Time and dose dependencies for priming effect of glucose on insulin secretion

1981 ◽  
Vol 240 (1) ◽  
pp. E24-E31 ◽  
Author(s):  
V. Grill
Keyword(s):  
Protein Synthesis ◽  
Insulin Secretion ◽  
Priming Effect ◽  
Rest Period ◽  
Short Term ◽  
Priming Effects ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Short Term Exposure ◽  
Effect Of Glucose

Short-term exposure to glucose increases insulin secretion during subsequent stimulation. This priming effect of glucose was further investigated in the perfused rat pancreas. A 5-min pulse of 27.7 mM glucose enhanced the response to a second pulse of the sugar after a 5- or 30-min period of 3.9 mM glucose. With a 10-min pulse of 27.7 mM glucose, the priming effect tended to persist also after a 60-min but not after a 90-min rest period. The priming effects of glucose were also evaluated from enhancement of stimulation 15 min later with 3-isobutyl-l-methylxanthine (IBMX). A 10-min pulse of 8.3 and 27.7, but not 5.6 mM glucose enhanced IBMX-induced insulin secretion. Cycloheximide did not abolish the priming effect of glucose on IBMX-induced insulin secretion. Conclusions are 1) priming is rapidly induced; 2) it persists longer than the time of induction; 3) threshold concentrations of glucose that induce priming are similar to those that initiate insulin secretions; and 4) mechanisms causing priming may not involve protein synthesis.

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.

Effect of somatostatin-28 on dynamics of insulin secretion in perfused rat pancreas

Diabetes ◽  
1991 ◽  
Vol 40 (9) ◽  
pp. 1163-1169 ◽  
Author(s):  
J. W. Ensinck ◽  
E. C. Laschansky ◽  
R. E. Vogel ◽  
D. A. D'Alessio
Keyword(s):  
Insulin Secretion ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Dynamics Of Insulin Secretion

Effects of PHI on hormonal secretion from perfused rat pancreas

1983 ◽  
Vol 245 (4) ◽  
pp. E313-E317
Author(s):  
J. Szecowka ◽  
D. Tendler ◽  
S. Efendic
Keyword(s):  
Amino Acids ◽  
Insulin Secretion ◽  
Glucagon Release ◽  
The Novel ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Isolated Perfused Rat Pancreas ◽  
Hormonal Secretion ◽  
D Cells

Effects of the novel gastrointestinal polypeptide PHI with N-terminal histidine, C-terminal isoleucine amide, and 27 amino acids have been studied in isolated perfused rat pancreas. PHI increased the release of insulin, glucagon, and somatostatin. The amounts of these hormones released were strictly dependent on the prevailing glucose concentrations. In the absence of glucose, PHI (1 nmol/liter) stimulated glucagon release. In the presence of 4.4 and 6.7 mmol/liter glucose, the same dose of this peptide stimulated insulin and somatostatin release. In the presence of 16.7 mmol/liter glucose, only insulin secretion was increased by PHI. When arginine was used as a secretagogue, PHI (10 nmol/liter) potentiated secretion of insulin, glucagon, and somatostatin. Thus, PHI may take part in the regulation of the function of the pancreatic A, B, and D cells.

Effect of Corticosterone on Carbamylcholine-, Leucine-, or Calcium-Induced Insulin Secretion by the Isolated Perfused Rat Pancreas*

Endocrinology ◽  
1984 ◽  
Vol 114 (4) ◽  
pp. 1086-1089 ◽  
Author(s):  
GEGHAM BARSEGHIAN ◽  
CYNTHIA TOMKINSON ◽  
DAVID L. HWANG ◽  
ARYE LEV-RAN
Keyword(s):  
Insulin Secretion ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Isolated Perfused Rat Pancreas

Minimal modeling of insulin secretion in the perfused rat pancreas: a drug effect case study

2014 ◽  
Vol 306 (6) ◽  
pp. E627-E634 ◽  
Author(s):  
Michela Riz ◽  
Morten Gram Pedersen ◽  
Gianna Maria Toffolo ◽  
Guido Haschke ◽  
Hans-Christoph Schneider ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Minimal Model ◽  
Cell Function ◽  
Fold Increase ◽  
Second Phase ◽  
Good Precision ◽  
Β Cell ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Β Cell Function

The experimental protocol of the perfused rat pancreas is commonly used to evaluate β-cell function. In this context, mathematical models become useful tools through the determination of indexes that allow the assessment of β-cell function in different experimental groups and the quantification of the effects of antidiabetic drugs, secretagogues, or treatments. However, a minimal model applicable to the isolated perfused rat pancreas has so far been unavailable. In this work, we adapt the C-peptide minimal model applied previously to the intravenous glucose tolerance test to obtain a specific model for the experimental settings of the perfused pancreas. Using the model, it is possible to estimate indexes describing β-cell responsivity for first (ΦD) and second phase (ΦS, T) of insulin secretion. The model was initially applied to untreated pancreata and afterward used for the assessment of pharmacologically relevant agents (the gut hormone GLP-1, the potent GLP-1 receptor agonist lixisenatide, and a GPR40/FFAR1 agonist, SAR1) to quantify and differentiate their effect on insulin secretion. Model fit was satisfactory, and parameters were estimated with good precision for both untreated and treated pancreata. Model application showed that lixisenatide reaches improvement of β-cell function similarly to GLP-1 (11.7- vs. 13.1-fold increase in ΦD and 2.3- vs. 2.8-fold increase in ΦS) and demonstrated that SAR1 leads to an additional improvement of β-cell function in the presence of postprandial GLP-1 levels.

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