Binge alcohol treatment of adolescent rats followed by alcohol abstinence is associated with site-specific differences in bone loss and incomplete recovery of bone mass and strength.

摘要

We previously demonstrated that alcohol-fed adolescent rats exhibit reductions in lumbar spine bone mineral density (BMD) and vertebral body height, suggesting that chronic alcohol consumption has negative consequences for skeletal development during adolescence. Binge alcohol consumption is common in adolescents and young adults, yet little is known about its consequences on skeletal integrity or the attainment of peak bone mass. We used a previously validated binge alcohol exposure model to test the hypothesis that binge alcohol treatment of adolescent rats would be associated with distinct temporal and site-specific bone loss profiles, with incomplete recovery from bone loss following a period of alcohol abstinence. Seventy-two male adolescent Sprague-Dawley rats were assigned to one of six treatment groups (n=12/group) receiving binge alcohol (3 g/kg) or saline intraperitoneal, 3 consecutive days (acute binge), 4 consecutive weekly (3-day) binge cycles (chronic binge), or 4 weekly binge cycles followed by a 30-day abstinence period without alcohol or saline injections (chronic binge with abstinence). Cancellous BMD was determined by quantitative computed tomography and compressive strength determined by biomechanical testing. Serum testosterone and osteocalcin levels were measured by enzyme-linked immunosorbent assay. Tibial cancellous BMD was significantly reduced by 25% (P<.05) after both acute and chronic binge alcohol treatment and vertebral cancellous BMD was significantly reduced by 15% (P<.05) after chronic binge exposure. Vertebral compressive strength was also significantly decreased by 31% (P<.05) after chronic binge alcohol treatment. Tibial cancellous BMD returned to control levels after the 30-day alcohol abstinence period, but vertebral cancellous BMD remained 15% below control values (P<.05) 30 days after termination of binge alcohol exposures. Serum osteocalcin levels were significantly decreased following acute binge alcohol exposure (P<.05). These results show that binge alcohol exposure can produce both short- and long-term skeletal damage in the adolescent rat. These data might have relevance to peak bone mass attainment and future risk of skeletal disease in adolescents and young adults who engage in repeated binge-drinking episodes.