Regulation of Calcium Fluxes and Their Regulatory Roles in Pancreatic Islets*

Malaisse, Willy; Herchuelz, André; Devis, Ghislain; Somers, Guido; Boschero, Antônio Carlos; Hutton, John C.; Kawazu, Shoji; Sener, Abdullah; Atwater, I; Duncan, G.; Ribalet, Bernard; Rojas, Eduardo

doi:10.1111/j.1749-6632.1978.tb41982.x

Cited by 120 publications

(66 citation statements)

References 31 publications

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“…The first phase of insulin release has been proposed to result from mobilization of intracellular Ca2+ [15]. It has also been suggested that glucose raises cytosolic Ca2+ by inhibiting the active extrusion of the ion by Na+/Ca2+ countertransport [14,15,18]. Even if such a mechanism would appear to explain how the sugar rapidly inhibits 45Ca efflux from P-cells, this inhibition may also reflect an initial lowering of cytosolic Ca2+ by stimulated sequestration of the cation in intracellular stores [5,6].…”

Section: Discussionmentioning

confidence: 99%

Dual effects of glucose on the cytosolic Ca²⁺ activity of mouse pancreatic β‐cells

et al. 1984

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The cytosolic Ca2+ activity of mouse pancreatic &cells was studied with the intracellular fluorescent indicator quin2. When the extracellular Ca2+ concentration was 1.20 mM, the basal cytosolic Ca2+ activity was 162 + 9 nM. Stimulation with 20 mM glucose increased this Ca2+ activity by 40%. In the presence of only 0.20 mM Ca2+ or after the addition of the voltage-dependent Ca2+ -channel blocker D-600, glucose had an opposite and more prompt effect in reducing cytosolic Ca2' by about 15%. It is concluded that an early result of glucose exposure is a lowering of the cytosolic Ca2+ activity and that this effect tends to be masked by a subsequent increase of the Ca2+ activity due to influx of Ca2+ through the voltagedependent Ca2+ channels. Cytosolic Ca2' Quin2Insulin secretion

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Section: Discussionmentioning

confidence: 99%

Dual effects of glucose on the cytosolic Ca²⁺ activity of mouse pancreatic β‐cells

et al. 1984

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“…To accomplish this we used noninvasive 31 P and 23 Na ϩ -neuclear magnetic resonance (NMR) technology, respirometry, and radioimmunoassays for insulin and c-AMP to compare the effect of high glucose (30 mmol/l) with the effect of GLY in continuously superfused ␤-HC9 cells complemented by selected studies with isolated ␤-HC9 cell mitochondria.…”

mentioning

confidence: 99%

Differential Effects of Glucose and Glyburide on Energetics and Na+ Levels of βHC9 Cells

et al. 2003

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In the present study, noninvasive 31 P and 23 Na ؉ -nuclear magnetic resonance (NMR) technology and respirometry were used to compare the effect of high glucose (30 mmol/l) with the effect of the antidiabetic sulfonylurea (SU) compound glyburide (GLY) on energy metabolism, Na ؉ flux, insulin, and cAMP release of continuously superfused ␤-HC9 cells encapsulated in microscopic agarose beads. Both high glucose and GLY increased oxygen consumption in ␤-HC9 cells (15-30%) with a maximal effect at 8 mmol/l for glucose and at 250 nmol/l for GLY. At the same time, insulin release from ␤-cells increased by 15-and 25-fold with high glucose or GLY, respectively. The P-creatine (PCr) level was greatly increased and inorganic phosphate (P i ) was decreased with 30 mmol/l glucose in contrast to the decreased level of PCr and increased P i with GLY. ATP levels remained unchanged during both interventions. Studies on isolated mitochondria of ␤-HC9 cells showed that GLY added to mitochondria oxidizing glutamine or glutamate abolished the stimulation of respiration by ADP (state 3) meanwhile leaving state 3 respiration unchanged during oxidation of other substrates. Exposure of ␤-HC9 cells to 5 mmol/l glucose decreased intracellular Na ؉ levels monitored by 23 Na ؉ -NMR spectroscopy and 30 mmol/l glucose resulted in a further decrease in cytosolic Na ؉ . In contrast, Na ؉ increased when 1 mol/l GLY was added to the perfusate containing 5 mmol/l glucose. These data support the hypothesis that glucose activates the ␤-cell through a "push mechanism" due to substrate pressure enhancing fuel flux, energy production, and extrusion of Na ؉ from the cells in contrast to SU receptor (SUR)-1 inhibitors, which may modify intermediary and energy metabolism secondarily through a "pull mechanism" due to higher energy demand resulting from increased ion fluxes and the exocytotic work load. Diabetes 52:394 -402, 2003

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“…However, it is unclear when the embryo gets the endocrine function. As there were a few reports indicating that hormone release from pancreatic endocrine cells was regulated by intracellular Ca2+ (20,38), Cat+-ATPase activity on endocrine cells also may be involved in their secretion. However, their relationship could not be demonstrated in the present study.…”

Section: Discussionmentioning

confidence: 99%

Developmental change of Ca2+-ATPase activity on plasma membrane of rat pancreas during perinatal period.

Lee

Araki

Takashima

1990

Acta Histochem. Cytochem

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Regulation of Calcium Fluxes and Their Regulatory Roles in Pancreatic Islets*

Cited by 120 publications

References 31 publications

Dual effects of glucose on the cytosolic Ca²⁺ activity of mouse pancreatic β‐cells

Dual effects of glucose on the cytosolic Ca²⁺ activity of mouse pancreatic β‐cells

Differential Effects of Glucose and Glyburide on Energetics and Na+ Levels of βHC9 Cells

Developmental change of Ca2+-ATPase activity on plasma membrane of rat pancreas during perinatal period.

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Regulation of Calcium Fluxes and Their Regulatory Roles in Pancreatic Islets*

Cited by 120 publications

References 31 publications

Dual effects of glucose on the cytosolic Ca2+ activity of mouse pancreatic β‐cells

Dual effects of glucose on the cytosolic Ca2+ activity of mouse pancreatic β‐cells

Differential Effects of Glucose and Glyburide on Energetics and Na+ Levels of βHC9 Cells

Developmental change of Ca2+-ATPase activity on plasma membrane of rat pancreas during perinatal period.

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Dual effects of glucose on the cytosolic Ca²⁺ activity of mouse pancreatic β‐cells

Dual effects of glucose on the cytosolic Ca²⁺ activity of mouse pancreatic β‐cells