Connelly D M, Nerurkar I, Taberner P V
Department of Pharmacology, University of Bristol Medical School, England.
Alcohol Alcohol Suppl. 1987;1:301-5.
Blood glucose levels and glucose uptake into cerebral cortex and diaphragm in vitro and into cerebral cortex and adipose tissue in vivo have been measured in LACG (normal) and C57Bl and CBA (diabetic) mice during chronic ethanol drinking and withdrawal. Chronic ethanol produced hypoglycaemia in diabetic mice but prevented insulin-provoked hypoglycaemia in normal mice. Insulin and ethanol had additive effects in diabetic mice. The hypoglycaemic effect of CET is not dependent upon insulin and can be explained by an increase in insulin-independent brain glucose uptake. Ethanol-induced hypoglycaemia and the changes in glucose uptake occur at relatively low blood levels of ethanol (4-20mM, 18-90mg%) and are rapidly reversible on withdrawal. Diabetic mice appear to be more sensitive to the effects of ethanol on glucoregulation.
在长期饮酒及戒酒过程中,对LACG(正常)、C57Bl和CBA(糖尿病)小鼠的血糖水平以及体外大脑皮层和膈肌、体内大脑皮层和脂肪组织的葡萄糖摄取情况进行了测量。长期饮酒使糖尿病小鼠出现低血糖,但可预防正常小鼠由胰岛素引发的低血糖。胰岛素和乙醇在糖尿病小鼠中具有相加作用。慢性乙醇中毒的低血糖效应不依赖胰岛素,可通过非胰岛素依赖性脑葡萄糖摄取增加来解释。乙醇诱导的低血糖以及葡萄糖摄取变化发生在相对较低的乙醇血浓度(4 - 20mM,18 - 90mg%)时,且在戒酒时迅速可逆。糖尿病小鼠似乎对乙醇对葡萄糖调节的影响更为敏感。