期刊
ENDOCRINE JOURNAL
卷 58, 期 4, 页码 305-313出版社
JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.K11E-056
关键词
Nesfatin-1; Insulin release; Islet beta-cell; Ca2+ signaling; L-type Ca channel
资金
- Japan Society for the Promotion of Science (JSPS) [18390065, 20390061, 22659044]
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Novo Nordisk
- Takeda Science Foundation
- Uehara Memorial Foundation
- Japan Diabetes Foundation
- KEIRIN RACE
- Grants-in-Aid for Scientific Research [18390065, 23390044, 22659044, 20390061] Funding Source: KAKEN
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 beta-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 beta-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 P-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+]; responses to nesfatin-1 were unaltered by inhibitors of protein kinase A (PKA) and phospholipase A(2) (PLA(2)). These results indicate that nesfain-1 potentiates glucose-induced insulin secretion by promoting Ca2+ influx through L-type Ca2+ channels independently of PKA and PLA(2) in mouse islet beta-cells.
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