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

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

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 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

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

Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

Diabetes ◽  
1988 ◽  
Vol 37 (7) ◽  
pp. 992-996 ◽  
Author(s):  
J. Turk ◽  
J. H. Hughes ◽  
R. A. Easom ◽  
B. A. Wolf ◽  
D. W. Scharp ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Human Pancreatic Islets

scholarly journals Pituitary Adenylate Cyclase-Activating Polypeptide Receptors Mediating Insulin Secretion in Rodent Pancreatic Islets Are Coupled to Adenylate Cyclase But Not to PLC

Endocrinology ◽  
2002 ◽  
Vol 143 (4) ◽  
pp. 1253-1259 ◽  
Author(s):  
Francoise Jamen ◽  
Raymond Puech ◽  
Joel Bockaert ◽  
Philippe Brabet ◽  
Gyslaine Bertrand
Keyword(s):  
Insulin Secretion ◽  
Adenylate Cyclase ◽  
Pancreatic Islets ◽  
Pituitary Adenylate Cyclase

scholarly journals Vitamin B6 deficiency disrupts serotonin signaling in pancreatic islets and induces gestational diabetes in mice

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ashley M. Fields ◽  
Kevin Welle ◽  
Elaine S. Ho ◽  
Clementina Mesaros ◽  
Martha Susiarjo
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Glucose Intolerance ◽  
Vitamin B6 ◽  
Serotonin Receptor ◽  
Dependent Manner ◽  
Β Cell ◽  
Vitamin B6 Deficiency ◽  
Maternal Glucose

AbstractIn pancreatic islets, catabolism of tryptophan into serotonin and serotonin receptor 2B (HTR2B) activation is crucial for β-cell proliferation and maternal glucose regulation during pregnancy. Factors that reduce serotonin synthesis and perturb HTR2B signaling are associated with decreased β-cell number, impaired insulin secretion, and gestational glucose intolerance in mice. Albeit the tryptophan-serotonin pathway is dependent on vitamin B6 bioavailability, how vitamin B6 deficiency impacts β-cell proliferation during pregnancy has not been investigated. In this study, we created a vitamin B6 deficient mouse model and investigated how gestational deficiency influences maternal glucose tolerance. Our studies show that gestational vitamin B6 deficiency decreases serotonin levels in maternal pancreatic islets and reduces β-cell proliferation in an HTR2B-dependent manner. These changes were associated with glucose intolerance and insulin resistance, however insulin secretion remained intact. Our findings suggest that vitamin B6 deficiency-induced gestational glucose intolerance involves additional mechanisms that are complex and insulin independent.

A nanostructured microfluidic device for plasmonic-assisted electrochemical detection of hydrogen peroxide released from cancer cells

Nanoscale ◽  
2021 ◽  
Author(s):  
Carolina del Real Mata ◽  
Roozbeh Siavash Moakhar ◽  
Sayed Iman Isaac Hosseini ◽  
Mahsa Jalali ◽  
Sara Mahshid
Keyword(s):  
Hydrogen Peroxide ◽  
Cancer Cells ◽  
Real Time ◽  
Electrochemical Detection ◽  
Microfluidic Device ◽  
Cancer Biomarker ◽  
Cancer Diagnostics ◽  
Liquid Biopsies ◽  
Non Invasive

Non-invasive liquid biopsies offer hope for a rapid, risk-free, real-time glimpse into cancer diagnostics. Recently, hydrogen peroxide (H2O2) is identified as a cancer biomarker due to continued release from cancer...

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