Background: The obese are usually protected against osteoporosis and have i
ncreased bone mineral density and plasma leptin concentrations. A recent in
vitro study demonstrated that leptin acts on human marrow stromal cells to
enhance differentiation to osteoblasts, suggesting an influence of leptin
on bone mass. However, little is known about the relationship between plasm
a leptin and bone mass in postmenopausal women with osteoporosis.
Objective: To investigate plasma leptin concentrations in postmenopausal wo
men with osteoporosis to improve the understanding of the role of leptin in
determining bone mass.
Methods: Fifty postmenopausal women with osteoporosis (ages 61.18 +/- 6.51
years: body mass index (BMI) 28.91 +/- 3.44 kg/m(2) mean +/- S.D.) and 30 a
ge- and BMI-matched healthy postmenopausal women were included in the study
Bone mineral densities (BMD) were measured by dual energy X-ray absorptiom
etry. Plasma leptin concentrations were determined using an immunoradiometr
ic assay
Results: The median spine BMD value in the patient group (0.695 +/- 8.26 g/
cm(2), median +/- S.E.M.) was significantly lower than that in the control
group (1.006 +/- 1.29 g/cm(2), median +/- S.E.M.; z = -7.454, P < 0.001). T
he median plasma leptin concentration in the patient group (18.70 +/- 1.78
ng/ml, median +/- S.E.M.) was not significantly different from that in the
control group (22.35 +/- 2.20 ng/ml, median +/- S.E.M.; z = -1.630, P = 0.1
03). Plasma leptin concentrations were correlated with BMI in both groups (
r(s) = 0.394, P = 0.031 in controls and r(s) = 0.404, P = 0.004 in the pati
ent group). There was no correlation between plasma leptin concentrations a
nd BMD values in controls (r(s) = -0.107, P = 0.575) but a weak correlation
was observed in the patient group (r(s) = 0.285, P = 0.045).
Conclusion: Our data suggest that circulating plasma leptin does not have a
significant direct influence on bone mass in postmenopausal women.