Molecular Malfunction May Lead To Diabetes

Researchers in the the department of bioengineering at the University of California, San Diego have discovered that molecular malfunction may be the reason behind the development of high blood pressure, diabetes and immune problems. Rogue versions of enzymes known as proteases roam the body, clipping off working segments of the receptors that allow insulin to enter cells and do its job. The report, published in the online issue of Hypertension reports that uncontrolled enzymatic activity also reduces the immune system’s response to infection and raises blood pressure. Thus the study presents a new mechanism for disease and injury to the body.

The author of the study Frank DeLano said,

“It is an idea that hasn’t been presented before. If we apply a protease inhibitor, we can prevent the damage we see in laboratory animals.”

The researchers have found that proteases, whose function is to clear away molecular debris, can go awry and split apart a number of different cell wall receptors. If insulin receptors are damaged, normal metabolism of glucose is not possible, and diabetes can be the result. Proteases can also damage receptors that are vital for the functioning of infection-fighting leukocytes. They also reported that the protein receptors on the surface of cells are clipped off as the rats develop high blood pressure. A major next step will be to show that the protease damage seen in laboratory rats occurs in humans.

“We will have to do human trials. We are working with other researchers on human trials,”

said DeLano in a statement.

The newly reported studies might also help explain why antioxidants such as vitamins C and E help against inflammation.


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