Nesfatin-1 enhances glucose-induced insulin secretion by promoting Ca2+ influx through L-type channels in mouse islet β-cells

Endocrine Journal

Toshihiko Yada²  Masanori Nakata²  Masatomo Mori¹  Sawako Yamamoto²  Kazunori Manaka² 

[1] Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Japan;Department of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan

关键词: Nesfatin-1;    Insulin release;    Islet β-cell;    Ca2+ signaling;    L-type Ca channel;   

DOI  :  10.1507/endocrj.K11E-056

学科分类：内分泌与代谢学

来源: Japan Endocrine Society

【 摘 要 】

References(36)Cited-By(35)Nucleobindin-2 (NUCB2)-derived nesfatin-1 located in the brain has been implicated in the satiety and control of energy metabolism.Nesfatin-1 is also produced in the periphery and present in the plasma.It has recently been reported that NUCB2/nesfatin-1 is localized in pancreatic islet β-cells in mice and rats and released from islets.However, its function in islets remains largely unknown.This study examined direct effects of nesfatin-1 on insulin release from pancreatic islets and on cytosolic Ca2+ concentration ([Ca2+]i) in single β-cells from ICR mice.In the presence of 8.3 mmol/L glucose, nesfatin-1 at 10-10-10-9 mol/L tended to increase and at 10-8 mol/L increased insulin release from isolated islets, while at 2.8 mmol/L glucose nesfatin-1 had no effect.Furthermore, nesfatin-1 at 10-10-10-8 mol/L increased [Ca2+]i in single β-cells in the presence of 8.3 but not 2.8 mmol/L glucose.The nesfatin-1-induced [Ca2+]i increase and insulin release were inhibited by removal of extracellular Ca2+ and by addition of nitrendipine, a blocker of voltage-dependent L-type Ca2+ channels.Unexpectedly, the [Ca2+]i responses to nesfatin-1 were unaltered by inhibitors of protein kinase A (PKA) and phospholipase A2 (PLA2).These results indicate that nesfain-1 potentiates glucose-induced insulin secretion by promoting Ca2+ influx through L-type Ca2+ channels independently of PKA and PLA2 in mouse islet β-cells.

【 授权许可】

Unknown