World M J, Ryle P R, Jones D, Shaw G K, Thomson A D
Alcohol Alcohol. 1984;19(4):281-90.
A six-months out-patient study of chronic alcoholics with undecompensated liver disease has shown a statistically significant inverse correlation between the change in mean corpuscular volume and the change in body weight (r = -0.4, P less than 0.01). A fall in body weight over this period was the best clinical indicator of apparently continuing alcohol abuse. Previous anthropometric studies have indicated that reduced adipose tissue is one cause of lower body weights in such patients. To determine whether this is due to the effects of alcohol or of poor nutrition, the epididymal fat pad weights of rats following 28 days administration of alcohol (36% of total calories) as part of a nutritionally adequate liquid diet were compared with those of pair-fed controls initially matched for body weight. At the end of the experiment, body weight gain was the same in both groups but the mean weight of the fat pads of alcohol-fed animals (371.7 mg +/- 60.0 mg SD) all of which developed hepatic steatosis was 29% greater than that of pair-fed controls (288.7 mg +/- 42.4 mg). This difference was statistically significant (P less than 0.025). This study shows that alcohol intake per se does not prevent an increase in body weight or fat even if hepatic steatosis is induced and that loss of adipose tissue in chronic alcoholics who continue to drink is probably due to simultaneous inadequate nutritional intake.
一项针对失代偿性肝病慢性酒精中毒患者的为期六个月的门诊研究表明，平均红细胞体积变化与体重变化之间存在统计学上显著的负相关（r = -0.4，P < 0.01）。在此期间体重下降是明显持续酗酒的最佳临床指标。先前的人体测量学研究表明，脂肪组织减少是此类患者体重降低的一个原因。为了确定这是由于酒精的作用还是营养不良所致，将给予酒精（占总热量的36%）28天作为营养充足的流质饮食一部分的大鼠附睾脂肪垫重量，与初始体重匹配的配对喂养对照组大鼠的附睾脂肪垫重量进行比较。实验结束时，两组的体重增加相同，但喂食酒精的动物（均出现肝脂肪变性）的脂肪垫平均重量（371.7毫克±60.0毫克标准差）比配对喂养对照组（288.7毫克±42.4毫克）高29%。这种差异具有统计学意义（P < 0.025）。这项研究表明，即使诱发了肝脂肪变性，酒精摄入本身也不会阻止体重或脂肪增加，持续饮酒的慢性酒精中毒患者脂肪组织减少可能是由于同时存在营养摄入不足。
