Insulin release from pancreatic islets of fetal rats mediated by leucine b-BCH, tolbutamide, glibenclamide, arginine, potassium chloride, and theophylline does not require stimulation of Ca2+ net uptake

Cell Calcium ◽  
1989 ◽  
Vol 10 (6) ◽  
pp. 441-450 ◽  
Author(s):  
H.P.T. Ammon ◽  
C. Glocker ◽  
R.G. Waldner ◽  
M.A. Wahl
Keyword(s):  
Potassium Chloride ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Fetal Rats ◽  
Net Uptake ◽  
Stimulation Of

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets

1990 ◽  
Vol 258 (6) ◽  
pp. E975-E984 ◽  
Author(s):  
G. Z. Fadda ◽  
M. Akmal ◽  
L. G. Lipson ◽  
S. G. Massry
Keyword(s):  
Insulin Secretion ◽  
Parathyroid Hormone ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Direct Effect ◽  
Indirect Evidence ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Stimulation Of

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

Mechanisms of synergism between glucose and cAMP on stimulation of insulin release

1984 ◽  
Vol 247 (6) ◽  
pp. E701-E708 ◽  
Author(s):  
W. Phang ◽  
L. Domboski ◽  
Y. Krausz ◽  
G. W. Sharp
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Ringer Solution ◽  
Intracellular Camp ◽  
Cyclic Monophosphate ◽  
Rat Pancreatic Islets ◽  
Individual Effects ◽  
The Individual ◽  
Isolated Rat ◽  
Stimulation Of

The mechanism of synergism between glucose and adenosine 3',5'-cyclic monophosphate (cAMP) on insulin release has been studied. Synergism may result from 1) inhibition of Na+-Ca2+ exchange by glucose and 2) a cAMP-induced sensitization of the release machinery to Ca2+. To distinguish between these two possibilities, isolated rat pancreatic islets were perifused with agents that raise intracellular levels of cAMP [3-isobutyl-1-methylxanthine (IBMX) and forskolin] and others that increase intracellular concentrations of Ca2+ either by blocking Na2+-Ca2+ exchange (ouabain and choline-Ringer solution) or by causing increased Ca2+ influx (KCl, carbachol, and 10 mM Ca2+). The results indicate that both the combination of cAMP and increased Ca2+ influx or blocked Na2-Ca2+ exchange and increased Ca2+ influx potentiated insulin release. When the relative potentiating abilities of cAMP and blocked Na2+-Ca2+ exchange were compared by determining the individual effects of IBMX and 1 mM ouabain (a concentration that causes similar inhibition of 45C2+ efflux as 16.7 mM glucose) in the presence of carbachol, cAMP was only 1.4 times more potent as a potentiating agent than blocked Na+-Ca2+ exchange. The greatest potentiation of insulin release was observed when Na+-Ca2+ exchange was blocked in the presence of increased levels of intracellular cAMP.

scholarly journals Cytosolic ratios of free [NADPH]/[NADP+] and [NADH]/[NAD+] in mouse pancreatic islets, and nutrient-induced insulin secretion

1987 ◽  
Vol 241 (1) ◽  
pp. 161-167 ◽  
Author(s):  
C J Hedeskov ◽  
K Capito ◽  
P Thams
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Coupling Factor ◽  
Mouse Pancreatic Islets ◽  
Cell Depolarization ◽  
K Permeability ◽  
Cell Glucose ◽  
Stimulation Of

When the extracellular concentration of glucose was raised from 3 mM to 7 mM (the concentration interval in which beta-cell depolarization and the major decrease in K+ permeability occur), the cytosolic free [NADPH]/[NADP+] ratio in mouse pancreatic islets increased by 29.5%. When glucose was increased to 20 mM, a 117% increase was observed. Glucose had no effect on the cytosolic free [NADH]/[NAD+] ratio. Neither the cytosolic free [NADPH]/[NADP+] ratio nor the corresponding [NADH]/[NAD+] ratio was affected when the islets were incubated with 20 mM-fructose or with 3 mM-glucose + 20 mM-fructose, although the last-mentioned condition stimulated insulin release. The insulin secretagogue leucine (10 mM) stimulated insulin secretion, but lowered the cytosolic free [NADPH]/[NADP+] ratio; 10 mM-leucine + 10 mM-glutamine stimulated insulin release and significantly enhanced both the [NADPH]/[NADP+] ratio and the [NADH]/[NAD+] ratio. It is concluded that the cytosolic free [NADPH]/[NADP+] ratio may be involved in coupling beta-cell glucose metabolism to beta-cell depolarization and ensuing insulin secretion, but it may not be the sole or major coupling factor in nutrient-induced stimulation of insulin secretion.

