Ethanol Stimulates Glycogenolysis and Inhibits both Glycogenesis via Gluconeogenesis and from Exogenous Glucose in Perfused Rat Liver
Ethanol Stimulates Glycogenolysis and Inhibits both Glycogenesis via Gluconeogenesis and from Exogenous Glucose in Perfused Rat Liver
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DOI：
10.1159/000080463
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发表时间：
2004-08
影响因子：
3.9
通讯作者：
O. Mokuda;H. Tanaka;T. Hayashi;H. Ooka;R. Okazaki;Y. Sakamoto
中科院分区：
文献类型：
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作者：
O. Mokuda;H. Tanaka;T. Hayashi;H. Ooka;R. Okazaki;Y. Sakamoto
目的：尽管人们普遍认为酒精抑制了血糖生成，但酒精摄入对血糖水平的影响仍存在争议。乙醇可以作用于肝脏中的葡萄糖产生和葡萄糖消耗。因此，我们研究了乙醇对肝脏中葡萄糖氧化、糖原生成、糖原分解的影响。方法：分离大鼠肝脏，用含50 mmol/l乙醇的培养液循环灌注。结果：20 min内，乙醇使肝脏中的14 C-葡萄糖氧化从1.09 ± 0.11 μmol增加到1.41 ± 0.14 μmol（p < 0.05）。乙醇处理12 min后，14 C-乳酸的葡萄糖异生作用显著降低，从8.0 ± 1.3 µmol降至1.5 ± 0.6 µmol（p < 0.01）。乙醇增加糖原分解（净肝葡萄糖输出，0.47 ± 0.10对0.22 ± 0.04 mmol/30 min，p < 0.01），然后降低肝糖原含量（179 ± 38对273 ± 39 mg，在1 mU/ml胰岛素存在下，灌注30 min后，p < 0.05）。30分钟内，乙醇使14 C-葡萄糖的直接糖原生成从0.55 ± 0.08 μmol/100 mg糖原降至0.33 ± 0.05 μmol/100 mg糖原（p < 0.01）。30 min内，乙醇抑制14 C-乳酸的间接糖原生成，从0.21 ± 0.04 µmol/100 mg糖原降至0.09 ± 0.01 µmol/100 mg糖原（p < 0.01）。讨论：乙醇对肝脏血糖调节的影响在空腹和进食状态下似乎不同。也就是说，乙醇具有通过减少糖原生成和增加葡萄糖氧化的降血糖作用和通过减少糖原生成和增加糖原分解的高血糖作用。
Aims: Although it is commonly recognized that ethanol suppresses gluconeogenesis, the influence of alcohol intake on blood glucose levels remains controversial. Ethanol may act on both glucose production and glucose consumption in the liver. Thus, we studied each effect of ethanol on glucose oxidation, gluconeogenesis, glycogenesis and glycogenolysis in the liver. Methods: The rat liver was isolated and cyclically perfused with a medium containing 50 mmol/l ethanol. Results: Ethanol enhanced 14C-glucose oxidation in the liver from 1.09 ± 0.11 to 1.41 ± 0.14 µmol for 20 min (p < 0.05). Gluconeogenesis from 14C-lactate was markedly reduced by ethanol from 8.0 ± 1.3 to 1.5 ± 0.6 µmol for 12 min (p < 0.01). Ethanol increased glycogenolysis (net hepatic glucose output, 0.47 ± 0.10 vs. 0.22 ± 0.04 mmol/30 min, p < 0.01), and then decreased hepatic glycogen content (179 ± 38 vs. 273 ± 39 mg in the presence of 1 mU/ml insulin after 30 min of perfusion, p < 0.05). Ethanol decreased the direct glycogenesis from 14C-glucose from 0.55 ± 0.08 to 0.33 ± 0.05 µmol per 100 mg glycogen for 30 min (p < 0.01). Ethanol inhibited the indirect glycogenesis from 14C-lactate from 0.21 ± 0.04 to 0.09 ± 0.01 µmol per 100 mg glycogen for 30 min (p < 0.01). Discussion: The influence of ethanol on the blood glucose regulation by the liver seems to be different between fasted and fed states. Namely, ethanol has both the hypoglycemic effects through decreased gluconeogenesis and increased glucose oxidation and the hyperglycemic effects through decreased glycogenesis and increased glycogenolysis.