scholarly journals Intracellular changes of Na+, K+, Ca++ & Mg++ in rat pancreatic islets in different glucose concentration and their relation with insulin secretion

2013 ◽  
Vol 18 (2) ◽  
pp. 17-20
Author(s):  
AN Chowdhury ◽  
S Saha ◽  
L Ali
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Maximum Level ◽  
Major Step ◽  
Pancreatic Cell ◽  
Stimulus Secretion Coupling ◽  
Intracellular Changes ◽  
Sensitive Electrode ◽  
Effect Of Glucose ◽  
K Permeability

Impairment of insulin secretion from pancreatic ?–cell constitutes an important pathophysiological factor in the development of diabetes mellitus. The changes of intracellular concentration of Na+, K+, Ca++ and Mg++ were observed in substimulatory and stimulatory different glucose concentrations. Pancreatic islets from Long-Evans rats were isolated by collagenase digestion. The concentrations of ions expressed in terms of islet protein in the homogenized islets were measured by using an ion-sensitive electrode based autoanalyzer. In the physiological medium, the islet content of all the four ions increased significantly in response to glucose with maximum level at 11 mM and no further increase at 20 mM. Initial depolarizing effect of glucose is due to reduction of K+ permeability. The reduction of K+ permeability by glucose in ?–cell is a major step in stimulus-secretion coupling for insulin release. DOI: http://dx.doi.org/10.3329/jdnmch.v18i2.16016 J. Dhaka National Med. Coll. Hos. 2012; 18 (02): 17-20

Nitric oxide donor SIN-1 inhibits insulin release

1996 ◽  
Vol 271 (4) ◽  
pp. C1098-C1102 ◽  
Author(s):  
A. Sjoholm
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Protein Kinase C ◽  
Insulin Secretion ◽  
Protein Kinase ◽  
Beta Cell ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Kinase C ◽  
Stimulus Secretion Coupling

Preceding the onset of insulin-dependent diabetes mellitus, pancreatic islets are infiltrated by macrophages secreting interleukin-1 beta, which exerts cytotoxic and inhibitory actions on islet beta-cell insulin secretion through induction of nitric oxide (NO) synthesis. The influence of the NO donor 3-morpholinosydnonimine (SIN-1) on insulin secretion from isolated pancreatic islets in response to various secretagogues was investigated. Stimulation of insulin release evoked by glucose, phospholipase C activation with carbachol, and protein kinase C activation with phorbol ester were obtained by SIN-1, whereas the response to adenylyl cyclase activation or K(+)-induced depolarization was not affected. It is concluded that enzymes involved in glucose catabolism, phospholipase C or protein kinase C, may be targeted by NO. Reversal of SIN-1 inhibition of glucose-stimulated insulin release by dithiothreitol suggests that NO may inhibit insulin secretion partly by S-nitrosylation of thiol residues in key proteins in the stimulus-secretion coupling. These adverse effects of NO on the beta-cell stimulus-secretion coupling may be of importance for the development of the impaired insulin secretion characterizing diabetes mellitus.

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.

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.

Roles of GTP and phospholipase C in the potentiation of Ca2+-induced insulin secretion by glucose in rat pancreatic islets

1997 ◽  
Vol 153 (1) ◽  
pp. 61-71 ◽  
Author(s):  
J Vadakekalam ◽  
M E Rabaglia ◽  
S A Metz
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Phospholipase C ◽  
Mycophenolic Acid ◽  
High Glucose ◽  
Secretory Response ◽  
Rat Pancreatic Islets ◽  
Isolated Rat Islets ◽  
Effect Of Glucose ◽  
Isolated Rat

