Sensitivity to Cd2+ but resistance to Ni2+ of Ca2+ inflow into rat pancreatic islets

1990 ◽  
Vol 258 (3) ◽  
pp. E529-E533 ◽  
Author(s):  
P. O. Plasman ◽  
M. Hermann ◽  
A. Herchuelz ◽  
P. Lebrun
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Islet Cells ◽  
Excitable Cells ◽  
45Ca Uptake ◽  
Rat Pancreatic Islets ◽  
Cell Plasma ◽  
Different Types ◽  
45Ca Efflux ◽  
Ca2 Channels

The presence of different types [long lasting (L) and transient (T)] of active voltage-operated Ca2+ channels in islet cells was investigated by comparing the effects of Cd2+, Ni2+, and 1,4-dihydropyridines on 45Ca uptake, 45Ca efflux, and insulin release in intact rat pancreatic islets. In several other excitable cells the L-channel has been shown to be modulated by 1,4-dihydropyridines and Cd2+, whereas the T-channel was reported to be sensitive to Ni2+. Nifedipine and Cd2+ inhibited whereas BAY K 8644 enhanced the glucose (11.1, 22.2 mM)-stimulated short-term 45Ca uptake, 45Ca efflux, and insulin release. In contrast, the stimulatory effects of glucose (11.1, 22.2 mM) on 45Ca uptake, 45Ca efflux, and insulin release were unaffected by Ni2+. These findings confirm that glucose provokes Ca2+ entry mainly by activating voltage-sensitive Ca2+ channels of the L-type and suggest that the B-cell plasma membrane is not equipped with active T-type Ca2+ channels.

scholarly journals Mechanism of 3-phenylpyruvate-induced insulin release. Metabolic aspects

1983 ◽  
Vol 210 (3) ◽  
pp. 921-927 ◽  
Author(s):  
W J Malaisse ◽  
A Sener ◽  
M Welsh ◽  
F Malaisse-Lagae ◽  
C Hellerström ◽  
...  
Keyword(s):  
Amino Acids ◽  
Pancreatic Islets ◽  
Glutamate Dehydrogenase ◽  
Production Rate ◽  
Insulin Release ◽  
Incubation Medium ◽  
Islet Cells ◽  
Metabolic Effects ◽  
Rat Pancreatic Islets ◽  
Endogenous Amino Acids

1. The metabolism and metabolic effects of 3-phenylpyruvate were examined in rat pancreatic islets. 2. Islet homogenates catalysed transamination reactions between 3-phenylpyruvate and L-glutamate, L-leucine, L-norleucine or L-valine. 3-Phenylpyruvate failed to activate glutamate dehydrogenase. 3. 3-Phenylpyruvate rapidly entered into islet cells, was extensively converted into phenylalanine but slowly oxidized. 4. The conversion of phenylpyruvate into phenylalanine coincided with a fall in the content of several amino acids (especially glutamate and aspartate) in the islets and incubation medium, the accumulation of 2-oxoglutarate and a modest fall in the NH4+ production rate. 5. 3-Phenylpyruvate failed to affect 14CO2 output from islets prelabelled with [U-14C]palmitate, but augmented 14CO2 output from islets prelabelled or incubated with L-[U-14C]glutamine. 6. In the presence of L-glutamine, 3-phenylpyruvate augmented the ATP/ADP ratio and NAD(P)H islet content, and caused a rapid and sustained decrease in the outflow of radioactivity from islets prelabelled with [2-3H]adenosine. 7. These data support the view that the insulin-releasing capacity of 3-phenylpyruvate coincides with an increase in the catabolism of endogenous amino acids acting as ‘partners’ in transamination reactions leading to the conversion of 3-phenylpyruvate into phenylalanine.

Inhibition by corticosterone of calcium inflow and insulin release in rat pancreatic islets

1984 ◽  
Vol 100 (2) ◽  
pp. 227-233 ◽  
Author(s):  
B. Billaudel ◽  
P. C. F. Mathias ◽  
B. C. J. Sutter ◽  
W. J. Malaisse
Keyword(s):  
Plasma Membrane ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Inhibitory Action ◽  
Islet Cells ◽  
Statistical Significance ◽  
Biological Response ◽  
Biophysical Properties ◽  
Rat Pancreatic Islets ◽  
Early Fall

