Type 2 diabetes raises serum sclerostin levels and disturbs the relation between sclerostin and bone mineral density : a call for caution with antisclerostin therapy in osteoporosis

Abstract EN

Background Sclerostin is an osteocyte-secreted protein that negatively regulates osteoblasts.

Wnt signaling may be crucial in the pathogenesis of impaired bone quality in type 2 diabetes mellitus ( T2DM).

The possibility that currently studied antisclerostin bone-forming agents could be useful to T2DM patients with osteoporosis needs further investigations.

Aim The aim of this study was to investigate the relationship between serum sclerostin and bone mineral density in T2DM patients, in comparison with nondiabetic individuals.

Patients and Methods This study was conducted on 21 T2DM patients and 22 nondiabetic individuals.

All participants were 60 years or older.

They underwent history taking, clinical examination, routine lab investigations, and glycated hemoglobin assessment.

Serum sclerostin was measured by ELISA.

Bone mineral density (BMD) was measured at the left femoral neck and lumbar spine.

Results Serum sclerostin level was signifi cantly higher in T2DM patients compared with nondiabetic individuals.

Male participants showed significantly higher sclerostin levels among the nondiabetic individuals, whereas this difference was not signifi cant among T2DM patients.

The Bone mineral density (BMD) and t-values of T2DM patients and the nondiabetic group were not signifi cantly different.

We found a signifi cant positive correlation between sclerostin level and lumbar spine BMD among nondiabetic individuals, whereas among T2DM patients, this correlation was not signifi cant.

Sclerostin levels did not show a signifi cant difference between diabetic osteoporotic and diabetic nonosteoporotic patients.

Conclusion Patients with T2DM have raised sclerostin levels that, unlike those in nondiabetic individuals, are not correlated with BMD.

This pathological condition that is specifi c to diabetes necessitates further study, careful assessment of the role of antisclerostin therapy, and probable dose adjustment for osteoporosis in T2DM patients.