Abstract
Plasma FGF-23 concentrations and its relationship with calcium-phosphate homeostasis were evaluated in 48 perimenopausal obese women and in 29 nonobese controls. Serum parathyroid hormone, 25-hydroxyvitamin D3, CTX1, osteocalcin, total calcium, phosphorus, creatinine, and plasma intact FGF-23 concentrations were assessed. DXA of lumbar spine and femoral neck was performed to determine bone mineral density (BMD). Plasma iFGF-23 concentration was significantly higher in obese patients (by 42%) and correlated with age and BMD of proximal femur (R = −0.346; R = 0.285, resp.) but not with markers of bone turnover. However, serum phosphorus level in obese subjects was significantly lower. iFGF-23 concentration correlated significantly with body mass index (R = 0.292) and fat content (R = 0.259) in all study subjects. Moreover, a significant correlation between iFGF-23 and iPTH (R = 0.254) was found. No correlation between serum phosphorus or eGFR and plasma iFGF-23 and between eGFR and serum phosphorus was found. Elevated serum iFGF-23 concentration may partially explain lower phosphorus levels in the obese and seems not to reflect bone turnover.
Highlights
Epidemiological studies have suggested a protective effect of obesity on postmenopausal bone loss [1]
Fibroblast growth factors regulate the development of subcutaneous white adipose tissue; only five of them (FGF-1, 2, 7, 9 and 18) and not FGF-23 were identified in scWAT [10]
There was a correlation between intact fibroblast growth factor 23 (iFGF-23) concentration and proximal femur bone mineral density (BMD) (R = 0.321; P = 0.010) but not lumbar spine BMD (R = 0.223; P = 0.099)
Summary
Epidemiological studies have suggested a protective effect of obesity on postmenopausal bone loss [1]. The regulation of bone metabolism is complex including hormones and a long list of cytokines and growth factors. A new hormone involved in calcium-phosphate homeostasis was found—fibroblast growth factor-23 (FGF23). Fibroblast growth factors regulate the development of subcutaneous white adipose tissue (scWAT); only five of them (FGF-1, 2, 7, 9 and 18) and not FGF-23 were identified in scWAT [10]. FGF-23 regulates serum phosphate and 1,25(OH)2D3 levels by acting on the kidney and intestines. FGF-23 reduces serum phosphorus level by suppressing proximal tubular phosphorus reabsorption ( to PTH) and, in indirect way, intestinal phosphorus absorption [14]. FGF-23 suppresses the expression of 1αhydroxylase and enhances the expression of 24α-hydroxylase in the kidney, causing the reduction of serum 1,25(OH)2D3 level [14]
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