The Stimulus-Secretion Coupling of Glucose-Induced Insulin Release: IX. The Participation of the Beta Cell Web

Diabetes ◽  
1972 ◽  
Vol 21 (Supplement_2) ◽  
pp. 594-604 ◽  
Author(s):  
W. J. Malaisse ◽  
D. L. Hager ◽  
L. Orci
Keyword(s):  
Beta Cell ◽  
Insulin Release ◽  
Stimulus Secretion Coupling ◽  
Cell Web

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: metabolism and cationic effects of leucine

Diabetes ◽  
1980 ◽  
Vol 29 (6) ◽  
pp. 431-437 ◽  
Author(s):  
W. J. Malaisse ◽  
J. C. Hutton ◽  
A. R. Carpinelli ◽  
A. Herchuelz ◽  
A. Sener
Keyword(s):  
Amino Acid ◽  
Insulin Release ◽  
Stimulus Secretion Coupling

Stimulus-secretion coupling of arginine-induced insulin release

1989 ◽  
Vol 38 (2) ◽  
pp. 327-330 ◽  
Author(s):  
A. Sener ◽  
P. Lebrun ◽  
F. Blachier ◽  
W.J. Malaisse
Keyword(s):  
Insulin Release ◽  
Stimulus Secretion Coupling

Pancreatic Beta-Cell Web: Its Possible Role in Insulin Secretion

Science ◽  
1972 ◽  
Vol 175 (4026) ◽  
pp. 1128-1130 ◽  
Author(s):  
L. Orci ◽  
K. H. Gabbay ◽  
W. J. Malaisse
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Cell Web

Similarities in the Stimulus-Secretion Coupling Mechanisms of Glucose- and 2-Keto Acid-Induced Insulin Release*

Endocrinology ◽  
1980 ◽  
Vol 106 (1) ◽  
pp. 203-219 ◽  
Author(s):  
JOHN C. HUTTON ◽  
ABDULLAH SENER ◽  
ANDRÉ HERCHUELZ ◽  
ILLANI ATWATER ◽  
SHOJI KAWAZU ◽  
...  
Keyword(s):  
Insulin Release ◽  
Keto Acid ◽  
Stimulus Secretion Coupling ◽  
Coupling Mechanisms

scholarly journals The stimulus–secretion coupling 4-methyl-2-oxopentanoate-induced insulin release

1979 ◽  
Vol 184 (2) ◽  
pp. 303-311 ◽  
Author(s):  
J C Hutton ◽  
A Sener ◽  
W J Malaisse
Keyword(s):  
Insulin Release ◽  
Metabolic Flux ◽  
Energy Charge ◽  
Hyperbolic Function ◽  
Maximal Response ◽  
Coupling Mechanism ◽  
Adenylate Energy Charge ◽  
Atp Content ◽  
45Ca Uptake ◽  
Stimulus Secretion Coupling

1. Pancreatic islet insulin secretion and 45Ca uptake showed similar responses to variation in the extracellular concentration of 4-methyl-2-oxopentanoate with a threshold at 4 mM and a maximal response at a 25 mM concentration. 2. Islet respiration, acetoacetate production and rates of substrate utilization, oxidation and amination all changed as a simple hyperbolic function of 4-methyl-2-oxopentanoate concentration and exhibited a maximal response at 25 mM. 3. The responses of ATP content, [ATP]/[ADP] ratio, adenylate energy charge and [NADH]/[NAD+] ratio were also hyperbolic in nature but were maximally elevated at lower concentrations of the secretagogue. The islet [NADPH]/[NADP+] ratio, however, was tightly correlated with parameters of metabolic flux, 45Ca uptake and insulin release. 4. NH4+ and menadione, agents that promote a more oxidized state in islet NADP, did not affect islet ATP content or the rates of [U-14C]4-methyl-2-oxopentanoate oxidation or amination, but markedly inhibited islet 45Ca uptake and insulin release. 5. It is proposed that changes in the redox state of NADP and Ca transport may serve as mediators in the stimulus-secretion coupling mechanism of insulin release induced by 4-methyl-2-oxopentanoate.

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