Diabetes medicine may help curb harmful blood clots

New research suggests that a medicine used for diabetes and certain heart-related conditions may help guard against dangerous blood clots by reducing the activity of platelets. The findings offer a possible explanation for the cardiovascular benefits seen with sotagliflozin, a drug that changes how the body processes sugar.

Platelets are tiny blood components that cluster together to stop bleeding. But when they become too active, they can also form clots that block blood flow to the heart or brain, leading to a heart attack or ischemic stroke.

The research team says the discovery could help improve prevention strategies while still preserving the body’s normal ability to stop bleeding. Because the results came from human blood samples and animal studies, they do not amount to a new clot-prevention treatment for all patients.

Scientists at the University of Michigan published the study in the Journal of Clinical Investigation. Instead of launching a new trial focused on heart attacks and strokes, they examined how sotagliflozin affects platelet behavior and compared it with empagliflozin.

Both drugs act on proteins called sodium-glucose cotransporters, which help transport sugar. Empagliflozin mainly blocks SGLT2 in the kidneys, while sotagliflozin blocks both SGLT2 and a related protein, SGLT1, which is also found in other tissues.

In blood samples from healthy volunteers and people with type 2 diabetes, sotagliflozin lowered platelet activation and reduced their tendency to clump together. Empagliflozin showed little or no effect in the same tests.

Researchers are also looking into how another diabetes medicine may help protect blood vessels as they age.

The same pattern appeared in mice with damaged blood vessels. Sotagliflozin cut clot formation by roughly 60%, compared with only about 5% to 10% for empagliflozin, suggesting that blocking SGLT2 alone did not explain the stronger response.

To explore the role of SGLT1, the team removed that protein specifically from mouse platelets. Clot formation dropped by about 40%, indicating that SGLT1 contributes to the effect, though it does not explain all of sotagliflozin’s action.

A drug that selectively blocks SGLT1 also failed to fully match sotagliflozin’s impact. The researchers therefore suspect other mechanisms may be involved, including possible effects on the cells that line blood vessels, which still need more study.

The experiments did not show that sotagliflozin weakened normal blood-clotting function. That is reassuring, but laboratory and animal findings cannot prove that every patient can use the drug without bleeding or other side effects.

The study also does not mean that all drugs in this class affect platelets in the same way. The comparison highlights a biological difference, while treatment decisions for diabetes and cardiovascular disease must still be based on evidence for each patient.

Further research could help determine how this mechanism contributes to clinical benefits and whether it applies to other groups. For now, the work gives scientists a clearer target for understanding how a sugar-lowering medicine may also influence harmful clot formation.

If you are interested in this topic, please read articles about A guide to healthy eating for diabetics, and Omega-3 fatty acids and heart health: What you need to know.

For more information, please see articles about Mediterranean diet could protect artery health, reduce heart disease risk, and Healthy eating for a happy heart: managing cholesterol levels through diet.

Source: University of Michigan Medical School.