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 Metabolic control of the potassium permeability in pancreatic islet cells

1980 ◽  
Vol 186 (2) ◽  
pp. 541-550 ◽  
Author(s):  
Jean-Claude Henquin
Keyword(s):  
Pancreatic Islet ◽  
Islet Cells ◽  
Reduced Glutathione ◽  
Pancreatic Islet Cells ◽  
Major Step ◽  
Metabolic Degradation ◽  
Glucose Metabolites ◽  
Effect Of Glucose ◽  
Phenazine Methosulphate ◽  
K Permeability

The K+ permeability of pancreatic islet cells was studied by monitoring the efflux of 86Rb+ (used as tracer for K+) from perifused rat islets and measuring the uptake of 42K+. Glucose markedly and reversibly decreased 86Rb+ efflux from islet cells and this effect was antagonized by inhibitors of the metabolic degradation of the sugar, i.e. mannoheptulose, iodoacetate, glucosamine and 2-deoxyglucose. Among glucose metabolites, glyceraldehyde reduced the K+ permeability even more potently than did glucose itself; pyruvate and lactate alone exhibited only a small effect, but potentiated that of glucose. Other metabolized sugars, like mannose, glucosamine and N-acetylglucosamine, also decreased 86Rb+ efflux from islet cells. Fructose was effective only in the presence of glucose. Non-metabolized sugars like galactose, 2-deoxyglucose and 3-O-methylglucose had no effect. The changes in K+ permeability by agents known to modify the concentrations of nicotinamide nucleotides, glutathione or ATP in islet cells were also studied. Increasing NAD(P)H concentrations in islet cells by pentobarbital rapidly and reversibly reduced 86Rb+ efflux; exogenous reduced glutathione produced a similar though weaker effect. By contrast, oxidizing nicotinamide nucleotides with phenazine methosulphate or Methylene Blue, or oxidizing glutathione by t-butyl hydroperoxide increased the K+ permeability of islet cells. Uncoupling the oxidative phosphorylations with dicumarol also augmented 86Rb+ efflux markedly. In the absence of glucose, but not in its presence, methylxanthines reduced 86Rb+ efflux from the islets; such was not the case for cholera toxin or dibutyryl cyclic AMP. Glucose and glyceraldehyde had no effect on 42K+ uptake after a short incubation (10min), but augmented it after 60min; the effect of glucose was suppressed by mannoheptulose and not mimicked by 3-O-methylglucose. The results clearly establish the importance of the metabolic degradation of glucose and other substrates for the control of the K+ permeability in pancreatic islet cells and support the concept that a decrease in the K+ permeability represents a major step of the B-cell response to physiological stimulation.

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

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
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