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

• Nakata Masanori

  Department of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan

• Manaka Kazunori

  Department of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan

• Yamamoto Sawako

  Department of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan

• Mori Masatomo

  Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Japan

• Yada Toshihiko

  Department of Physiology, Division of Integrative Physiology, Jichi Medical University School of Medicine, Shimotsuke, Japan Department of Developmental Physiology, Division of Adaptation Development, National Institute for Physiological Sciences, Okazaki, Japan

Bibliographic Information

Other Title

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

Abstract

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.

Journal

• Endocrine Journal

  Endocrine Journal 58 (4), 305-313, 2011

  The Japan Endocrine Society

Keywords

• Nesfatin-1
• Insulin release
• Islet β-cell
• Ca²⁺ signaling
• L-type Ca channel

Details

• CRID: 1390001206298571648
• NII Article ID: 130004443687
• DOI: 10.1507/endocrj.k11e-056
• ISSN: 13484540
• ISSN: 09188959
• Web Site: http://www.jstage.jst.go.jp/article/endocrj/58/4/58_K11E-056/_pdf
• Text Lang: en
• Data Source:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed