Protective effects of Clec11a in islets against lipotoxicity via modulation of proliferation and lipid metabolism in mice

The lipotoxicity is considered as one of the risk for diabetes. Here we report C-type lectin domain family 11, member A (Clec11a) as a new regulator in islet playing a protective role in lipotoxicity induced dysfunction. Islet transcriptome sequencing was performed using the high-fat diet induced obesity (DIO) mice model. We found a significant decrease of Clec11a expression in islets of DIO mice compared to normal control mice, which was further confirmed by real-time PCR. Immunostaining demonstrated the localization of the Clec11a protein in mouse islets. Administration of recombinant human Clec11a (rClec11a) protein promoted the proliferation of islet cells and rescued the inhibition of fatty acid on cell proliferation, which involved the activation of Erk signaling pathway. We also found that the rClec11a altered the expression of genes involved in lipid metabolism. •The expression of Clect11a decreases in the islets of high-fat diet induced obesity (DIO) mice model.•Clec11a plays a regulatory role on proliferation and lipid metabolism in islets, which could be a novel protective factor for the lipotoxicity in islets.•Clec11a plays a regulatory role on proliferation and lipid metabolism in islets.