Sampson H W, Perks N, Champney T H, DeFee B
Department of Human Anatomy and Neurobiology, College of Medicine, Texas A&M University, Health Science Center, College Station 77843-1114, USA.
Alcohol Clin Exp Res. 1996 Nov;20(8):1375-84. doi: 10.1111/j.1530-0277.1996.tb01137.x.
Adolescence is an age of widespread alcohol abuse, but the effect of alcohol consumption on bone formation has not been studied in the young population. This study addresses the effect of alcohol on the early phases of bone growth and development in an animal model. Four-week-old, female Sprague-Dawley rats were divided into three groups. Alcohol-treated animals were fed a modified Lieber-DeCarli diet ad libitum containing 35% ethanol-derived calories, whereas the pair-fed animals (weight-matched to ethanol rats) received an isocaloric liquid diet in which maltose-dextrin substituted calories supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae (primarily cancellous bone) and femora (primarily cortical bone) were removed for analysis after 2, 4, 6, or 8 weeks on the diets. Serum was collected for analysis of calcium levels, osteocalcin, corticosterone, growth hormone, parathyroid hormone, and 25-hydroxyvitamin D. The most rapid weight gain occurred between 6 and 8 weeks of age, it was significantly delayed in alcohol and pair-fed animals. Almost all morphological parameters of bone were lower in the alcohol groups. No significant difference in serum calcium levels, osteocalcin, or growth hormone levels were found, and small difference in calciotropic hormone levels was found between groups. The results indicated that chronic alcohol consumption during the age of bone development reduces bone density and peak bone mass in both cortical and cancellous bone. The mechanism whereby this effect occurs is not fully understood, but, our results suggest that the negative impact of alcohol on growing bone is not due to the secondary effects of altered bone mineral regulating hormones.
青春期是酒精滥用普遍存在的一个年龄段，但饮酒对年轻人骨骼形成的影响尚未得到研究。本研究探讨了酒精对动物模型中骨骼生长和发育早期阶段的影响。将四周龄的雌性斯普拉格-道利大鼠分为三组。给接受酒精处理的动物随意喂食一种改良的利伯-德卡利饮食，其中含有35%来自乙醇的热量，而配对喂食的动物（体重与乙醇组大鼠匹配）则接受一种等热量的流质饮食，其中麦芽糖糊精替代了由乙醇提供的热量。正常饮食组动物随意喂食标准大鼠饲料。在按照饮食方案喂养2、4、6或8周后，取出近端胫骨（主要为松质骨）和股骨（主要为皮质骨）进行分析。采集血清以分析钙水平、骨钙素、皮质酮、生长激素、甲状旁腺激素和25-羟基维生素D。体重增加最快的时期出现在6至8周龄之间，在酒精组和配对喂食组动物中体重增加明显延迟。酒精组几乎所有骨骼形态学参数都较低。未发现血清钙水平、骨钙素或生长激素水平有显著差异，且各组之间在钙调节激素水平上存在微小差异。结果表明，在骨骼发育年龄期间长期饮酒会降低皮质骨和松质骨的骨密度和峰值骨量。这种影响发生的机制尚未完全了解，但我们的结果表明，酒精对生长中骨骼的负面影响并非由于骨矿物质调节激素改变的继发效应。