Abstract Glucose can augment insulin secretion independently of K+ channel closure, provided cytoplasmic free Ca2+ concentration is elevated. A role for phospholipase C (PLC) in this phenomenon has been both claimed and refuted. Recently, we have shown a role for GTP in the secretory effect of glucose as well as in glucose-induced PLC activation, using islets pre-treated with GTP synthesis inhibitors such as mycophenolic acid (MPA). Therefore, in the current studies, we examined first, whether glucose augments Ca2+-induced PLC activation and second, whether GTP is required for this effect, when K+(ATP) channels are kept open using diazoxide. Isolated rat islets pre-labeled with [3H]myo-inositol were studied with or without first priming with glucose. There was a 98% greater augmentation of insulin secretion by 16·7 mm glucose (in the presence of diazoxide and 40 mm K+) in primed islets; however, the ability of high glucose to augment PLC activity bore no relationship to the secretory response. MPA markedly inhibited PLC in both conditions; however, insulin secretion was only inhibited (by 46%) in primed islets. None of these differences were attributable to alterations in labeling of phosphoinositides or levels of GTP or ATP. These data indicate that an adequate level of GTP is critical for glucose's potentiation of Ca2+-induced insulin secretion in primed islets but that PLC activation can clearly be dissociated from insulin secretion and therefore cannot be the major cause of glucose's augmentation of Ca2+-induced insulin secretion. Journal of Endocrinology (1997) 153, 61–71

Influence of thiol groups, calcium, and glucose metabolism on cholinergic-induced insulin release and on methylscopolamine binding to muscarinic receptors in pancreatic islets of the rat

1985 ◽  
Vol 109 (3) ◽  
pp. 355-360 ◽  
Author(s):  
V. Grill ◽  
K. Fåk
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Muscarinic Receptors ◽  
Priming Effect ◽  
Thiol Groups ◽  
Short Term ◽  
Effect Of Glucose ◽  
Stimulation Of

Abstract. Short-term regulation of [3H]methylscopolamine binding to muscarinic receptors and acetylcholineinduced stimulation of insulin release was investigated in pancreatic islets of the rat. Binding of methylscopolamine was reversible; 47% of label was displaced 10 min and 70% 30 min after addition of unlabelled substance. 0.1 mm chloromercuribensoic acid, when present during binding incubations, inhibited binding by 54%, whereas acetylcholine-induced insulin release was unaffected by the presence of the thiol reactant. Pre-incubation for 60 min in a calcium-deprived medium or in the presence of 50 μm trifluoroperazine likewise inhibited binding. Pre-incubation with 1.0 mm 3-isobutyl-l-methylxanthine or 16.7 m glucose failed to influence subsequent binding although acetylcholine-induced insulin release was 4-fold enhanced by priming with glucose. We conclude that 1) binding to muscarinic receptors is influenced by thiol interaction, 2) short-term alterations in calcium fluxes influence binding, whereas short-term changes in cyclic AMP (cAMP) or glucose metabolism do not, 3) a priming effect of glucose on insulin secretion is not mediated by changes in receptor binding.

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.

Real Time Electrochemical Detection of 5-HT/Insulin Secretion from Single Pancreatic Islets: Effect of Glucose and K+Depolarization

1996 ◽  
Vol 228 (1) ◽  
pp. 100-104 ◽  
Author(s):  
Rui M. Barbosa ◽  
Amélia M. Silva ◽  
Angelo R. Tomé ◽  
Jonathan A. Stamford ◽  
Rosa M. Santos ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Real Time ◽  
Electrochemical Detection ◽  
Effect Of Glucose

Real Time Electrochemical Detection of 5-HT/Insulin Secretion from Single Pancreatic Islets: Effect of Glucose and K+Depolarization

1997 ◽  
Vol 231 (2) ◽  
pp. 519
Author(s):  
Rui M. Barbosa ◽  
Amélia M. Silva ◽  
Angelo R. Tomé ◽  
Jonathan A. Stamford ◽  
Rosa M. Santos ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Real Time ◽  
Electrochemical Detection ◽  
Effect Of Glucose

Pulsatile insulin secretion from isolated human pancreatic islets

Diabetes ◽  
1994 ◽  
Vol 43 (6) ◽  
pp. 827-830 ◽  
Author(s):  
P. Marchetti ◽  
D. W. Scharp ◽  
M. Mclear ◽  
R. Gingerich ◽  
E. Finke ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Human Pancreatic Islets ◽  
Pulsatile Insulin Secretion

Intraportal transplantation of pancreatic islets into livers of diabetic rats. Reinnervation of islets and regulation of insulin secretion by the hepatic sympathetic nerves

Diabetes ◽  
1994 ◽  
Vol 43 (11) ◽  
pp. 1345-1352 ◽  
Author(s):  
A. Gardemann ◽  
K. Jungermann ◽  
V. Grosse ◽  
L. Cossel ◽  
F. Wohlrab ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Sympathetic Nerves ◽  
Diabetic Rats
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