Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, School of Medicine, Southeast University, Nanjing 210009, China; School of Medicine, Southeast University, Nanjing, 210009, China.
Department of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing 210009, China.
Exp Cell Res. 2019 Nov 1;384(1):111613. doi: 10.1016/j.yexcr.2019.111613. Epub 2019 Sep 5.
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.
脂毒性被认为是糖尿病的一个风险因素。在这里，我们报告 C 型凝集素结构域家族 11，成员 A（Clec11a）作为胰岛中的一种新的调节剂，在脂毒性诱导的功能障碍中发挥保护作用。使用高脂肪饮食诱导肥胖（DIO）小鼠模型进行胰岛转录组测序。我们发现与正常对照组小鼠相比，DIO 小鼠胰岛中的 Clec11a 表达显著降低，实时 PCR 进一步证实了这一点。免疫染色显示 Clec11a 蛋白在小鼠胰岛中的定位。给予重组人 Clec11a（rClec11a）蛋白可促进胰岛细胞的增殖，并挽救脂肪酸对细胞增殖的抑制作用，这涉及 Erk 信号通路的激活。我们还发现 rClec11a 改变了参与脂质代谢的基因的表达。
