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Albert Salehi

S Albert Salehi

Research team manager

Albert Salehi

Signal transduction in islet hormone release: interaction of nitric oxide with basal and nutrient-induced hormone responses

Author

  • S Albert Salehi
  • Fariborz Parandeh
  • Ingmar Lundquist

Summary, in English

We examined the relation between the islet NO system and islet hormone secretion induced by either the non-glucose nutrient alpha-ketoisocaproic acid (KIC) or, in some experiments, glucose. KIC dose dependently stimulated insulin but inhibited glucagon secretion. In a medium devoid of any nutrient, the NO synthase (NOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) induced an increase in basal insulin release but a decrease in glucagon release. These effects were evident also in K+-depolarised islets. KIC-induced insulin release was increased by L-NAME. This increase was abolished in K+-depolarised islets. In contrast, glucose- induced insulin release was potentiated by L-NAME after K+ depolarisation. The intracellular NO donor hydroxylamine dose dependently inhibited KIC-stimulated insulin release and reversed KIC-induced suppression of glucagon release. Our data suggest that islet hormone secretion in a medium devoid of nutrients is greatly affected by the islet NO system, whereas KIC-induced secretion is little affected. Glucose-induced insulin release, however, is accompanied by increased NOS activity, the NOS-activating signal being derived from the glycolytic-pentose shunt part of glucose metabolism. The observed NO effects on islet hormone release can proceed independently of membrane-depolarisation events.

Department/s

  • Islet cell physiology

Publishing year

1998

Language

English

Pages

645-651

Publication/Series

Cellular Signalling

Volume

10

Issue

9

Document type

Journal article

Publisher

Elsevier

Topic

  • Microbiology

Status

Published

Research group

  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 1873-3913