Xu D, Thambirajah R, Palmer T N
Department of Biochemistry, University of Western Australia, Nedlands.
Biochem J. 1992 Dec 1;288 ( Pt 2)(Pt 2):445-50. doi: 10.1042/bj2880445.
The pattern of glycogen deposition in individual cardiothoracic and skeletal muscles in response to oral and intraperitoneal glucose administration was examined in 40 h-starved rats. Rates of glycogen synthesis were consistently higher in oxidative muscles than in non-oxidative muscles. Intragastric ethanol administration was associated with an impaired glycaemic response and the almost total abolition of glycogen deposition in oxidative muscles in response to oral or intraperitoneal glucose re-feeding. This effect was dose-dependent and differential, in that ethanol produced no equivalent impairment in glycogen deposition in non-oxidative muscles. Ethanol treatment also selectively promoted glycogenolysis in oxidative muscles in the starved state. There was positive correlation (P < 0.001) between the decrease in glycogen levels in soleus and diaphragm muscles in response to increasing ethanol doses and blood glucose and lactate concentrations after intraperitoneal glucose administration, implying that the basis for the impairment in glycogen synthesis may be diminished glucose availability. The mechanism whereby ethanol may differentially compromise carbohydrate metabolism in oxidative muscles is discussed.
在禁食40小时的大鼠中，研究了口服和腹腔注射葡萄糖后，个体心胸肌和骨骼肌中糖原沉积的模式。氧化型肌肉中糖原合成速率始终高于非氧化型肌肉。胃内给予乙醇与血糖反应受损以及口服或腹腔注射葡萄糖再喂养后氧化型肌肉中糖原沉积几乎完全消失有关。这种效应具有剂量依赖性和差异性，因为乙醇对非氧化型肌肉中的糖原沉积没有产生同等程度的损害。乙醇处理还选择性地促进了饥饿状态下氧化型肌肉中的糖原分解。比目鱼肌和膈肌中糖原水平随乙醇剂量增加而降低，与腹腔注射葡萄糖后血糖和乳酸浓度呈正相关（P < 0.001），这意味着糖原合成受损的基础可能是葡萄糖可用性降低。本文讨论了乙醇可能差异性损害氧化型肌肉中碳水化合物代谢的机制。
