Effect of exogenous ATP upon inositol phosphate production, cationic fluxes and insulin release in pancreatic islet cells

1988 ◽  
Vol 970 (2) ◽  
pp. 222-229 ◽  
Author(s):  
F. Blachier ◽  
W.J. Malaisse
Keyword(s):  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Inositol Phosphate ◽  
Pancreatic Islet Cells ◽  
Inositol Phosphate Production

scholarly journals Effect of glucose on the intracellular pH of pancreatic islet cells

1984 ◽  
Vol 218 (3) ◽  
pp. 887-892 ◽  
Author(s):  
P Lindström ◽  
J Sehlin
Keyword(s):  
Insulin Release ◽  
Intracellular Ph ◽  
Pancreatic Islet ◽  
Basal Insulin ◽  
Islet Cells ◽  
Maximum Effect ◽  
Maximal Effect ◽  
Pancreatic Islet Cells ◽  
Bicarbonate Buffer ◽  
Effect Of Glucose

To characterize the effect of glucose on the intracellular pH (pHi) of pancreatic islet cells, we measured the accumulation of 14C-labelled 5,5-dimethyloxazolidine-2,4-dione ([14C]DMO) in beta-cell-rich islets from ob/ob mice. D-Glucose (20 mM) stimulated insulin release and enhanced the [14C]DMO equilibrium uptake corresponding to an increase of pHi by about 0.15 unit. The glucose effect on DMO uptake was concentration-dependent, with half-maximal effect at about 4 mM-glucose and maximum effect at about 10 mM-glucose. It was inhibited by 20 mM-mannoheptulose and potentiated by 4 mM-L-5-hydroxytryptophan, but not affected by 2 mM-theophylline. Mannoheptulose is an inhibitor and L-5-hydroxytryptophan and theophylline are potentiators of glucose-stimulated insulin release. The glucose-induced increase in pHi appeared rapidly (7 min) and persisted for at least 30 min and it was observed both in bicarbonate/CO2-buffered and in Hepes [4-(2-hydroxyethyl)-1-piperazine-ethanesulphonic acid]-buffered media. Addition of extracellular bicarbonate buffer lowered the pHi, but did not affect basal insulin release, whereas 5 mM-NH4+ increased pHi and induced a 4-fold increase of basal insulin release. We conclude that, in contrast with previous assumptions, glucose increases intracellular pH in the islet cells. This effect may be coupled to the glucose metabolism and associated with triggering of insulin release.

scholarly journals The coupling of metabolic to secretory events in pancreatic islets. The cytosolic redox state

1984 ◽  
Vol 220 (2) ◽  
pp. 433-440 ◽  
Author(s):  
A Sener ◽  
F Malaisse-Lagae ◽  
S P Dufrane ◽  
W J Malaisse
Keyword(s):  
Pancreatic Islets ◽  
Malate Dehydrogenase ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Flow Rate ◽  
Isocitrate Dehydrogenase ◽  
Malic Enzyme ◽  
Redox State ◽  
Islet Cells ◽  
Pancreatic Islet Cells

NADP-linked isocitrate dehydrogenase and malic enzyme [malate dehydrogenase (decarboxylating) (NADP)] activities were characterized in the cytosol of pancreatic islet cells. D-Glucose and L-leucine augmented the cytosolic NADPH/NADP+ ratio, as judged from the isocitrate/2-oxoglutarate and malate/pyruvate islet contents. The flow rate through the malic enzyme was judged from the output of labelled pyruvate by islets exposed to either L-[U-14C]glutamine or L-[U-14C]leucine. The cytosolic generation of NADPH, e.g. at the level of the malic enzyme, may play a role in the coupling of metabolic to secretory events in the process of nutrient-stimulated insulin release.

The Possible Importance of Contact between Pancreatic Islet Cells for the Control of Insulin Release*

Endocrinology ◽  
1982 ◽  
Vol 111 (1) ◽  
pp. 86-94 ◽  
Author(s):  
PHILIPPE A. HALBAN ◽  
CLAES B. WOLLHEIM ◽  
BENIGNA BLONDEL ◽  
PAOLO MEDA ◽  
ERIC N. NIESOR ◽  
...  
Keyword(s):  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells

scholarly journals Gatifloxacin Induces Augmented Insulin Release and Intracellular Insulin Depletion of Pancreatic Islet Cells

2007 ◽  
Vol 30 (4) ◽  
pp. 644-647 ◽  
Author(s):  
Takashi Tomita ◽  
Mariko Onishi ◽  
Eiji Sato ◽  
Yasuhiro Kimura ◽  
Kenji Kihira
Keyword(s):  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells

scholarly journals A role for calcium in the breakdown of inositol phospholipids in intact and digitonin-permeabilized pancreatic islets

1986 ◽  
Vol 238 (3) ◽  
pp. 773-779 ◽  
Author(s):  
L Best
Keyword(s):  
Lipid Metabolism ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Islet Cells ◽  
Inositol Phosphate ◽  
Significant Stimulation ◽  
Inositol Phospholipids ◽  
Inositol Phosphate Production ◽  
Small Inhibition ◽  
Stimulation Of

Glucose (20 mM) and 4-methyl-2-oxopentanoate (10 mM) both caused a pronounced stimulation of insulin release and of [3H]inositol phosphate production in rat pancreatic islets prelabelled with myo-[3H]inositol. Secretory responses to these nutrients were markedly impaired by lowering the Ca2+ concentration of the incubation medium to 10(-4)M or less, whereas stimulated inositol phosphate production was sensitive to Ca2+ within the range 10(-6)-10(-4)M. Inositol phosphate formation in response to carbamoylcholine was also found to be dependent on the presence of 10(-5)M-Ca2+ or above. Raising the concentration of K+ in the medium resulted in a progressive, Ca2+-dependent stimulation of inositol phosphate production in islets, although no significant stimulation of insulin release was observed. In islets prelabelled with myo[3H]inositol, then permeabilized by exposure to digitonin, [3H]inositol phosphate production could be triggered by raising the Ca2+ concentration from 10(-7) to 10(-5)M. This effect was dependent on the concentration of ATP and the presence of Li+, and involved detectable increases in the levels of InsP3 and InsP2 as well as InsP. A potentiation of inositol phosphate production by carbamoylcholine was observed in permeabilized islets at lower Ca2+ concentrations, although nutrient stimuli were ineffective. No significant effects were observed with guanine nucleotides or with neomycin, although NADH produced a modest increase and adriamycin a small inhibition of inositol phosphate production in permeabilized islets. These results strongly suggest that Ca2+ ions play an important role in the stimulation of inositol lipid metabolism in islets in response to nutrient secretagogues, and that inositide breakdown may actually be triggered by Ca2+ entry into the islet cells.

The dynamics of insulin release from mouse pancreatic islet cells in suspension

1976 ◽  
Vol 366 (2-3) ◽  
pp. 185-188 ◽  
Author(s):  
Lars-�ke Idahl ◽  
�ke Lernmark ◽  
Janove Sehlin ◽  
Inge-Bert T�ljedal
Keyword(s):  
Insulin Release ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Mouse Pancreatic Islet

Monolayer cultures of adult pancreatic islet cells on osmotically disrupted fibroblasts

Diabetes ◽  
1980 ◽  
Vol 29 (6) ◽  
pp. 497-500 ◽  
Author(s):  
P. Meda ◽  
E. L. Hooghe-Peters ◽  
L. Orci
Keyword(s):  
Pancreatic Islet ◽  
Islet Cells ◽  
Pancreatic Islet Cells ◽  
Monolayer Cultures
Sign in / Sign up

Export Citation Format

Share Document