Clinical studies evaluating the role of leptin and adiponectin on bone metabolism had shown conflicting results, and data about the effect of anticatabolic drugs on these adipokines are scarce. Our aims were to determine adiponectin and leptin levels in osteoporotic postmenopausal women and their relationship with bone mass and bone turnover and to analyze changes on adiponectin and leptin levels after treatment with raloxifene or alendronate.
We selected 53 women (mean ± SD age, 63 ± 7 y) with postmenopausal osteoporosis divided into two treatment groups: raloxifene (60 mg/d; n = 20) or alendronate (70 mg/wk; n = 33) during a period of 1 year. Bone mineral density by dual-energy x-ray absorptiometry and serum levels of leptin, adiponectin, and bone turnovers markers were determined at baseline and at 1 year after treatment.
Baseline levels of leptin were correlated to body mass index (r = 0.47; P < 0.01), waist circumference (r = 0.38, P = 0.01), and estradiol (r = 0.4, P = 0.003). Adiponectin was inversely related to bone-specific alkaline phosphatase (r = −0.41, P < 0.01) and serum crosslaps (r = −0.35; P < 0.01). There was no correlation between bone mineral density, leptin, and adiponectin. After 12 months, no changes were observed in leptin and adiponectin in the alendronate group; however, a significant increase in leptin levels (973.5 ± 637.4 pM/mL vs 1,305.7 ± 793.5 pM/mL; P = 0.031) was detected in the raloxifene group, whereas adiponectin levels showed no significant changes (P = 0.46).
In postmenopausal women with osteoporosis, raloxifene induces a significant increase in leptin levels without significant changes in adiponectin serum levels. The antiresorptive effect of raloxifene and alendronate is not substantially influenced by changes in leptin or adiponectin levels.
The antiresorptive effect of raloxifene and alendronate is not substantially influenced by changes in leptin or adiponectin levels.
From the 1Bone Metabolic Unit, Endocrinology Division, Hospital Universitario San Cecilio, Granada; 2Endocrinology Division, Hospital Virgen de la Victoria, CIBER Fisiopatologìa de la Obesidad y Nutriciòn (06/03), Instituto de Salud Carlos III, Málaga; and 3Endocrinology Division, Hospital Torrecárdenas, Almería, Spain.
Received April 28, 2011; revised and accepted June 7, 2011.
Funding/support: This work was not supported by any specific grant.
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Manuel Muñoz-Torres, MD, PhD, Bone Metabolic Unit. Endocrinology. Hospital Universitario San Cecilio, Av. Dr. Oloriz 16, 18012 Granada, Spain. E-mail: firstname.lastname@example.org