Salaspuro M P, Shaw S, Jayatilleke E, Ross W A, Lieber C S
Hepatology. 1981 Jan-Feb;1(1):33-8. doi: 10.1002/hep.1840010106.
Acute ethanol administration results in increased hepatic NADH/NAD+ ratio and inhibition of galactose elimination, tricarboxylic acid cycle activity, and fatty acid oxidation. To determine how this redox change is affected by chronic alcohol consumption and to assess the resulting metabolic consequences, we studied baboons which were fed alcohol as 50% of their total calories. Redox changes were evaluated through measurement of galactose elimination in vivo and lactate/pyruvate ratios in liver slices in vitro. The metabolic consequences of these changes were assessed through measurement of CO2 production and fatty acid oxidation in liver slices and hepatic lipid accumulation. Chronic alcohol feeding resulted in attenuation of inhibition of galactose elimination, increase in the lactate/pyruvate ratio, and decrease in fatty acid oxidation which were caused by acute ethanol administration. These metabolic adaptations were associated with reduced accumulation of hepatic fat.
急性给予乙醇会导致肝脏中NADH/NAD⁺比值升高，并抑制半乳糖清除、三羧酸循环活性和脂肪酸氧化。为了确定这种氧化还原变化如何受到长期饮酒的影响，并评估由此产生的代谢后果，我们研究了以总热量的50%摄入酒精的狒狒。通过测量体内半乳糖清除率和体外肝切片中的乳酸/丙酮酸比值来评估氧化还原变化。通过测量肝切片中的二氧化碳产生、脂肪酸氧化和肝脏脂质积累来评估这些变化的代谢后果。长期给予酒精导致急性给予乙醇所引起的半乳糖清除抑制减弱、乳酸/丙酮酸比值升高以及脂肪酸氧化减少。这些代谢适应性变化与肝脏脂肪积累减少有关。
