Overview
- Researchers at IIT Kanpur reported Thursday that activating a receptor called GPR18 on pancreatic macrophages triggers a rapid release of sphingolipid fats that block insulin release from neighbouring beta cells.
- The team traced the mechanism step by step: GPR18 activation in macrophages causes sphingolipid release, beta cells take up those lipids through a surface transporter, and the lipids then interfere with the cells' insulin‑release machinery.
- In mouse experiments, precision genetic switching of the macrophage pathway reduced insulin secretion and turning the pathway off or blocking GPR18 restored normal release.
- The same GPR18–sphingolipid pathway was confirmed ex vivo in donated human pancreatic tissue, where activating it likewise suppressed insulin secretion, but the work remains preclinical and was not done in living patients.
- The authors identify three candidate therapeutic targets—GPR18, the sphingolipid signal, and the beta‑cell uptake transporter—and say follow‑up studies must test safety, specificity, and whether blocking the pathway can help people with obesity or type 2 diabetes.