Scientists have found the hidden cause of diabetes in pancreatic cells
Researchers have found that disrupting the formation of proteins inside cells that produce insulin may play an important role in the development of diabetes. The work of scientists, published in the journal Science Daily, showed how a malfunction in the insulin assembly system leads to damage to pancreatic beta cells and may become a new target for future treatments. All the details are in the Izvestia article.
An error inside the cell that interferes with the work of insulin
Scientists from the Sanford Burnham Prebis Medical Research Institute and the University of Michigan have studied the process that occurs inside the beta cells of the pancreas - they are responsible for the production of insulin and control of blood sugar levels.
Researchers have found that for cells to function properly, they need to form proteins correctly. If this process is disrupted, damaged proteins begin to accumulate inside the cells, which causes stress and can lead to deterioration of beta cells.
The scientists paid special attention to proinsulin, a precursor protein from which cells create insulin. Previously, it was known that improper formation of proinsulin is associated with the development of diabetes, but it remained unclear which proteins help control this process.
Randal J. Kaufman, Ph.D., is a professor at the Center for Metabolic and Liver Diseases at the Sanford Burnham Davis Institute and senior and lead author of the study.
Our goal was to study how these partner proteins coordinate proinsulin folding and eliminate any errors associated with protein folding, as these steps are essential for the health of insulin-producing cells.
Why does insulin depend on "helpers"
In the course of the study, the scientists studied the role of the binding immunoglobulin protein (BiP) and its partner p58IPK, which are involved in the proper formation and transport of proinsulin inside cells.
Experiments have shown that when p58IPK was removed from cells, the amount of improperly formed proinsulin increased in them. Similar results were obtained in studies on mice: in the absence of this protein, beta cells produced less proinsulin and insulin.
After the return of p58IPK to the altered cells, their ability to properly form and move proinsulin improved, and the number of damaged proteins decreased. However, scientists have found that this protein cannot completely replace BiP — both participants in the process are necessary for the normal operation of the system.
The researchers compared this system to teamwork: a single protein is not able to independently perform all the tasks necessary to maintain the health of insulin-producing cells.
A new approach to protecting cells from diabetes
Today, most diabetes medications are aimed at controlling blood sugar levels.: they help tissues absorb glucose or stimulate the release of insulin. However, existing methods do not correct the problems associated with the improper formation of proinsulin and damage to beta cells.
Randall J. Kaufman
If we can learn how to influence the coordinated activity of BiP as a key regulator of proinsulin clotting, we may find a promising treatment strategy for early intervention to prevent or reduce damage to insulin-producing cells.
Scientists have yet to determine how this process can be influenced in the human body. However, the results show that protein formation disorders may be one of the factors that contribute to cell deterioration in type II diabetes.
Переведено сервисом «Яндекс Переводчик»
