Fisher H, Yu Y L, Sekowski A, Federico E, Ulman E, Wagner G C
Department of Nutritional Sciences, Rutgers University, New Brunswick, NJ 08903, USA.
Alcohol. 1996 Mar-Apr;13(2):195-200. doi: 10.1016/0741-8329(95)02046-2.
Experiments were carried out in which a nutritionally balanced liquid diet previously used in this laboratory was modified as to total calorie content and high or low carbohydrate and fat concentration. Ethanol was added at 4.5% and 6.2% of diet weight and provided either 27% or 34-37% of total calories depending upon the changes in nutrient content. Measurements included 8-day food/calorie and ethanol consumption, plasma ethanol level, liver alcohol dehydrogenase (ADH) activity, and rate of audiogenic-induced withdrawal seizures. The original liquid diet with 4.5% ethanol was consumed in significantly lesser amounts than the alcohol-free diet, and essentially no body weight gain occurred, regardless if the major nonalcohol, nonprotein calorie source was fat or carbohydrate. When the calorie content of the diet was boosted through the addition of extra carbohydrate or fat (at the expense of water), appreciable weight gain was noted; in the case of the higher calorie diet boosted with more carbohydrate (maltodextrin) calories, growth was similar to that observed on the alcohol-free control diet. On this latter diet ethanol calories appeared to be utilized close to their theoretical value of 7 kcal/g. Blood alcohol levels were significantly higher on the lower calorie diets and were lowest on the high-calorie, high-carbohydrate, 4.5% ethanol diet. This diet also allowed for the lowest rate of withdrawal seizures despite an ethanol intake that was as high as on the lower calorie diets. Essentially, no differences were noted among ADH activities for the dietary treatments studied and thus, did not explain the differences observed among blood ethanol levels. When the alcohol concentration in the high-carbohydrate, high-calorie diet was raised to 6.2% from 4.5% to provide 34% of total calories, the rats responded by decreasing their food (and alcohol) intake to the same level as did the animals receiving a much lower calorie diet, but with 37% of caloric alcohol content. This suggests that at a diet alcohol concentration of 34-37%, one or more nutrient metabolites become limiting in the utilization of ethanol, resulting in food intake adjustments that maintain similar amounts of alcohol consumption.
进行了多项实验，其中本实验室之前使用的营养均衡液体饮食在总热量含量以及高或低碳水化合物和脂肪浓度方面进行了调整。乙醇按饮食重量的4.5%和6.2%添加，根据营养成分的变化，提供总热量的27%或34 - 37%。测量指标包括8天的食物/热量和乙醇消耗量、血浆乙醇水平、肝脏乙醇脱氢酶（ADH）活性以及声源性诱导戒断性癫痫发作的发生率。含4.5%乙醇的原始液体饮食的消耗量明显低于无酒精饮食，无论主要的非酒精、非蛋白质热量来源是脂肪还是碳水化合物，体重基本没有增加。当通过添加额外的碳水化合物或脂肪（以减少水为代价）来提高饮食的热量含量时，体重显著增加；在热量更高且碳水化合物（麦芽糊精）热量增加的饮食中，生长情况与无酒精对照饮食相似。在这种后期饮食中，乙醇热量的利用率似乎接近其理论值7千卡/克。低热量饮食的血液酒精水平显著更高，而在高热量、高碳水化合物、含4.5%乙醇的饮食中最低。尽管乙醇摄入量与低热量饮食一样高，但这种饮食的戒断性癫痫发作率也是最低的。在所研究的饮食处理中，ADH活性基本没有差异，因此无法解释所观察到的血液乙醇水平差异。当高碳水化合物、高热量饮食中的酒精浓度从4.5%提高到6.2%以提供总热量的34%时，大鼠的反应是将食物（和酒精）摄入量减少到与接受热量低得多但酒精热量含量为37%的动物相同的水平。这表明在饮食酒精浓度为34 - 37%时，一种或多种营养代谢产物在乙醇利用中成为限制因素，导致食物摄入量调整以维持相似的酒精消耗量。
