Body mass index (BMI) and parameters of bone formation and resorption in postmenopausal women

Objectives: Aim of this study was to evaluate increased body mass index (BMI) as an anthropometric factor, predisposing to lower rates of bone turnover or changes in bone balance after menopause. Material and methods: For this purpose, we calculated BMI, and measured spinal (BMDSP) and femoral bone mineral density (BMDFN) and biochemical markers of bone formation (serum osteocalcin (S-OC), serum procollagen type I C propeptide (S-PICP), serum bone-specific alkaline phosphatase (S-B-ALP)) and resorption (urine N- and C-terminal cross-linking telopeptide of type I collagen (U-NTX-I and U-CTX-I), pyridinoline (U-PYD) and deoxypyridinoline (U-DPD)) in 130 healthy postmenopausal women, aged 46-85 years. Bone balance indices were calculated by subtracting z-scores of resorption markers from z-scores of formation markers, to evaluate bone balance. Results: S-PICP (r = -0.297, P = 0.002), S-OC (r = -0.173, P = 0.05) and bone balance indices (zPICP-zDPD) and (zPICP-zPYD) were negatively. correlated with BMI (r = -0.25, P = 0.01 and r = -0.21, P = 0.037) and with BMDSP (r = -0.196, P = 0.032 and r = -0.275 and P = 0.022). Women were grouped according to their BMI, in normals (BMI < 25 kg/m(2)), overweight (BMI = 25-30 kg/m(2)), and obese (BMI > 30 kg/m(2)). Overweight and obese women had approximately 30% lower levels of S-PICP compared to normals (68.11 +/- 24.85 and 66.41 +/- 24.93 ng/ml versus 97.47 +/- 23.36 ng/ml, respectively; P = 0.0001). zPICP-zDPD, zPICP-zCTX-I and zPICP-zPYD were significantly declined in obese women compared to normals (P = 0.0072, 0.02 and 0.0028). Conclusions: We conclude that in postmenopausal women, BMI is inversely associated with levels of collagen I formation marker, serum PICR In obesity formation of collagen I was reduced, in favor of degradation, but since this finding is not followed by simultaneous decrease in bone mineral density, it seems that increased body weight may have different effects on mature estrogen-deficient bone and extraskeletal tissues containing collagen I. (C) 2003 Elsevier Ireland Ltd. All rights reserved

Mechanisms of disease: is osteoporosis the obesity of bone?

Osteoporosis and obesity, two disorders of body composition, are growing in prevalence. Interestingly, these diseases share several features including a genetic predisposition and a common progenitor cell. With aging, the composition of bone marrow shifts to favor the presence of adipocytes, osteoclast activity increases, and osteoblast function declines, resulting in osteoporosis. Secondary causes of osteoporosis, including diabetes mellitus, glucocorticoids and immobility, are associated with bone-marrow adiposity. In this review, we ask a provocative question: does fat infiltration in the bone marrow cause low bone mass or is it a result of bone loss? Unraveling the interface between bone and fat at a molecular and cellular level is likely to lead to a better understanding of several diseases, and to the development of drugs for both osteoporosis and obesity