ABSTRACT Corticosterone (0·6 μmol/l) inhibited both 45Ca outflow and insulin release evoked by glucose, the combination of leucine and glutamine, 2-ketoisocaproate, gliclazide or the association of gliclazide and a tumour-promoting phorbol ester in rat pancreatic islets perifused at normal extracellular Ca2+ concentration (1·0 mmol/l). In all cases, the inhibitory action of corticosterone reached statistical significance within 10–22 min of exposure to this steroid and failed to be rapidly reversible. Corticosterone failed to affect basal 45Ca outflow and insulin release. The steroid also failed to affect the inhibitory action of glucose upon 45Ca outflow, as judged from either the glucose-induced early fall in effluent radioactivity from islets maintained at normal extracellular Ca2+ concentration or the steady-state values for 45Ca outflow from glucose-stimulated but Ca2+-deprived islets. Corticosterone caused a modest increase in 86Rb outflow from islets perifused in the presence of glucose (16·7 mmol/l). It is concluded that corticosterone impairs Ca2+ inflow into the islet cells and, by doing so, causes a progressive inhibition of insulin release. The pancreatic B cell might thus serve as a further model for the study of the rapid biological response to steroids, as presumably mediated by alteration in the biophysical properties of the plasma membrane. J. Endocr. (1984) 100, 227–233

Regulation of calcium fluxes in pancreatic islets: two calcium movements' dissociated response to glucose

1980 ◽  
Vol 238 (2) ◽  
pp. E87-E95
Author(s):  
A. Herchuelz ◽  
W. J. Malaisse
Keyword(s):  
Glucose Metabolism ◽  
Low Temperature ◽  
Pancreatic Islets ◽  
Islet Cells ◽  
Calcium Fluxes ◽  
Rat Pancreatic Islets ◽  
Early Fall ◽  
45Ca Efflux ◽  
Secondary Rise

At normal extracellular 40Ca concentration (1.0--1.5 mM), D-glucose initially reduces and subsequently increases 45Ca efflux from prelabeled rat pancreatic islets, whether in the absence or presence of 20 mM Ca-EGTA. Thus, the initial fall cannot be attributed to a reuptake of effluent 45Ca. Both the fall and rise in effluent 45Ca represent sustained and rapidly reversible phenomena partially masked by one another. The dose-action relationship for the initial fall in 45Ca efflux (Km = 4.2 mM) differs vastly from that characterizing the secondary rise in 45Ca efflux (Km = 9.1 mM). Mannoheptulose, iodoacetate, and low temperature inhibit both the early fall and secondary rise in effluent radioactivity normally evoked by glucose. D-Glucose (8.3 mM) and D-glyceraldehyde (10 mM) exert comparable effects on 45Ca efflux. The initial fall and later increase in 45Ca efflux evoked by glucose, although dependent on the integrity of glucose metabolism, correspond to two distinct processes in the rapid regulation of Ca handling by the islet cells.

Impairment by aminooxyacetate of ionic response to nutrients in pancreatic islets

1983 ◽  
Vol 245 (1) ◽  
pp. E38-E46
Author(s):  
P. Lebrun ◽  
W. J. Malaisse ◽  
A. Herchuelz
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Redox State ◽  
Islet Cells ◽  
Inhibitory Effect ◽  
High Concentration ◽  
Perifused Islets ◽  
45Ca Efflux ◽  
Reduced State ◽  
Stimulation Of

Aminooxyacetate, an inhibitor of transamination reactions, was recently reported to prevent the induction of a more reduced state in the cytosolic redox couple, as normally evoked by glucose or 2-ketoisocaproate in rat pancreatic islets. The cationic effects of aminooxyacetate were examined, therefore, in perifused islets prelabeled with either 86Rb or 45Ca. Aminooxyacetate augmented the outflow of 86Rb from the islets whether in the absence or presence of an exogenous nutrient and slightly impaired the capacity of nutrients, especially 2-ketoisocaproate, to decrease 86Rb outflow. Aminooxyacetate abolished the nutrient-induced rise in 45Ca efflux that normally results from the stimulation by glucose or 2-ketoisocaproate of 40Ca influx into the islet cells. Aminooxyacetate, however, failed to suppress the early inhibitory effect of nutrients on 45Ca efflux. The alteration by aminooxyacetate of the cationic response to nutrient secretagogues coincided with a suppression of insulin release, whereas the cationic response to a nonnutrient stimulation by a high concentration of extracellular K+ was unaffected by aminooxyacetate. These findings suggest that the induction of a more reduced cytosolic redox state represents an essential link between metabolic events and both the decrease in K+ conductance and stimulation of Ca2+ inflow in the process of nutrient-induced insulin release.

scholarly journals Insulin release and arachidonic acid metabolism in neonatal rat pancreatic islets. (2)

1984 ◽  
Vol 36 ◽  
pp. 96
Author(s):  
Naoko Tanaka ◽  
Shohei Nagawa ◽  
Keiko Murakoso ◽  
Kunio Haito ◽  
Shizuo Shimizu ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Neonatal Rat ◽  
Rat Pancreatic Islets

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 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 porcine rubulavirus LPMV infects rat pancreatic islets resulting in an impairment of glucose stimulated insulin release

2000 ◽  
Vol 50 ◽  
pp. 151
Author(s):  
Pablo Hernandez Jauregui ◽  
Alia Jacoub ◽  
Ann Andersson ◽  
Aaron Pimentel ◽  
G Frisk ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Rat Pancreatic Islets ◽  
Porcine Rubulavirus
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