Sampson H W, Chaffin C, Lange J, 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. 1997 Apr;21(2):352-9.
Alcohol consumption by young actively growing rats has been previously demonstrated to decrease bone density. This study addresses the mechanism of alcohol action on the early phases of bone growth and development using histomorphometric techniques. 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 were supplied by ethanol. Chow animals were fed a standard rat chow ad libitum. Proximal tibiae, including epiphyseal growth plate, were removed for analysis after 2, 4, 6, or 8 weeks on the diets. Trabecular volume and number were greatly reduced in the alcohol-fed animals; however, bone formation rates and mineralization rates were normal. Epiphyseal growth rate and proliferation rate were essentially stopped in the alcohol-fed animals.
先前已证明,幼年正处于生长活跃期的大鼠饮酒会降低骨密度。本研究使用组织形态计量学技术,探讨酒精对骨骼生长发育早期阶段的作用机制。将四周龄的雌性斯普拉格-道利大鼠分为三组。接受酒精处理的动物随意进食改良的利伯-德卡利饮食,其中35%的热量来自乙醇;而配对喂养的动物(体重与乙醇喂养的大鼠匹配)则接受等热量的流质饮食,其中麦芽糖糊精替代的热量由乙醇提供。正常饮食的动物随意进食标准大鼠饲料。在进食饲料2、4、6或8周后,取出包括骨骺生长板在内的近端胫骨进行分析。喂食酒精的动物的骨小梁体积和数量大幅减少;然而,骨形成率和矿化率正常。喂食酒精的动物的骨骺生长率和增殖率基本停止。