RESUMO
Moderate amounts of alcohol intake have been reported to have a protective effect on the cardiovascular system and this may involve enhanced insulin sensitivity. We established an animal model of increased insulin sensitivity by low ethanol consumption and here we investigated metabolic parameters and molecular mechanisms potentially involved in this phenomenon. For that, Wistar rats have received drinking water either without (control) or with 3% ethanol for four weeks. The effect of ethanol intake on insulin sensitivity was analyzed by insulin resistance index (HOMA-IR), intravenous insulin tolerance test (IVITT) and lipid profile. The role of liver was investigated by the analysis of insulin signaling pathway, GLUT2 gene expression and tissue glycogen content. Rats consuming 3% ethanol showed lower values of HOMA-IR and plasma free fatty acids (FFA) levels and higher hepatic glycogen content and glucose disappearance constant during the IVITT. Neither the phosphorylation of insulin receptor (IR) and insulin receptor substrate-1 (IRS-1), nor its association with phosphatidylinositol-3-kinase (PI3-kinase), was affected by ethanol. However, ethanol consumption enhanced liver IRS-2 and protein kinase B (Akt) phosphorylation (3 times, P<0.05), which can be involved in the 2-fold increased (P<0.05) hepatic glycogen content. The GLUT2 protein content was unchanged. Our findings point out that liver plays a role in enhanced insulin sensitivity induced by low ethanol consumption.
Assuntos
Consumo de Bebidas Alcoólicas/metabolismo , Resistência à Insulina/fisiologia , Fígado/fisiologia , Animais , Northern Blotting , Western Blotting , Peso Corporal/efeitos dos fármacos , Colesterol/sangue , Ingestão de Alimentos/efeitos dos fármacos , Etanol/administração & dosagem , Etanol/farmacologia , Ácidos Graxos não Esterificados/sangue , Expressão Gênica/efeitos dos fármacos , Transportador de Glucose Tipo 2 , Glicogênio/metabolismo , Insulina/farmacologia , Proteínas Substratos do Receptor de Insulina , Peptídeos e Proteínas de Sinalização Intracelular , Lipoproteínas/sangue , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , Proteínas de Transporte de Monossacarídeos/genética , Proteínas de Transporte de Monossacarídeos/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Fosfoproteínas/metabolismo , Fosforilação/efeitos dos fármacos , Proteínas Serina-Treonina Quinases/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , Proteínas Proto-Oncogênicas c-akt , Ratos , Ratos Wistar , Receptor de Insulina/metabolismo , Triglicerídeos/sangueRESUMO
As alpha-glucosidase inhibitor, the antidiabetic drug acarbose reduces postprandial glucose levels by retarding the intestinal digestion of polysaccharides. However, it is unknown if acarbose also affects the expression of intestinal glucose transporters, especially the Na(+)-glucose cotransporter (SGLT1) and the glucose transporters GLUT1 and GLUT2. To unravel this question, Wistar rats received standard powdered chow either without (control) or with acarbose (40 mg acarbose/100 g chow) for 40 days. While food intake was slightly enhanced by acarbose, the drug had no influence on weight gain or plasma glucose and insulin levels. The acarbose-treatment did not alter the SGLT1 and GLUT2 gene expression in both upper and middle small intestine, whereas GLUT1 protein was increased by 75% in middle small intestine. Despite the territorial change in GLUT1 protein, the intestinal glucose absorption in an acarbose-free perfusion study was unaltered. In conclusion, the chronic use of acarbose did not alter the acarbose-free glucose absorption profile.