A primary treatment goal in type 1 and type 2 diabetes is normalization of pancreatic β-cell homeostasis. Kondegowda et al. report that the TNF receptor superfamily member osteoprotegerin — which is involved in bone formation — stimulates β-cell proliferation and enhances glucose homeostasis in young, aged and diabetic mice. These effects were mediated through binding receptor activator of NF-κB ligand (RANKL) and modulation of the CREB and GSK3 pathways. Treatment of humanized diabetic mice with the RANKL-specific antibody denosumab (an osteoporosis drug that is approved in the US) induced β-cell proliferation.
References
Kondegowda, N. et al. Osteoprotegerin and Denosumab stimulate human beta cell proliferation through inhibition of the receptor activator of NF-κB ligand pathway. Cell Metab. 22, 77–85 (2015)
Rights and permissions
About this article
Cite this article
Crunkhorn, S. Osteoporosis drug promotes β-cell proliferation. Nat Rev Drug Discov 14, 528 (2015). https://doi.org/10.1038/nrd4699
Published:
Issue Date:
DOI: https://doi.org/10.1038/nrd4699
