Campus Action: IIT Kanpur researchers identify mechanism of pancreatic immune cells to suppress insulin secretion


Kanpur, Nov 12 (INB) Researchers at the Indian Institute of Technology (IIT) Kanpur have identified a molecular mechanism through which immune cells in the pancreas can rapidly suppress insulin secretion, offering a new direction for research into obesity-associated insulin dysfunction and type 2 diabetes, it said on Thursday. The study, published in The Journal of Clinical Investigation family of journals, explains how immune cells called macrophages communicate with insulin-producing beta cells and interfere with their functioning, according to an institute statement. The researchers found that activated macrophages release sphingolipids, a class of lipid molecules that are taken up by neighbouring beta cells and disrupt the machinery responsible for insulin secretion. The team traced this process to GPR18, a receptor that triggers the signalling pathway in macrophages. Using genetic approaches in experimental models, the researchers demonstrated that activating this pathway significantly reduces insulin secretion, while inhibiting it improves insulin release, it stated. The findings were also validated in human pancreatic tissue in collaboration with the Indiana Biosciences Research Institute (IBRI), US. The team confirmed the presence of GPR18 in immune cells within human pancreatic islets and found that activation of the pathway suppresses insulin secretion in donated human tissue. The research was conducted predominantly at IIT Kanpur under the supervision of Prof Sai Prasad Pydi of the Department of Biological Sciences and Bioengineering (BSBE). Simran Singh and Ashish K jointly led the study as co-first authors, it added The researchers said the findings identify a previously unexplored molecular pathway that could inform future drug development. However, the discovery does not represent an immediate treatment for diabetes.
Research paper: [ https://www.jci.org/articles/view/202344](www.jci.org/articles/view/202344?utm_source=chatgpt.com)

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