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
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 T2...
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Published in | Egyptian Rheumatology and Rehabilitation Vol. 41; no. 1; pp. 37 - 43 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
The Egyptian Society for Rheumatology and Rehabilitation
2014
Springer Berlin Heidelberg Medknow Publications and Media Pvt. Ltd Springer Nature B.V SpringerOpen |
Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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ISSN: | 1110-161X 2090-3235 |
DOI: | 10.4103/1110-161X.128136 |