Effect of 11β-HSD1 dehydrogenase activity on bone histomorphometry of glucocorticoid-induced osteoporotic male Sprague-Dawley rats

<p><b>INTRODUCTION</b>Glucocorticoids cause osteoporosis by decreasing bone formation and increasing bone resorption activity. Glucocorticoid action in bones depends on the activity of 11-beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) enzyme, which plays an important role in regulating corticosteroids. 11β-HSD1 is expressed by human and rat osteoblasts. We aimed to investigate the relationship between 11β-HSD1 dehydrogenase activity and bone histomorphometric changes in glucocorticoid-induced osteoporotic bone in rats.</p><p><b>METHODS</b>A total of 30 male Sprague-Dawley rats (aged three months, weighing 200-250 g) were divided into three groups of ten each. Group 1 rats were the baseline control, which were sacrificed untreated at the beginning of the study. Group 2 rats underwent sham operation and were administered with vehicle olive oil intramuscularly at 0.05 ml/kg. Group 3 rats were adrenalectomised and administered with an intramuscular injection of dexamethasone 120 μg/kg body weight/day. The treatment was started two weeks after the operation, for a duration of two months. Plasma osteocalcin, plasma pyrodinoline, plasma corticosterone and 11β-HSD1 were measured, and bone histomorphometry analysis was performed.</p><p><b>RESULTS</b>Dexamethasone treatment caused an increase in plasma corticosterone level, together with a significant reduction in 11β-HSD1 dehydrogenase activity of the bone, along with a higher plasma level of the bone resorption marker, pyridinoline. Dexamethasone treatment also caused a reduction in trabecular volume, number and thickness, and an increase in trabecular separation.</p><p><b>CONCLUSION</b>Long-term glucocorticoid treatment reduces the 11β-HSD1 dehydrogenase activity in the bone, which can otherwise lead to bone loss due to the increased level of active glucocorticoids.</p>

effects of Vitamin E on bodyweight and fat mass in intact and ovariectomized female rats

The aim of this study was to determine the effect of vitamin E deficiency and supplementation on body weight and body composition in intact and ovariectomized growing female rats. One hundred and twenty female Wistar rats aged 3 months were ovariectomized [OVX] or left intact [sham-operated]. The intact and OVX rats were divided into 6 groups and given different dietary treatments, i.e. vitamin E deficient diets [VED, 75%VED, 50%VED, 25%VED], normal rat chow diet [RC] and rat chow with oral supplementation of 30mg/kg body weight of alpha -tocopherol [RC+ATF]. Body weight of intact and OVX rats in the RC and the RC+ATF groups showed increased significantly after 15 weeks of dietary treatment. Intact and ovariectomized rats fed with VED, 75%VED, 50%VED and 25%VED did not gain weight after 15 weeks. OVX rats had significantly higher body weight than intact rats in the 50%VED, 25%VED, RC and RC+ATF groups. Fat mass of intact rats was increased only in the RC and RC+ATF groups. For OVX rats, fat mass was increased in the VED, 50%VED, RC and RC+ATF groups. OVX groups had significantly higher fat mass when compared with intact groups, however, the significance was greater for the RC and RC+ATF groups. Other parameters of body composition were not significantly affected. In conclusion, vitamin E played an important role in the weight gain of female rats and the gain was primarily due to the increase in fat mass, irrespective of the effect of ovariectomy. Alpha-Tocopherol supplementation conferred little benefit compared to giving RC diet alone in both the intact and ovariectomized female rats. The results also indicate that excessive vitamin E intake might contribute towards obesity in female rats