摘要
O objetivo deste trabalho foi avaliar a influ那ncia do tratamento com etanol (Et) sobre a gliconeog那nese em ratos intolerantes 角 glicose. A intolerancia 角 glicose foi induzida pela inje o de dexametasona (DEXA) (0,1 mg kg-1; s.c., quatro dias). O teste de tolerancia 角glicose (GTT) e os experimentos de perfus o de f赤gado in situ (avalia o da gliconeog那nese) foram realizados em ratos submetidos a jejum de 15h dos grupos experimentais: Controle (salina 0,9%, s.c., quatro dias); DEX (DEXA 0,1 mg kg-1; s.c., quatro dias); DEX+Et 3% (per os, 14 dias); DEX+Et 20% (per os, 14 dias); DEX+Met (Mettformina 300 mg kg-1, per os, quatro dias). Os animais tratados com DEX apresentaram elevada concentra o de glicose sangu赤nea e tamb谷m no perfusato coletado. O tratamento com metformina promoveu redu o significativa na concentra o de glicose no perfusato obtido de animais intolerantes 角 glicose. Entretanto, somente o tratamento com Et 3% promoveu redu o na intolerancia 角 glicose, mas n o na produ o da glicose hep芍tica observada em animais DEX. Os dados obtidos demonstram que a administra o de Et 3% melhora a intolerancia 角 glicose induzida pela DEX sem influenciar na gliconeog那nese, diferentemente do observado pelo tratamento com a metformina. In this work, the influence of ethanol (Et) treatment on gluconeogenesis in glucose-intolerance rats was evaluated. Glucose intolerance in rats was induced by dexamethasone (DEXA) injection (0.1 mg kg-1; s.c., 4 days). The glucose tolerance test (GTT) and liver perfusion in situ experiments (gluconeogenesis evaluation) were performed with 15-hour fasted rats in the following experimental groups: Control (saline 0.9%, s.c., 4 days); DEX (DEXA 0.1 mg kg-1; s.c., 4 days); DEX+Et 3% (per os, 14 days); DEX+Et 20% (per os, 14 days); DEX+Met (Metformin 300 mg kg-1, per os, 4 days). DEX-treated animals showed high glucose concentration in blood and also in the perfusate collected. Metformin treatment resulted in a significant reduction in the concentration of perfusate glucose in intolerant animals. However, only the Et 3% treatment reduced glucose intolerance, but not glucose hepatic production observed in DEX animals. Data showed that Et 3% administration improves glucose intolerance induced by DEX without influence on gluconeogenesis, unlike the result observed with Metformin treatment.