Relationships between serum adipocyte hormones (adiponectin, leptin, resistin), bone mineral density and bone metabolic markers in osteoporosis patients

Abstract

The purpose of this study was to investigate the relationship between fasting serum leptin, adiponectin and resistin levels and bone mineral density (BMD) in osteoporosis patients and a non-osteoporosis control group. We studied 81 non-diabetic osteoporosis patients (92 % female, 8 % male; mean age 54.5 ± 15.5 years and body mass index [BMI] 28.2 ± 4.6) and 120 non-diabetic individuals with normal BMD as controls (86 % female, 14 % male; mean age 39.7 ± 10.4 years and BMI 28.8 ± 4.4). BMD was studied by dual-energy X-ray absorptiometry from the lumbar spine (L1-L4) and femoral neck and fasting blood samples were taken for biochemical measurement of fasting blood glucose, leptin, adiponectin and resistin. Fasting levels of plasma adiponectin had a significant negative correlation with BMD of the femoral neck and lumbar spine in the osteoporosis group (r = -0.478, P = 0.003, r = -0.513, P = 0.023) but not in the non-osteoporosis group (r = -0.158, P = 0.057, r = -0.23, P = 0.465). Fasting plasma levels of resistin were significantly correlated only with femur BMD in the osteoporosis group, and not significantly correlated with lumbar spine BMD (r = -0.244, P = 0.048 vs r = 0.276, P = 0.56). Leptin did not have a significant correlation with BMD in either the osteoporosis or non-osteoporosis groups (P > 0.05). Adiponectin had a significant negative correlation with BMD of the lumbar spine and femoral neck. The correlation between leptin and resistin are not inconclusive.

Long-Term Supplementation of Green Tea Extract Does Not Modify Adiposity or Bone Mineral Density in a Randomized Trial of Overweight and Obese Postmenopausal Women

“…Research has shown that receptors for adiponectin are present on osteoblasts and may influence proliferation, differentiation, and the mineralization effects of these bone-remodeling cells (46,47). However, this association is not consistent (48). The impact of leptin on bone metabolism has also been studied, but results remain controversial.…”

Bone-adiposity cross-talk: implications for pediatric obesity

“…Similarly, it increases RANKL expression (a stimulus for osteoclast formation, function and survival) in osteoblasts, but inhibits them via the sympathetic nervous system [38]. The influence of this adipocytokine on bone mass via different pathways has been supported in adult study [39]. However, its action remains controversial.…”

Cytokines and Hormones That Contribute to the Positive Association between Fat and Bone

“…Plasma concentrations of adiponectin are inversely related to visceral fat mass and BMI, possibly due to the inhibition of adiponectin secretion by cytokines and hormones that are increased in obesity, by adipose tissue hypoxia, or by a negative effect of adiponectin on its own production (37). Clinical studies consistently show inverse relationships between circulating adiponectin concentrations and BMD, which persist after adjustment for potential confounding factors, including BMI, serum leptin, and central fat mass (33, 36, 41–43). There is a suggestion that an increased level of circulating adiponectin is a risk factor for fracture independent of body composition and BMD (36).…”

“…Clinical studies of the effect of leptin in bone are inconclusive, with some finding a positive correlation between leptin serum levels and BMD (31, 32) and others finding no correlation (33–35). Circulating leptin levels were not associated with fracture risk in a large prospective cohort study (36).…”