Effect of a sodium-channel activator (BDF 9148) on insulin secretion in mouse pancreatic islets

1997 ◽  
Vol 355 (3) ◽  
pp. 417-421 ◽  
Author(s):  
M. A. Wahl ◽  
K. Anulukanapakorn ◽  
Hermann P. T. Ammon
Keyword(s):  
Insulin Secretion ◽  
Sodium Channel ◽  
Pancreatic Islets ◽  
Mouse Pancreatic Islets ◽  
Bdf 9148 ◽  
Channel Activator

scholarly journals Taurine supplementation: involvement of cholinergic/phospholipase C and protein kinase A pathways in potentiation of insulin secretion and Ca2+handling in mouse pancreatic islets

2010 ◽  
Vol 104 (8) ◽  
pp. 1148-1155 ◽  
Author(s):  
Rosane A. Ribeiro ◽  
Emerielle C. Vanzela ◽  
Camila A. M. Oliveira ◽  
Maria L. Bonfleur ◽  
Antonio C. Boschero ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Protein Kinase ◽  
Pancreatic Islets ◽  
Phospholipase C ◽  
Islet Cells ◽  
Taurine Supplementation ◽  
Adult Mice ◽  
Intracellular Ca ◽  
Mouse Pancreatic Islets ◽  
Methyl Xanthine

Taurine (TAU) supplementation increases insulin secretion in response to high glucose concentrations in rodent islets. This effect is probably due to an increase in Ca2+handling by the islet cells. Here, we investigated the possible involvement of the cholinergic/phospholipase C (PLC) and protein kinase (PK) A pathways in this process. Adult mice were fed with 2 % TAU in drinking water for 30 d. The mice were killed and pancreatic islets isolated by the collagenase method. Islets from TAU-supplemented mice showed higher insulin secretion in the presence of 8·3 mm-glucose, 100 μm-carbachol (Cch) and 1 mm-3-isobutyl-1-methyl-xanthine (IBMX), respectively. The increase in insulin secretion in response to Cch in TAU islets was accompanied by a higher intracellular Ca2+mobilisation and PLCβ2protein expression. The Ca2+uptake was higher in TAU islets in the presence of 8·3 mm-glucose, but similar when the islets were challenged by glucose plus IBMX. TAU islets also showed an increase in the expression of PKAα protein. This protein may play a role in cation accumulation, since the amount of Ca2+in these islets was significantly reduced by the PKA inhibitors:N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline sulfonamide (H89) and PK inhibitor-(6–22)-amide (PKI). In conclusion, TAU supplementation increases insulin secretion in response to glucose, favouring both influx and internal mobilisation of Ca2+, and these effects seem to involve the activation of both PLC–inositol-1,4,5-trisphosphate and cAMP–PKA pathways.

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.

Gastrin Releasing Peptide Augments Glucose Mediated45Ca2+Uptake, Electrical Activity, and Insulin Secretion of Mouse Pancreatic Islets*

Endocrinology ◽  
1991 ◽  
Vol 128 (6) ◽  
pp. 3247-3252 ◽  
Author(s):  
MARTIN A. WAHL ◽  
ROLAND J. PLEHN ◽  
EBERHARD A. LANDSBECK ◽  
EUGEN J. VERSPOHL ◽  
HERMANN P. T. AMMON
Keyword(s):  
Insulin Secretion ◽  
Electrical Activity ◽  
Pancreatic Islets ◽  
Gastrin Releasing Peptide ◽  
Mouse Pancreatic Islets

scholarly journals Cytosolic ratios of free [NADPH]/[NADP+] and [NADH]/[NAD+] in mouse pancreatic islets, and nutrient-induced insulin secretion

1987 ◽  
Vol 241 (1) ◽  
pp. 161-167 ◽  
Author(s):  
C J Hedeskov ◽  
K Capito ◽  
P Thams
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Coupling Factor ◽  
Mouse Pancreatic Islets ◽  
Cell Depolarization ◽  
K Permeability ◽  
Cell Glucose ◽  
Stimulation Of

When the extracellular concentration of glucose was raised from 3 mM to 7 mM (the concentration interval in which beta-cell depolarization and the major decrease in K+ permeability occur), the cytosolic free [NADPH]/[NADP+] ratio in mouse pancreatic islets increased by 29.5%. When glucose was increased to 20 mM, a 117% increase was observed. Glucose had no effect on the cytosolic free [NADH]/[NAD+] ratio. Neither the cytosolic free [NADPH]/[NADP+] ratio nor the corresponding [NADH]/[NAD+] ratio was affected when the islets were incubated with 20 mM-fructose or with 3 mM-glucose + 20 mM-fructose, although the last-mentioned condition stimulated insulin release. The insulin secretagogue leucine (10 mM) stimulated insulin secretion, but lowered the cytosolic free [NADPH]/[NADP+] ratio; 10 mM-leucine + 10 mM-glutamine stimulated insulin release and significantly enhanced both the [NADPH]/[NADP+] ratio and the [NADH]/[NAD+] ratio. It is concluded that the cytosolic free [NADPH]/[NADP+] ratio may be involved in coupling beta-cell glucose metabolism to beta-cell depolarization and ensuing insulin secretion, but it may not be the sole or major coupling factor in nutrient-induced stimulation of insulin secretion.

scholarly journals Protection of the pancreatic β-cell glucoreceptor mechanism for insulin secretion during culture in chemically defined medium

1978 ◽  
Vol 174 (3) ◽  
pp. 959-964 ◽  
Author(s):  
Erik Gylfe
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Culture Media ◽  
Early Stage ◽  
Insulin Response ◽  
Defined Medium ◽  
Β Cell ◽  
Before And After ◽  
Mouse Pancreatic Islets ◽  
High Concentrations

High concentrations of glucose have a protective effect on the glucoreceptor mechanism for insulin secretion during culture of pancreatic islets in chemically defined media. To study at what level glucose exerts this effect, insulin secretion from β-cell-rich mouse pancreatic islets was measured before and after culture for 1 week in the presence of different substances. Before culture, glucose and inosine were potent stimulators, mannose and fructose were less potent and xylitol had no effect on secretion. Culture in 3mm-glucose resulted in a 10-fold decrease in the insulin response to glucose stimulation. A less marked decrease was noted after culture in 20mm- or 30mm-glucose. Inosine-stimulated secretion was much decreased after culture in high concentrations of glucose, whereas the responses to mannose or fructose were unchanged. After culture in 30mm-mannose, glucose-stimulated secretion was similar to that observed after culture in high concentrations of glucose, whereas the response to mannose had much decreased. There were no secretory responses to glucose or fructose after culture in 30mm-fructose, or to glucose or xylitol after culture in 30mm-xylitol. Culture in 10mm-inosine did not preserve any significant response to glucose or inosine. The insulin contents of islets and culture media were higher after culture in high concentrations of glucose, mannose or inosine than after culture in fructose, xylitol or low concentrations of glucose. It is suggested that glucose, and to some extent mannose, preserves the glucoreceptor mechanism for insulin secretion by influencing an early stage in glucose metabolism, presumably glucokinase activity.

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