Regulation of Bone Mineral Density in Morbidly Obese Women

Introduction

Obesity is defined as an excess of body fat, and the main assumption of the body mass index (BMI) guidelines is clearly associated with body fat; consequently is associated with its morbidity and mortality especially in morbid obesity with a BMI higher than 40Kg/m. Moderate obese women generally have increased bone mineral density (BMD) and reduced risk of fractures, but the effects of extreme obesity on BMD have not been well examined and remain controversial (1). On the other hand, significant changes in body composition occur with aging and a progressive increase in body fat and progressive reduction in free-fat mass have been observed (2, 3). Body weight influences both bone turnover and BMD and a high BMI is protective against osteoporotic and hip fractures in men and women (1). There is evidence of an inverse relationship between BMI and osteoclast activity in normal postmenopausal women and an increase in bone resorption following weight loss (4). The mechanisms for this fat-bone relationship have been described. They include the effect of soft tissue mass on skeletal loading, the association of fat mass with the secretion of active hormones from the pancreatic beta cells such as insulin (5) and amylin (6) that directly stimulate osteoblast proliferation, and the secretion of active hormones (estrogens, leptin, adiponectin, and resistin) from the adipocyte (7–9). In the morbid obese population—especially women—lean mass was the main determinant of BMD, before and after bariatric surgery and the insulin growth factor-I (IGF-I), adipocytokines, and circulating proinflammatory cytokines were not clearly associated with changes in BMD in this obese women population (10–12). In this review we analyze the most relevant aspects of BMD regulation in morbidly obese women and its evolution after bariatric surgery.

Abstract

Keywords

body mass index, bone mineral density, insulin growth factor, leptin, morbid obesity, vitamin D