Impaired insulin signaling limits osteogenic potential of bone marrow stromal cells in type 2 diabetes
Authors' conclusion
These findings demonstrate impaired insulin signaling in human BMSCs from patients with T2D and link reduced insulin responsiveness to diminished osteogenic potential and bone formation. Disrupted insulin-Wnt pathway signaling in BMSCs may contribute to the low bone turnover phenotype observed in T2D.
Study context
- Population
- Adults with long-standing T2D; Bone marrow stromal cells (BMSCs) and iliac crest bone biopsies
- Exposure
- T2D BMSCs vs healthy controls
- T2Dn = 16
- Outcome
- Insulin signaling and osteogenic capacity of BMSCs
Methodological detailsprimary human BMSCs, age- and sex-matched healthy controls, phosphoproteomics, single-cell RNA sequencing
- Primary human BMSCs
- Age- and sex-matched healthy controls
- Phosphoproteomics
- Single-cell RNA sequencing
Main finding
As reported in the abstract
- A BMSC subset enriched for inflammatory genes correlated with fasting insulin levels
- Insulin responsiveness in BMSCs correlated positively with in vitro osteogenic differentiation and in vivo bone formation rate
- T2D BMSCs: baseline hyperphosphorylation and attenuated insulin-stimulated canonical Wnt signaling vs healthy controls
Observational data: associations, not effects.
Original publication
Impaired insulin signaling limits osteogenic potential of bone marrow stromal cells in type 2 diabetes. Eur J Endocrinol. Published 15 April 2026. doi:10.
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