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

Salehi, S Albert LU ; Parandeh, Fariborz and Lundquist, Ingmar LU (1998) In Cellular Signalling 10(9). p.645-651
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cellular Signalling
volume
10
issue
9
pages
645 - 651
publisher
Elsevier
external identifiers
  • pmid:9794246
  • scopus:0031718360
ISSN
1873-3913
DOI
10.1016/S0898-6568(98)00005-9
language
English
LU publication?
yes
id
705d34fe-b0c8-4777-9893-81ceac557fd8 (old id 1113481)
date added to LUP
2008-07-15 10:39:59
date last changed
2017-01-01 04:46:34
@article{705d34fe-b0c8-4777-9893-81ceac557fd8,
  abstract     = {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.},
  author       = {Salehi, S Albert and Parandeh, Fariborz and Lundquist, Ingmar},
  issn         = {1873-3913},
  language     = {eng},
  number       = {9},
  pages        = {645--651},
  publisher    = {Elsevier},
  series       = {Cellular Signalling},
  title        = {Signal transduction in islet hormone release: interaction of nitric oxide with basal and nutrient-induced hormone responses},
  url          = {http://dx.doi.org/10.1016/S0898-6568(98)00005-9},
  volume       = {10},
  year         = {1998},
}