Dual Role of Nitric Oxide in Pancreatic β-Cells

被引：35

作者：

Kaneko, Yukiko Kurohane ^{[1
]}

Ishikawa, Tomohisa ^{[1
]}

机构：

[1] Univ Shizuoka, Sch Pharmaceut Sci, Dept Pharmacol, Suruga Ku, Shizuoka 4228526, Japan

来源：

JOURNAL OF PHARMACOLOGICAL SCIENCES | 2013年 / 123卷 / 04期

关键词：

nitric oxide; pancreatic islet; beta-cell; insulin secretion; apoptosis; ENDOPLASMIC-RETICULUM STRESS; SENSITIVE K+ CHANNELS; STIMULATED INSULIN-SECRETION; INDUCED APOPTOSIS; RINM5F CELLS; SYNTHASE; RAT; GLUCOSE; RELEASE; INHIBITION;

D O I：

10.1254/jphs.13R10CP

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

An involvement of inducible nitric oxide (NO) synthase (NOS) in pancreatic beta-cell degeneration during the process of type 1 diabetes has been well discussed. Recently, there is growing evidence for pivotal roles of constitutive NOS (cNOS) in beta-cells; the presence of NOS1 and NOS3 in pancreatic beta-cells and the effects of low-concentration NO, which is assumed to be derived from cNOS, on beta-cell functions have been reported. However, the roles of cNOS-derived NO in beta-cells are still under debate. One of the reasons seems to be that NO has multiple biological activities, which are dependent on its concentration. In beta-cells, NO has been shown to exert positive and negative regulation of insulin secretion and anti- and pro-apoptotic activities, which is likely to be dependent on concentrations. In this review article, we will describe the current understanding of the roles of NO in pancreatic beta-cells, especially focusing on cNOS-derived NO and its differential roles depending on concentrations.

引用

页码：295 / 300

页数：6

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