Affordable Access

Involvement of cyclic guanosine 3',5'-monophosphate in nitric oxide-induced glucagon secretion from pancreatic alpha cells.

Authors
  • Mori, T
  • Murakami, Y
  • Koshimura, K
  • Hamaguchi, K
  • Kato, Y
Type
Published Article
Journal
Metabolism
Publisher
Elsevier
Publication Date
Jun 01, 2001
Volume
50
Issue
6
Pages
703–707
Identifiers
PMID: 11398148
Source
Medline
License
Unknown

Abstract

It has been reported that nitric oxide (NO) is a positive modulator of glucagon release. The involvement of cyclic guanosine 3',5'-monophosphate (cGMP) in NO-induced glucagon secretion and the possible role of NO in glucagon release induced by l-arginine were investigated in mouse clonal alpha-cell line clone 6 (alpha TC6) cells, which predominantly secrete glucagon. NOC12, an NO donor, elicited an increase in glucagon release from alpha Tc6 cells in perifusion and static incubation. An inhibitor of cGMP-dependent protein kinase inhibited NOC12-induced glucagon release. NOC12 (1 mmol/L) also increased the cellular level of cGMP. In addition, a permeable cGMP agonist increased glucagon release. l-arginine (15 mmol/L) increased perifusate concentrations of glucagon and nitrite in alpha Tc6 cells, which were inhibited by N(G)-nitro-L-arginine methyl ester. NO synthase (NOS) activity was shown in alpha Tc6 cells by l-citrulline formation assay. Our present findings suggest that NO plays a stimulating role in glucagon release from the alpha cells, and that a cGMP-dependent pathway is involved in NO action. These findings also provide further evidence that l-arginine might play a stimulating role in regulating glucagon secretion, at least partly, through generation of NO in the islets.

Report this publication

Statistics

Seen <100 times