People with type 2 diabetes have an increased risk of bone fractures, but some diabetes treatment options can adversely affect the bone health of patients, according to study authors Patrick R. Griffin, The Scripps Research Institute (TSRI), and B. Lecka-Czernik, University of Toledo.
This is because diabetes drugs have to combat the transcription factor known as PPAR&gamma, which is instrumental in regulating stem cells and controlling bone formation, bone resorption and fat.
A drug class known as glitazones (TZDs) targets PPARγ, but the interaction leads to the glitazones driving stem cells to fat at the expense of bone. This then increases the risk of fractures and severe bone loss.
This new drug class is designed to achieve healthy bone balance. SR10171 is a dual-targeting drug candidate: it sensitises patients to insulin, and also increases bone mass by expanding the formation of new bone and replacing old bone.
In type 2 diabetic and normal mouse models, SR10171 treatment inhibited fat formation in the bone marrow without affecting their metabolic state.
“Using structural biology techniques and rational design synthetic chemistry, SR10171 was constructed to engage the PPARγ protein in a unique way possessing an optimal balance with the receptor’s other family member, PPARα, to treat diabetes and, at the same time, improve bone health,” said Griffin.
There is currently no word on planned subsequent studies for the compound, so a potential treatment could still take a long time to develop and put through clinical trials.
The study appears in the online journal EBioMedicine.