Novel Drug Candidate Could Treat Type 2 Diabetes, Osteoporosis

Findings from a recent study suggest that a new class of drugs could treat both type 2 diabetes and bone loss.

Patients with type 2 diabetes, especially postmenopausal women, have an increased risk of bone fractures. Since anti-diabetic drugs can potentially increase this risk, patients have limited treatment options.

The drug candidate, SR10171, increases bone mass by expanding bone formation and bone turnover, according to a study published by EBio Medicine. These 2 processes ensure healthy bone maintenance, and are negatively affected by diabetes.

Researchers examined how different molecules can increase sensitivity to insulin, and have developed a class of drugs that target the peroxisome proliferator-activated receptors gamma (PPARγ), which regulates stem cells that control bone formation and bone resorption, and is also a fat regulator.

Glitazones (TZDs) are anti-diabetic drugs that target the PPARγ protein, but can lead to bone loss and increased fractures because they differentiate stem cells into fat cells instead of bone cells, according to the study. However, SR10171 avoids this effect, and in the animal models treated with it, researchers found that fat formation in bone marrow was blocked.

“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, PPARa, to treat diabetes and, at the same time, improve bone health," said co-leader of the study Patrick R. Griffin, PhD. “This targeted polypharmacological approach demonstrates that the target isn't the problem if you target it correctly.”

SR10171 increases bone mass by protecting and increasing the activity of bone cells, according to the study.

“SR10171 improves bone mass regardless of body mass index, normal to obese," Dr Griffin concluded. “So you could use such a drug to treat osteoporosis whether patients are diabetic or not.”