Researchers at the University of Michigan Medical School have revealed a potential mechanism explaining the role of the drug "sotagliflozin" in reducing the formation of blood clots. Experiments showed that it reduces platelet activity and aggregation, which may help explain its association with a lower risk of heart attacks and strokes in some patients.
The researchers conducted laboratory experiments on blood samples from healthy individuals and those with type 2 diabetes, alongside experiments on mouse models, to compare the effects of "sotagliflozin" with "empagliflozin," a drug used in diabetes treatment. The results showed that sotagliflozin reduced platelet activation, aggregation, and clot formation, whereas the effect of empagliflozin was limited or not significant in most tests.
The experiments indicated that the effect of sotagliflozin in reducing clot formation was not accompanied by any significant disturbance in the bleeding cessation mechanism within the studied models. Researchers believe these findings may help explain some of the cardiovascular protective effects associated with the drug, in addition to its effect on regulating blood sugar levels.
The drug's effect is linked to sodium-glucose transporters, proteins that contribute to glucose transport within the body. Sotagliflozin inhibits two types of these transporters, while empagliflozin's effect is limited to the second type. The results suggest that inhibiting the first transporter may play a role in reducing platelet activity, but the precise mechanisms still require further research.
The study provides additional understanding of the relationship between diabetes medications and blood clotting. However, the results of laboratory and animal experiments alone are not sufficient to prove that this effect directly reduces clots in patients, necessitating further studies to determine the mechanism and its clinical significance.
Source: Syrian Arab News Agency (SANA)
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