Bone Abstracts

Aim: Aim of our study was to investigate the serum adiponectin, leptin, and osteoprotegerin (OPG) levels and its expressions in the adipose tissue, and their relationships with bone metabolism and in patients with severe C chronic obstructive pulmonary disease (COPD).

Materials and methods: Serum leptin, adiponectin, OPG, the receptor activator of nuclear factor-kB ligand (RANKL), and bone turnover markers (osteocalcin and type 1 collagen C-telopeptide (CTx)) were determinated in 52 patients with severe COPD and 42 age- and sex-matched healthy controls. Bone mineral density (BMD) and body composition was assessed by dual energy X-ray absorptiometry at the lumbar spine (LS) and left femur neck (FN). Subcutaneous adipose tissue samples were analyzed by immunocytochemical analyses.

Results: Adipose tissue expression of leptin (LepR) was low and adipose tissue expression of adiponectin (AdipoR1) was higher in COPD group than in control. Compared to patients without osteoporosis, those with the disease had significantly lower serum leptin, OPG levels, and LepR, in association with increased serum CTx, RANKL, adiponectin, and AdipoR1 expressions (P<0.05). LepR was inversely related to serum CTx (P<0.01), and directly to serum leptin (P<0.01), to fat free mass (FFM) (r=0.44, P<0.01) and to BMD FN and BMD LS (P<0.05 for all relationships). Serum leptin was correlated positively with OPG (P<0.05) and negatively with RANKL (P<0.05); serum adiponectin was negative association with serum OPG (P<0.05) and positive correlation with RANKL (P<0.05) in severe COPD. AdipoR1 expression was negatively related to FFM (r<−0.51, P=0.01) and directly to serum adiponectin and CTx (P<0.01). Adipose tissue OPG expression was related to BMD FN only (P<0.05).

Conclusion: Our results suggest that adipose tissue leptin, adiponectin, and OPG expressions are related to development of osteoporosis in severe COPD, and appear to act as mediators between fat mass and bone density.