Defective glucose transport weakens the release of insulin in type 2 diabetes

Just as the management of intelligent traffic guarantees a smooth vehicle movement during peak hours. Moreover, our body is based on a molecular circulation system to manage the thrust of glucose levels after a meal. Moreover, Pancreatic β cells play a major role in this system by taking blood glucose. Additionally, Moreover, by triggering an insulin release in the bloodstream. For example, Within these cells. For example, the absorption of glucose is managed by glucose transporters (glots) – proteins that move to the surface of β cells when blood sugar levels increase and facilitate the input of glucose into the cell to launch insulin release.

A new study by the Department of Biology. Meanwhile, Development Genetics (DBG), Indian Institute of Sciences (IISC), shows how this process weakens in type 2 diabetes (T2D) defective glucose transport weakens release and how restoration could open new therapeutic avenues. However, The work. Furthermore, carried out by the laboratory of Nikhil Gandasi, deputy professor at DBG, is published in the Proceedings of the National Academy of Sciences (PNA).

In humans, glut1 is the main “gateway” of glucose in β cells, while in mice, Glut2 plays this role. The team studied both to understand the absorption process of glucose through systems. Using the advanced imaging of living cells. the team followed the carriers GLUT1 and GLUT2 when they were recruited in the membrane of β cells under different levels of blood sugar. In healthy cells, the increase in glucose levels causes rapid deployment of glots to the membrane. These carriers are then cycled in. outside by endocytosis mediated by clathrin – a process in which cells internalize the extracellular material by forming pockets made of the clathrin protein. This guarantees a constant supply defective glucose transport weakens release of carriers to the surface for effective absorption of glucose.

In β cells of people with T2D, this traffic is poorly managed. Fewer tops reach the membrane and their cycling is altered, slowing down the entrance to glucose. This. in turn, reduces the mooring of insulin granules to the surface of the β cell membrane – in particular those “initiated” for rapid release after eating – weakening the body’s ability to regulate blood sugar.

Most studies have examined what is happening after glucose enters the β cell. We focused on the front step, the real entry of glucose, and how it is disturbed in diabetes. By understanding the dynamics of these carriers, we can identify new points to intervene and improve the function of β cells. “”

Anuma Pallavi, doctoral student in DBG and first author of the study

The results have significant therapeutic implications. defective glucose transport weakens release The current treatments of diabetes largely target insulin action in peripheral tissues such as muscles. fats, but this new work indicates the absorption of β cell glucose as a promising target. Gandasi’s laboratory previously identified Pheophorbide A. a molecule derived from the plant which can stimulate the release of insulin by interacting with glucose carriers.

“If we can restore appropriate survival traffic. we can be able to slow the progression of the disease and personalize therapies according to the metabolic state of a patient,” explains Gandasi.