic homeostasis, which may be related to its positive impact on Il6 and Slc2a4/GLUT4 expression in SAT. (AU)

• Processo FAPESP: 13/18841-1 - Regulação do metabolismo da glicose pelo osso: ações da osteocalcina na resistência à insulina e inflamação em tecidos adiposo e hepático
• Beneficiário: Daniela Tomie Furuya
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores
• Processo FAPESP: 12/04831-1 - Novos moduladores do controle glicêmico e do desenvolvimento de complicações crônicas no Diabetes mellitus: perspectivas preventivas e terapêuticas
• Beneficiário: Ubiratan Fabres Machado
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 14/10007-5 - Regulação do metabolismo da glicose pelo osso: ações da osteocalcina na resistência à insulina e inflamação em tecidos adiposo e hepático
• Beneficiário: Daniela Tomie Furuya
• Modalidade de apoio: Bolsas no Brasil - Jovens Pesquisadores