Obesity protects from osteoporosis. Bone remodeling and energy metabolism could be regulated by the adipocyte-derived hormone, leptin acting on osteoblasts though hypothalamic pathways. Hypothalamic lesions cause obesity. Since most of these patients are also hypopituitary with low IGF1 which could affect bone metabolism the aim of our study was to investigate whether obesity would protect them from osteoporosis.
Three groups of patients were studied: (1) eight hypothalamic obese patients (HO −4 female, mean age 25.5±2.1 years, BMI-38.4±2.8 kg/m2), (2) seven normal weight hypopituitary (HN −4 female, mean age 32.1±2.2 years, BMI-23.8±1.3 kg/m2) and (3) four diet induced obese patients (DIO-3 female, mean age 27.2±3.1 years, BMI −44.3±3.8 kg/m2). Patients were sex and age matched. The etiology of obesity in the HO and HN group was due to hypothalamo-pituitary tumor operation or hypothalamo-pituitary disconnection. All patients received standard hormone replacement therapy except for growth hormone replacement after overnight fast serum leptin, IGF1, osteocalcin-OCL, CTx and 25-OH-vitamin D levels were measured. Body composition (Fat%) and bone mineral density (BMD) were estimated by DEXA (Hologic). Relevant parameters are presented as mean±S.E.M. in Table.
|Groups||BMI (kg/m2)||Leptin (ng/ml)||OCL (ng/ml)||CTx (ng/ml)||Vit. D (nmol/l)||IGF 1 (ng/ml)||DEXA Z score||BMD (g/m2)||TBMC (kg)||Fat%|
|*P<0.05 DIO vs HO; †P<0.05 DIO vs HN|
1. Obesity induced by hypothalamic lesion with concomitant hypopituitarism (low IGF1), protects from bone loss when compared with normal weight hypopituitary patients with low IGF 1 levels.
2. When compared with diet-induced obesity despite significanlty lower IGF1 levels bone mineral density and biochemical markers of bone turnover were similar.
03 - 07 May 2008
European Society of Endocrinology