Mumbai, Nov 12 (PTI) Researchers at the Indian Institute of Technology Kanpur have discovered how immune cells in the pancreas can suppress insulin release within minutes, uncovering a new cellular communication pathway that could open fresh avenues in diabetes research.
The study was jointly led by Simran Singh and Ashish Kumar, who are the co-first authors of the research, under the supervision of Dr Sai Prasad Pydi at the Department of Biological Sciences and Bioengineering, IIT Kanpur, the institute said in a statement.
The team has also confirmed that the same pathway is present and active in human pancreatic tissue, which makes it a target for drugs meant to protect insulin production in people with obesity and type 2 diabetes.
The human pancreas contains several types of cells, including insulin-producing beta cells and immune cells called macrophages. While beta cells regulate blood glucose by secreting insulin, macrophages help maintain tissue health and immune balance.
The study reveals how macrophages directly interact with neighbouring beta cells to regulate insulin secretion.
While obesity was previously believed to trigger low-grade inflammation that gradually damages beta cells over months and years, this IIT Kanpur study reveals a much faster, direct exchange of signals between immune cells and insulin-producing cells.
“We discovered that immune cells that are present next to beta cells can switch off insulin release within minutes. And they do it without giving any of the classical inflammation signals we have been studying for decades. The findings change our fundamental understanding of how immune cells influence insulin production.
“The effect is not slow damage from inflammation but instruction that is delivered in minutes. The fact that this works the same way in human tissue is what makes it exciting. It is not just a finding in tissues of laboratory mice, but a real biological circuit that could be targeted with a drug," said Dr Pydi.
The team traced the trigger to GPR18, a receptor on macrophages that sits at the top of the chain. Blocking GPR18, or any of the steps below it, restored normal insulin release.
The pathway therefore has three points at which a potential drug could act - the receptor, the lipid signal and the uptake step.
Working with the Indiana Biosciences Research Institute in the United States, the IIT Kanpur team confirmed that GPR18 is heavily concentrated in the immune cells of human pancreatic islets.
When the researchers activated the pathway in donated human pancreatic tissue, insulin secretion was blocked there as well.
While the study does not offer a diabetes treatment, the validation establishes a foundation for further research into how disrupting the pathway can help preserve insulin secretion in people with obesity and type 2 diabetes.
