An osteoporosis medication could help restore insulin production in people with type 1 diabetes

Type 1 diabetes (T1D) is caused by an autoimmune attack on insulin-producing beta cells, but studies have shown that many adults with long-term T1D are able to maintain some of their beta cells. One potential approach to curing the disease is stimulating these remaining cells to replicate, survive and produce insulin.

A team of JDRF-supported researchers led by Rupangi Vasavada, Ph.D., at the Icahn School of Medicine at Mt. Sinai in New York City have found that denosumab, a drug used to prevent bone loss in people with osteoporosis, promotes the replication and survival of insulin-producing beta cells. In a recently published Cell Metabolism paper, the research team demonstrated that a protein called osteoprotegerin (OPG) triggers an increase of beta cells in diabetic mouse models. This finding prompted Dr. Vasavada and her colleagues to look for an existing drug that acts like the OPG protein and subsequently triggers beta cell proliferation. Denosumab, which works along the OPG-production pathway, was among the drugs they tested. Their tests showed that denosumab therapy induced beta cell proliferation in mouse models and in human islets in vitro. When the drug was given to mouse models that had received human islet grafts, there was also a substantial increase in beta cells.

Dr. Vasavada’s work shows the potential for repurposing denosumab or developing new drugs with similar activities to trigger beta-cell regeneration as a part of a future cure for T1D. Further research is ongoing to learn more about how denosumab and OPG modulate beta-cell regeneration and function, and to determine the potential for human clinical trials.