The pore-forming subunit Kir6.1 of the K-ATP channel negatively regulates the NLRP3 inflammasome to control insulin resistance by interacting with NLRP3

• Main Authors: Ren-Hong Du, Ming Lu, Cong Wang, Jian-Hua Ding, Guangyu Wu, Gang Hu
• Format: Article
• Language: English
• Published: Nature Publishing Group 2019-08-01
• Series: Experimental and Molecular Medicine
• Online Access: https://doi.org/10.1038/s12276-019-0291-6
• ISSN: 1226-3613; 2092-6413

Diabetes: Inflammation in insulin resistance A potassium-regulating molecule, Kir6.1, blocks inflammation and prevents insulin resistance (IR), a hallmark of type 2 diabetes. Insulin triggers cellular glucose absorption, lowering blood glucose levels. In IR, cells resist insulin signals, causing unhealthy blood sugar levels. Inflammasomes, multi-protein complexes that assemble in response to infection and trigger an inflammatory response, were previously implicated in development of IR, but the details are poorly understood. Gang Hu at Nanjing Medical University in China and co-workers investigated how inflammation and IR are linked to Kir6.1. Mice lacking Kir6.1 showed high levels of inflammation and developed IR; treating the mice with Kir6.1 restored insulin sensitivity. Further study showed that Kir6.1 binds to one of the components of the inflammasome, preventing it from assembling. Kir6.1 shows promise for development of new treatments for inflammatory diseases, including IR.