Beta-adrenergic blockade increases GLUT4 and improves glycemic control in insulin-treated diabetic Wistar rats

Autor(es)

Alves-Wagner, Ana Barbara ^[1] ; Mori, Rosana Cristina ^[1] ; Sabino-Silva, Robinson ^[2] ; Fatima, Luciana Alves ^[1] ; Alves, Adilson da Silva ^[1] ; Britto, Luiz Roberto ^[1] ; Schaan, Beatriz D'Agord ^[3] ; Machado, Ubiratan Fabres ^[1]

Afiliação do(s) autor(es)

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

^[2] Univ Fed Uberlandia, Inst Biomed Sci ICBIM, BR-38400 Uberlandia, MG - Brazil

^[3] Univ Fed Rio Grande do Sul, Hosp Clin Porto Alegre, Div Endocrine, Porto Alegre, RS - Brazil

• Tipo de documento: Artigo Científico
• Fonte: AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL; v. 193, p. 108-116, DEC 2015.
• Citações Web of Science: 6

Resumo

Objective: Unequivocal modulation of glycemic homeostasis by chronic beta-adrenergic blockade in diabetes has never been demonstrated. This study investigates the participation of beta-adrenergic system in glycemic control and muscle glucose transporter GLUT4 expression in insulin-treated diabetic rats. Methods: Insulin-treated diabetic Wistar (W) or spontaneously hypertensive rats (SHR) were additionally treated with propranolol, and glycemic homeostasis and expression of some target mRNAs and proteins in soleus and extensor digitorum longus (EDL) muscles were analyzed. Results: Insulin improved glycemic control in both strains. Importantly, in W, propranolol promoted a further improvement in glycemic control, which was accompanied by decreased PKA and Tnf expression, and increased Slc2a4 and GLUT4 in EDL Those effects were not observed in diabetic-SHR. Discussion: Propranolol-induced decrease in beta-adrenergic activity in skeletal muscles of insulin-treated diabetic Wistar rats increases GLUT4 expression in EDL, improving glycemic control. These outcomes represent a positive effect of nonselective beta-blockade, which might be extended to autonomic neuropathy. (C) 2015 Elsevier B.V. All rights reserved. (AU)

• 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: 07/54805-9 - Efeito do sistema nervoso autonomo simpatico beta-adrenergico sobre a expressao do gene do glut4 em ratos espontaneamente hipertensos (shr) diabeticos.
• Beneficiário: Ana Bárbara Teixeira Alves Wagner
• Modalidade de apoio: Bolsas no Brasil - Doutorado