Effects of Insulin Resistance Induced by Dexamethasone on Bone Mass in Ovariectomized Rats

Abstract

Glucocorticoids therapy is the most common cause of secondary iatrogenic osteoporosis.The bone loss occurs predominantly due to a decrease in bone formation, although increased bone resorption also occurs. Insulin resistance is the key pathology in type 2 diabetes negatively influence bone remodeling and leads to reduced bone strength. Loss of sex steroids, particularly oestradiol, as in ovariectomized rats,leads to increased skeletal remodeling over and above the age-related increment, together with excessive osteoclast activity. In this study, ovariectomy DEX group has highly significant increase in relative cortical resorptioncompared to ovaiectomy and sham DEX groups, also ovariectomy and DEX group has highly significant decrease in bone thickness compared to ovariectomy and sham DEX groups. The consequent increase in remodeling activation increases the overall resorption rate without a compensatory increase in formation, leading to rapid bone loss.This negative effect on bone which is due to the glucocorticoid excess is also mediated by indirect mechanisms such as the calcium malabsorption and hypercalciuria. In response to the enhanced supply of calcium from the skeleton, PTH secretion tends to be diminished, thereby reducing vitamin D [1,25(OH)2 cholecalciferol] concentration with a consequent reduction in calcium absorption.