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Abdullah Sener - One of the best experts on this subject based on the ideXlab platform.
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Stimulus-secretion coupling of hypotonicity-induced Insulin Release in BRIN-BD11 cells.
Endocrine, 2006Co-Authors: Renaud Beauwens, Willy Malaisse, L. Best, Nicolas Markadieu, Raphaël Crutzen, Karim Louchami, Peter D. Brown, Allen P. Yates, Abdullah SenerAbstract:The stimulus-secretion coupling for hypotonicity-induced Insulin Release was investigated in BRIN-BD11 cells. A 50 mM decrease in extracellular NaCI caused a twofold increase in Insulin Release. The Release of Insulin evoked by hypotonicity progressively decreased in an exponential manner. The response to extracellular hypotonicity displayed a threshold value close to 20 mOsmol/L and amaximal response at about 70 mOsmol/L. Hypotonicity also caused a rapid increase in cell volume followed by a regulatory volume decrease (RVD), cell membrane depolarization with induction of spike activity, and a rise in cytosolic Ca2+ concentration. 5-Nitro-2-(3-phenylpropylamino) benzoate inhibited the secretory response to hypoosmolarity, failed to affect the early increase in cell volume but prevented the RVD, and suppressed the hypotonicity-induced plasma membrane depolarization. Insulin Release provoked by hypotonicity was inhibited by verapamil, absence of Ca2+, thapsigargin, furosemide, tributyltin, and diazoxide. On the contrary, tolbutamide augmented modestly Insulin Release recorded in the hypoosmolar medium. Last, a rise in extracellular K+ concentration, while augmenting basal Insulin output, failed to affect Insulin Release in the hypoosmolar medium. Thus, the Insulin secretory response to hypotonicity apparently represents a Ca2+-dependent process triggered by the gating of volume-sensitive anion channels with subsequent depolarization and gating of voltage-sensitive Ca2+ channels.
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Stimulus-Secretion Coupling of Arginine-Induced Insulin Release: Comparison with Histidine-Induced Insulin Release*
Endocrinology, 1990Co-Authors: Abdullah Sener, François Blachier, Joanne Rasschaert, Willy MalaisseAbstract:L-Histidine, when tested at a 10-mM concentration, caused a rapid and sustained stimulation of Insulin Release from rat islets exposed to either D-glucose (7.0 or 8.3 mM) or L-leucine (10.0 mM). The stimulation of Insulin Release could not be ascribed to an increase in oxygen uptake, to the generation of histamine from L-histidine, or to its participation in a transglutaminase-catalyzed reaction. Like other cationic amino acids, however, L-histidine rapidly accumulated in islet cells, increased 86Rb outflow from prelabeled islets perifused in the presence or absence of extracellular Ca2+, and stimulated the entry of Ca2+ into islet cells. Yet, the amount of exogenous L-histidine present in the islet cells with a positively charged side chain was estimated to be below the threshold value required for stimulation of Insulin Release by fully ionized cationic amino acids, such as L-arginine. Hence, the present findings argue against the view that the Insulinotropic action of cationic amino acids is solely attributable to the accumulation of these positively charged molecules inside the islet B cell with subsequent depolarization of the plasma membrane.
Willy Malaisse - One of the best experts on this subject based on the ideXlab platform.
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Stimulus-secretion coupling of hypotonicity-induced Insulin Release in BRIN-BD11 cells.
Endocrine, 2006Co-Authors: Renaud Beauwens, Willy Malaisse, L. Best, Nicolas Markadieu, Raphaël Crutzen, Karim Louchami, Peter D. Brown, Allen P. Yates, Abdullah SenerAbstract:The stimulus-secretion coupling for hypotonicity-induced Insulin Release was investigated in BRIN-BD11 cells. A 50 mM decrease in extracellular NaCI caused a twofold increase in Insulin Release. The Release of Insulin evoked by hypotonicity progressively decreased in an exponential manner. The response to extracellular hypotonicity displayed a threshold value close to 20 mOsmol/L and amaximal response at about 70 mOsmol/L. Hypotonicity also caused a rapid increase in cell volume followed by a regulatory volume decrease (RVD), cell membrane depolarization with induction of spike activity, and a rise in cytosolic Ca2+ concentration. 5-Nitro-2-(3-phenylpropylamino) benzoate inhibited the secretory response to hypoosmolarity, failed to affect the early increase in cell volume but prevented the RVD, and suppressed the hypotonicity-induced plasma membrane depolarization. Insulin Release provoked by hypotonicity was inhibited by verapamil, absence of Ca2+, thapsigargin, furosemide, tributyltin, and diazoxide. On the contrary, tolbutamide augmented modestly Insulin Release recorded in the hypoosmolar medium. Last, a rise in extracellular K+ concentration, while augmenting basal Insulin output, failed to affect Insulin Release in the hypoosmolar medium. Thus, the Insulin secretory response to hypotonicity apparently represents a Ca2+-dependent process triggered by the gating of volume-sensitive anion channels with subsequent depolarization and gating of voltage-sensitive Ca2+ channels.
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Mechanisms of sulfonylurea-induced Insulin Release.
