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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1113481
- author
- Salehi, S Albert
LU
; Parandeh, Fariborz
and Lundquist, Ingmar
LU
- organization
- publishing date
- 1998
- 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
- 2016-04-01 12:02:11
- date last changed
- 2022-01-26 21:50:47
@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}},
doi = {{10.1016/S0898-6568(98)00005-9}},
volume = {{10}},
year = {{1998}},
}