The abundant bone protein osteocalcin is a key component, both in bone and in circulation of the response of bone to chronic alcohol consumption and/or stress. Data to support this hypothesis will be obtained by evaluating the effects of alcohol consumption by the animals alone and in combination with mental stressors. Individually, alcohol consumption and chronic stress have both been shown to have deleterious effects on bone, but there are no reports in which both factors have been investigated in the same experiments.
The specific aims of the study are: (1) to determine the effects of prolonged alcohol consumption on bone quality, serum osteocalcin, and biosynthesis of enzymes of the catecholamine pathway, with and without the addition of acute (one time) or chronic restraint stress: and (2) identify extraskeletal sites where increased uptake of radiolabeled osteocalcin in restraint stressed animals will indicate potential regulatory influence on mineral homeostasis. The effect of alcohol consumption on bone will be evaluated in rats given 5% ethanol in a liquid diet form (ELD), compared with those given control liquid diet (CLD). Bones are expected to smaller in ELD rats and to contain less osteocalcin. A one time restrain immobilization of these rats is will show that ELD abolishes the rapid increase in serum osteocalcin which will be seen in CLD rats. Chronic restrain combined with ELD will magnify the deleterious effects of ELD on bone and further depress circulating levels of osteocalcin. Bones and serum from the animals will be analyzed for biochemical and hormonal components, comparing values in ELD and CLD with and without imposition of acute or chronic stress. Bone quality,. As distinguished from quantity, will be evaluated by determination of breaking strength and by density gradient separation of finely powdered bone particles. These experiments are based on the need to understand mechanisms leading to osteoporotic problems in humans consuming high levels of ethanol, with and without interaction with environmental stressors.
