Clinical data have suggested that obesity protects against osteoporosis. Leptin, mainly secreted by white adipose tissue, might be involved by mediating an effect on bone metabolism. This study was conducted to investigate a possible relationship of leptin and bone turn-over in postmenopausal women with osteoporosis.
We measured bone mineral density (BMD), serum leptin levels and markers of bone metabolism, including osteocalcin and cross-laps in 44 patients with osteoporosis. The main group consisted of 32 postmenopausal women.
Mean serum leptin was 13.1 microg/L and showed no statistically significant difference to the levels measured in a collective of normal persons adjusted for age and BMI. When related to serum cross-laps as markers of bone resorption, a positive correlation (p<0.05) was observed, whereas no correlation with osteocalcin could be seen.
A dual control of bone formation by leptin is assumed: This involves local mechanisms acting on osteoblasts and a central inhibitory effect on bone metabolism via a hypothalamic relay. Our data indicate that the net effect of circulating leptin may cause bone loss and is significantly related to high-turnover serum bone markers, at least in postmenopausal women with osteoporosis.
"However, clinical data on the association between circulating leptin and adiponectin levels and OC are controversial. Previous human studies that have evaluated the relationship between leptin and OC yielded conflicting results, showing either no correlation      , positive , or negative correlation    . Similarly, some studies reported a positive association between serum adiponectin and OC      , whereas other studies were not able to demonstrate a significant and independent relationship [16, 20, 28–30]. "
[Show abstract][Hide abstract] ABSTRACT: Introduction. Experiments on genetically modified animals have discovered a complex cross-regulation between adipokines (leptin, adiponectin) and osteocalcin. The relationships between these molecules in human osteoporosis are still unclear. We evaluated the hypothesis of a bidirectional link between adipokines and osteocalcin. Materials and Methods. In a cross-sectional study of 294 older patients with osteoporotic hip fracture, we estimated serum concentrations of leptin, adiponectin, resistin, osteocalcin, parameters of mineral metabolism, and renal function. Results. After adjustment for multiple potential confounders, serum osteocalcin concentration was inversely associated with resistin and positively with leptin, leptin/resistin ratio, and adiponectin/resistin ratio. In multivariate regression models, osteocalcin was an independent predictor of serum leptin, resistin, leptin/resistin, and adiponectin/resistin ratios. Conclusions. Our data support the bidirectional regulation between osteocalcin and adipokines, but contrary to the genetically modified animal models, in older subjects with osteoporotic hip fracture, serum osteocalcin is positively associated with leptin and inversely with resistin.
International Journal of Endocrinology 02/2012; 2012:684323. DOI:10.1155/2012/684323 · 1.95 Impact Factor
"Leptin-deficient (ob/ob) and leptinreceptor–deficient (db/db) mice present increased bone formation . In addition, circulating leptin may cause bone loss and has been significantly related to high-turnover serum bone markers in postmenopausal women with osteoporosis . "
[Show abstract][Hide abstract] ABSTRACT: Information regarding nutrition and body composition in patients diagnosed with osteogenesis imperfecta (OI) is scarce. In the present study, nutritional status, bone mineral density, and biochemical parameters of subjects with OI were evaluated.
Patients with type I OI (n = 13) and type III OI (n = 13) and healthy controls (n = 8) were selected. Nutritional status and bone mineral density were assessed by a 3-d food diary and dual-energy X-ray absorptiometry at the lumbar spine, respectively. Body mass index, serum albumin, calcium, creatinine, cross-linked C-telopeptide, parathyroid hormone, and 25-hydroxivitamin D(3) were also evaluated.
Patients with OI had lower bone mineral density (P < 0.05 versus controls). Patients with type III OI had the highest body mass index (P < 0.05 versus patients with type I OI and controls) and the lowest lean body mass (P < 0.05 versus patients with type I OI and controls). In patients with OI, the number of fractures was positively correlated with body mass index (r = 0.581, P = 0.002) and the percentage of body fat (r = 0.451, P = 0.027) and negatively correlated to lean body mass (r = -0.523, P = 0.009). Even when taking dietary supplements, 58% and 12% of subjects with OI did not achieve the calcium and vitamin D recommendations, respectively.
Body composition is a risk factor for bone fractures in subjects with OI. Individualized nutritional support is recommended not only to improve body composition but also to potentiate pharmacologic and physical therapies.
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