Binge Alcohol Treatment Increases Vertebral Bone Loss Following Ovariectomy: Compensation by Intermittent Parathyroid Hormone
- 29 March 2006
- journal article
- Published by Wiley in Alcohol: Clinical and Experimental Research
- Vol. 30 (4), 665-672
- https://doi.org/10.1111/j.1530-0277.2006.00078.x
Abstract
Background: Postmenopausal estrogen deficiency and alcohol abuse are known risk factors for osteoporosis. Previous studies of the combined effect of alcohol and ovariectomy on bone loss using chronic alcohol‐feeding models have not demonstrated additional alcohol‐induced bone loss in ovariectomized (OVX) animals. Binge alcohol treatment causes rapid bone loss in male rats. We hypothesized that binge alcohol would cause additional bone loss in OVX rats. Methods: Ninety‐six adult (400 g) female Sprague–Dawley rats (48 sham‐operated and 48 OVX, pair fed) were randomly divided into 4 treatment groups: (a) saline‐treated, (b) binge alcohol‐treated (3 g/kg alcohol as a 20% weight to volume alcohol/saline solution, intraperitoneal (IP), 3 times per week), (c) parathyroid hormone (PTH)‐treated (80 μg/kg, SC, 5 d/wk), and (d) binge alcohol plus PTH. Rats were treated for either 2 or 4 weeks. Following treatment periods, blood was collected for alcohol concentration (BAC) measurements; lumbar vertebrae were removed for bone mineral density (BMD) levels, trabecular microarchitecture assessment, and vertebral compressive strength analysis. Results: Peak binge BACs averaged 300 mg/dL. Alcohol and OVX decreased cancellous BMD: alcohol and OVX treatment in combination caused additional cancellous BMD loss and significant cortical BMD reductions. Compressive strength was also decreased by OVX and alcohol. Combination treatment resulted in further declines in bone strength. Micro‐CT analysis revealed a significant effect of combined OVX and alcohol treatment resulting in decreased trabecular bone volume/total volume (BV/TV). Intermittent PTH administration compensated for losses of BMD, compressive strength, and restored BV/TV deficits caused by OVX, alcohol, or their combination. Conclusions: Bone loss following OVX can be significantly increased by concurrent binge alcohol treatment. The effects of alcohol and OVX are compensated by concurrent intermittent treatment with PTH. These results suggest that postmenopausal women who abuse alcohol may place their skeleton at additional risk for osteoporotic fracture.Keywords
This publication has 55 references indexed in Scilit:
- The 12-month prevalence and trends in DSM-IV alcohol abuse and dependence: United States, 1991–1992 and 2001–2002Drug and Alcohol Dependence, 2004
- Both hPTH(1–34) and bFGF Increase Trabecular Bone Mass in Osteopenic Rats but They Have Different Effects on Trabecular Bone ArchitectureJournal of Bone and Mineral Research, 2003
- Adverse Outcomes of Osteoporotic Fractures in the General PopulationJournal of Bone and Mineral Research, 2003
- Disuse Exaggerates the Detrimental Effects of Alcohol on Cortical BoneAlcohol: Clinical and Experimental Research, 2003
- Episodic heavy drinking in four Nordic countries: a comparative surveyAddiction, 2001
- Effects of Parathyroid Hormone on Bone Formation in a Rat Model for Chronic Alcohol AbuseAlcohol: Clinical and Experimental Research, 2001
- Moderate Alcohol Consumption Suppresses Bone Turnover in Adult Female RatsJournal of Bone and Mineral Research, 2001
- Dietary Ethanol Does Not Accelerate Bone Loss in Ovariectomized RatsAlcohol: Clinical and Experimental Research, 1998
- Mechanisms of alcohol abuse and alcoholism in adolescents: A case for developing animal modelsBehavioral and Neural Biology, 1994
- Ethanol reduces bone formation and may cause osteoporosisAmerican Journal Of Medicine, 1989