Diazoxide unmasks glucose inhibition of insulin release by counteracting entry of Ca2+

1988 ◽  
Vol 255 (4) ◽  
pp. E422-E427 ◽  
Author(s):  
P. Bergsten ◽  
E. Gylfe ◽  
N. Wesslen ◽  
B. Hellman
Keyword(s):  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Secretory Response ◽  
Glucose Stimulation ◽  
Glucose Inhibition ◽  
Insulin Secretory Response ◽  
Stimulation Of

The interaction of diazoxide with the effects of glucose on the insulin-releasing mechanism was analyzed in beta-cell-rich pancreatic islets isolated from ob/ob mice. When added at a concentration of 400 microM to a medium containing 1.28 mM Ca2+, diazoxide converted glucose stimulation of insulin release into inhibition. Further addition of 2 mM theophylline restored the insulin secretory response to glucose. The paradoxical glucose inhibition of insulin release was accounted for by a diazoxide interaction with the entry of Ca2+, unmasking a capacity of the sugar to lower cytoplasmic Ca2+ below its resting concentration.

Demonstration of glucose inhibition of insulin release in the presence of diazoxide

1987 ◽  
Vol 115 (2) ◽  
pp. 170-174 ◽  
Author(s):  
Peter Bergsten ◽  
Bo Hellman
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Β Cell ◽  
Glucose Stimulation ◽  
Inhibitory Component ◽  
Glucose Inhibition ◽  
Stimulation Of

Abstract. β-Cell-rich pancreatic islets from ob/ob mice were taken for measurements of insulin release in response to glucose after culture in RPMI 1640 medium. The stimulatory effect of 20 mmol/l glucose was converted into an inhibition when the medium was supplemented with 400 μmol/l diazoxide. Glucose inhibition of insulin release was observed when the islets had been cultured in the presence of 1 or 20 mmol/l glucose in media either containing or lacking Ca2+. The data provide further evidence for an inhibitory component in the action of glucose on insulin release, suggesting that glucose stimulation of the Ca2+ efflux is essential for the appearance of this inhibition.

Respiratory, ionic, and functional effects of succinate esters in pancreatic islets

1993 ◽  
Vol 264 (3) ◽  
pp. E428-E433 ◽  
Author(s):  
W. J. Malaisse ◽  
J. Rasschaert ◽  
M. L. Villanueva-Penacarrillo ◽  
I. Valverde
Keyword(s):  
Succinic Acid ◽  
Insulin Release ◽  
Methyl Esters ◽  
O2 Uptake ◽  
Biosynthetic Activity ◽  
Insulin Secretagogues ◽  
Net Uptake ◽  
Characteristic Features ◽  
45Ca Efflux ◽  
Stimulation Of

The methyl esters of succinic acid were introduced a few years ago as new potent insulin secretagogues. In the present study, they were found to increase O2 uptake by rat islets incubated in the absence or presence of D-glucose; to decrease 86Rb outflow from prelabeled islets; to stimulate biosynthetic activity in the islets, with a preferential effect on the synthesis of proinsulin; to inhibit 45Ca efflux from prelabeled islets perifused in the absence of extracellular Ca2+ but to augment 45Ca net uptake and to cause a biphasic stimulation of 45Ca outflow in islets incubated or perifused in the presence of extracellular Ca2+; and to evoke a biphasic stimulation of insulin release. The insulinotropic action of these methyl esters coincided with a shift to the left of the sigmoidal relationship between insulin output and D-glucose concentration, was concentration related in the 2-10 mM range, failed to be duplicated by succinic acid, displayed both Ca2+ dependency and resistance to a lowering of extracellular pH, and was operative in the absence of D-glucose whether or not the islets were stimulated by non-nutrient secretagogues. It is concluded that the respiratory, cationic, biosynthetic, and secretory responses of the islets to succinate methyl esters display the characteristic features usually encountered in the process of nutrient-stimulated insulin release.

scholarly journals Cerulenin, an inhibitor of protein acylation, selectively attenuates nutrient stimulation of insulin release: a study in rat pancreatic islets

Diabetes ◽  
2000 ◽  
Vol 49 (5) ◽  
pp. 712-717 ◽  
Author(s):  
H. Yajima ◽  
M. Komatsu ◽  
S. Yamada ◽  
S. G. Straub ◽  
T. Kaneko ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Rat Pancreatic Islets ◽  
Protein Acylation ◽  
Stimulation Of
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