Australian researchers have discovered a new biological path that causes the risk of developing type 2 diabetes patients with serious blood clots, which exposes them to the risk of heart attacks and strokes. The discovery paves the way for new treatments that reduce this danger.
The study was conducted by researchers from Sydney University in Australia, and its results were published in the Journal of Clinical Research on August 15, and the American Journal of Newsweek was written about it.
Farida Bassam, a professor of hematology and research author, told Newsweek: “Type -second diabetes patients suffer from a greater risk of heart attacks and strokes, and this is partly due to their hyperactivity.”
Platelets are small fragments of cells that are in our blood that constitute clots to help stop bleeding, but Dr. Farida explained that high blood sugar levels in diabetics cause biochemical changes that make the blood “more viscous”, which allows him to clot when there is no need.
Dr. Farida continued: “Medicines such as aspirin prevent platelets, but they are 3 times less effective in type 2 diabetes. Understanding the reason for increasing platelets in diabetics opens the door to developing medicines targeting this newly discovered path.”
Discovered protein
The research team in their study found that the levels of protein called SEC 61B (SEC61B) rises significantly in platelets in type 2 diabetics.
The researchers explained that this protein appears to be disrupted by the calcium balance within the platelets, which makes it more vulnerable to blocs and clotting.
The researchers found that the inhibition of the “SEC 61B” activity using an antibiotic called Anisomycin reduces the platelette lump in both human samples and animal models.
“People with type 2 diabetes are more likely to develop blood clots. These exciting results determine a completely new way to reduce this risk and help prevent life -threatening complications such as heart attacks and strokes.”
The team analyzed in their studies of platelets in humans and mice, and discovered that the “SEC 61B” gene contributes to the leakage of calcium from the stock of platelets, making the cell fragments more interactive.
This increased sensitivity to platelets to clotting reduces the effectiveness of traditional anticoagulants in type 2 diabetes, reducing the options available to reduce the risk of cardiovascular disease.
The treatments targeting the JEC 61B gene are still in their early stages, and researchers believe that animal experiments may begin in a year to two years, and possible treatments for patients are likely to be available during the next decade.