Diabetes Care, 1990Co-Authors: Willy Malaisse, Philippe LebrunAbstract:The mechanisms responsible for the stimulation of Insulin Release from the pancreatic beta-cell by hypoglycemic sulfonylureas are reviewed herein. One hypothesis postulates that these agents act, at the level of the plasma membrane, by causing the closure of a class of K+ channels characterized by their sensitivity to ATP. This may lead to depolarization of the plasma membrane, gating of voltage-sensitive Ca2+ channels, increase in cytosolic Ca2+ activity, and activation of the effector system for Insulin Release. However, it is not evident that the closure of ATP-sensitive K+ channels accounts for effects of sulfonylureas such as inhibition of K+ inflow into the islet cells, increase in their Na+ content, or even stimulation of Ca2+ inflow and Insulin Release at physiological or higher concentrations of D-glucose.
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Stimulus-Secretion Coupling of Arginine-Induced Insulin Release: Comparison with Histidine-Induced Insulin Release*
Endocrinology, 1990Co-Authors: Abdullah Sener, François Blachier, Joanne Rasschaert, Willy MalaisseAbstract:L-Histidine, when tested at a 10-mM concentration, caused a rapid and sustained stimulation of Insulin Release from rat islets exposed to either D-glucose (7.0 or 8.3 mM) or L-leucine (10.0 mM). The stimulation of Insulin Release could not be ascribed to an increase in oxygen uptake, to the generation of histamine from L-histidine, or to its participation in a transglutaminase-catalyzed reaction. Like other cationic amino acids, however, L-histidine rapidly accumulated in islet cells, increased 86Rb outflow from prelabeled islets perifused in the presence or absence of extracellular Ca2+, and stimulated the entry of Ca2+ into islet cells. Yet, the amount of exogenous L-histidine present in the islet cells with a positively charged side chain was estimated to be below the threshold value required for stimulation of Insulin Release by fully ionized cationic amino acids, such as L-arginine. Hence, the present findings argue against the view that the Insulinotropic action of cationic amino acids is solely attributable to the accumulation of these positively charged molecules inside the islet B cell with subsequent depolarization of the plasma membrane.
Michael J. Macdonald - One of the best experts on this subject based on the ideXlab platform.
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Stimulation of Insulin Release from pancreatic islets by quinones
Bioscience reports, 1991Co-Authors: Michael J. MacdonaldAbstract:Coenzyme Q (CoQ0) and other quinones were shown to be potent Insulin secretagogues in the isolated pancreatic islet. The order of potency was CoQ0≃benzoquinone≃hydroquinonemenadione. CoQ6 and CoQ10 (ubiquinone), duroquinone and durohydroquinone did not stimulate Insulin Release. CoQ0's Insulinotropism was enhanced in calcium-free medium and CoQ0 appeared to stimulate only the second phase of Insulin Release. CoQ0 inhibited inositol mono-, bis- and trisphosphate formation. Inhibitors of mitochondrial respiration (rotenone, antimycin A, FCCP and cyanide) and the calcium channel blocker verapamil, did not inhibit CoQ0-induced Insulin Release. Dicumarol, an inhibitor of quinone reductase, did not inhibit CoQ0-induced Insulin Release, but it did inhibit glucose-induced Insulin Release suggesting that the enzyme and quinones play a role in glucose-induced Insulin Release. Quinones may stimulate Insulin Release by mimicking physiologically-occuring quinones, such as CoQ10, by acting on the plasma membrane or in the cytosol. Exogenous quinones may bypass the quinone reductase reaction, as well as many reactions important for exocytosis.
Atsushi Niki - One of the best experts on this subject based on the ideXlab platform.
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EFFECTS OF SOMATOSTATIN ON Insulin Release FROM DIGITONIN-PERMEABILIZED ISLETS
Biomedical Research, 1993Co-Authors: Tatsuo Tamagawa, Hatsumi Niki, Ichiro Niki, Kazumasa Uemura, Hisayuki Miura, Akihisa Iguchi, Atsushi NikiAbstract:Somatostatin is known to be a powerful inhibitor of Insulin Release, but its cellular mechanism has not been established. We studied the effects of somatostatin on Insulin Release from digitonin-permeabilized rat pancreatic islets. A rise a free Ca 2+ concentration in the medium of 0.1μM to 1-10 μM induced Insulin Release in a concentration-dependent manner when the islets had been treated with digitonin. Forskolin, an activator of adenylate cyclase, cAMP and 12-O-tetradecanoyl-phorbol-13-acetate, an activator of protein kinase C, augmented Insulin Release induced by 1 μM Ca 2+
H.p. Chase - One of the best experts on this subject based on the ideXlab platform.
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First-phase Insulin Release in normal children.
The Journal of pediatrics, 1993Co-Authors: Holley Allen, B.w. Jeffers, Georgeanna J. Klingensmith, H.p. ChaseAbstract:Normal values for the first-phase Insulin Release during an intravenous glucosetolerance test are not yet well defined for children and adolescents. In this study, 69 normal subjects (aged 7 to 22 years) who had no family history of type I diabetes, a normal glycohemoglobin value, and a negative islet cell antibody test result underwent a standard intravenous glucose tolerance test. The mean (±SEM) first-phase Insulin Release increased with age and pubertal status: 7 to 10 years, 93±10.1 mIU/L; 11 to 15 years, 172.7±22.3 mIU/L; and 16 to 22 years, 163±28.5 mIU/L. The mean intraindividual variability in 11 subjects who underwent a second test was 23.6%. Acute stress, as estimated by observer assessment or by blood catecholamine levels, did not significantly correlate with firstphase Insulin Release. We conclude that first-phase Insulin Release is markedly lower in prepubertal children than in adolescents and young adults.