Aspects of Novel Sites of Regulation of the Insulin Stimulus-Secretion Coupling in Normal and Diabetic Pancreatic Islets

Endocrine ◽  
1998 ◽  
Vol 9 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Ake Sjöholm
Keyword(s):  
Pancreatic Islets ◽  
Stimulus Secretion Coupling

Nitric oxide donor SIN-1 inhibits insulin release

1996 ◽  
Vol 271 (4) ◽  
pp. C1098-C1102 ◽  
Author(s):  
A. Sjoholm
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Kinase C ◽  
Stimulus Secretion Coupling

Preceding the onset of insulin-dependent diabetes mellitus, pancreatic islets are infiltrated by macrophages secreting interleukin-1 beta, which exerts cytotoxic and inhibitory actions on islet beta-cell insulin secretion through induction of nitric oxide (NO) synthesis. The influence of the NO donor 3-morpholinosydnonimine (SIN-1) on insulin secretion from isolated pancreatic islets in response to various secretagogues was investigated. Stimulation of insulin release evoked by glucose, phospholipase C activation with carbachol, and protein kinase C activation with phorbol ester were obtained by SIN-1, whereas the response to adenylyl cyclase activation or K(+)-induced depolarization was not affected. It is concluded that enzymes involved in glucose catabolism, phospholipase C or protein kinase C, may be targeted by NO. Reversal of SIN-1 inhibition of glucose-stimulated insulin release by dithiothreitol suggests that NO may inhibit insulin secretion partly by S-nitrosylation of thiol residues in key proteins in the stimulus-secretion coupling. These adverse effects of NO on the beta-cell stimulus-secretion coupling may be of importance for the development of the impaired insulin secretion characterizing diabetes mellitus.

scholarly journals Effect of perchlorate on calcium uptake and insulin secretion in mouse pancreatic islets

1987 ◽  
Vol 248 (1) ◽  
pp. 109-115 ◽  
Author(s):  
J Sehlin
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Glucose Oxidation ◽  
Calcium Uptake ◽  
Maximum Effect ◽  
Mouse Pancreatic Islets ◽  
Stimulus Secretion Coupling ◽  
Ca2 Channels

Microdissected beta-cell-rich pancreatic islets of non-inbred ob/ob mice were used in studies of how perchlorate (CIO4-) affects stimulus-secretion coupling in beta-cells. CIO4- at 16 mM potentiated D-glucose-induced insulin release, without inducing secretion at non-stimulatory glucose concentrations. The potentiation mainly applied to the first phase of stimulated insulin release. In the presence of 20 mM-glucose, the half-maximum effect of CIO4- was reached at 5.5 mM and maximum effect at 12 mM of the anion. The potentiation was reversible and inhibitable by D-mannoheptulose (20 mM) or Ca2+ deficiency. CIO4- at 1-8 mM did not affect glucose oxidation. The effects on secretion were paralleled by a potentiation of glucose-induced 45Ca2+ influx during 3 min. K+-induced insulin secretion and 45Ca2+ uptake were potentiated by 8-16 mM-CIO4-. The spontaneous inactivation of K+-induced (20.9 mM-K+) insulin release was delayed by 8 mM-CIO4-. The anion potentiated the 45Ca2+ uptake induced by glibenclamide, which is known to depolarize the beta-cell. Insulin release was not affected by 1-10 mM-trichloroacetate. It is suggested that CIO4- stimulates the beta-cell by affecting the gating of voltage-controlled Ca2+ channels.

The Stimulus-Secretion Coupling of Amino Acid-induced Insulin Release: Secretory and Oxidative Response of Pancreatic Islets to L-Asparagine

Diabetes ◽  
1984 ◽  
Vol 33 (5) ◽  
pp. 464-469 ◽  
Author(s):  
F. Malaisse-Lagae ◽  
M. Welsh ◽  
P. Lebrun ◽  
A. Herchuelz ◽  
A. Sener ◽  
...  
Keyword(s):  
Amino Acid ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Oxidative Response ◽  
Stimulus Secretion Coupling

Stimulus-secretion coupling of arginine-induced insulin release. Metabolism of l-arginine and l-ornithine in pancreatic islets

1989 ◽  
Vol 1013 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Willy J. Malaisse ◽  
François Blachier ◽  
Ali Mourtada ◽  
Javier Camara ◽  
Amador Albor ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Stimulus Secretion Coupling

The stimulus-secretion coupling of amino acid-induced insulin release. Secretory and oxidative response of pancreatic islets to L-asparagine

Diabetes ◽  
1984 ◽  
Vol 33 (5) ◽  
pp. 464-469 ◽  
Author(s):  
F. Malaisse-Lagae ◽  
M. Welsh ◽  
P. Lebrun ◽  
A. Herchuelz ◽  
A. Sener ◽  
...  
Keyword(s):  
Amino Acid ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Oxidative Response ◽  
Stimulus Secretion Coupling

scholarly journals Phenotyping of Individual Pancreatic Islets Locates Genetic Defects in Stimulus Secretion Coupling to Niddm1i Within the Major Diabetes Locus in GK Rats

Diabetes ◽  
2001 ◽  
Vol 50 (12) ◽  
pp. 2737-2743 ◽  
Author(s):  
J.-M. Lin ◽  
H. Ortsater ◽  
H. Fakhrai-Rad ◽  
J. Galli ◽  
H. Luthman ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Genetic Defects ◽  
Gk Rats ◽  
Stimulus Secretion Coupling
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