Effects of leptin, acetylcholine and vasoactive intestinal polypeptide on insulin secretion in isolated ob/ob mouse pancreatic islets

2004 ◽  
Vol 41 (3) ◽  
pp. 104-112 ◽  
Author(s):  
S. Persson-Sj�gren ◽  
A. Elmi ◽  
P. Lindstr�m
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Vasoactive Intestinal Polypeptide ◽  
Mouse Pancreatic Islets ◽  
Intestinal Polypeptide

Effects of gastric inhibitory polypeptide, vasoactive intestinal polypeptide and peptide histidine isoleucine on the secretion of hormones by isolated mouse pancreatic islets

1990 ◽  
Vol 125 (3) ◽  
pp. 375-379 ◽  
Author(s):  
C. J. Bailey ◽  
L. C. Wilkes ◽  
J. M. Conlon ◽  
P. H. Armstrong ◽  
K. D. Buchanan
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Vasoactive Intestinal Polypeptide ◽  
Pancreatic Polypeptide ◽  
Glucose Concentration ◽  
Gastric Inhibitory Polypeptide ◽  
Glucagon Release ◽  
Islet Hormones ◽  
Mouse Pancreatic Islets ◽  
Intestinal Polypeptide

ABSTRACT The release of insulin, glucagon, somatostatin and pancreatic polypeptide (PP) by isolated mouse pancreatic islets was determined during 30-min incubations at 5.6 and 16.7 mmol glucose/l in the absence and presence of gastric inhibitory polypeptide (GIP), vasoactive intestinal polypeptide (VIP) and peptide histidine isoleucine (PHI) at concentrations of 1–1000 nmol/l. Insulin release was enhanced (>50%) by GIP (100–1000 nmol/l) and VIP (1 μmol/l) at 5.6 mmol glucose/l, but not at 16.7 mmol glucose/l. Glucagon release was increased by GIP (100–1000 nmol/l), and by VIP and PHI (1—1000 nmol/l) at both glucose concentrations in a dose-related manner (maximum increases > tenfold). Somatostatin release was similarly increased by GIP (10–1000 nmol/l) at both glucose concentrations. Only the highest concentration (1 μmol/l of PHI tested increased somatostatin release (twofold) at 5.6 mmol glucose/l, whereas PHI and VIP (1–1000 nmol/l reduced (>37%) somatostatin release at 16.7 mmol glucose/l. PP release was increased (49–58%) by 100–1000 nmol GIP/l, but was not significantly altered by VIP, and was reduced (39–56%) by PHI. The results indicate that GIP, VIP and PHI each stimulate glucagon release in a dose-related manner, but they exert discretely different effects on other islet hormones depending upon the dose and the prevailing glucose concentration. Journal of Endocrinology (1990) 125, 375–379

scholarly journals Innervation of the pancreas by substance P, enkephalin, vasoactive intestinal polypeptide and gastrin/CCK immunoractive nerves.

1979 ◽  
Vol 27 (9) ◽  
pp. 1283-1284 ◽  
Author(s):  
L I Larsson
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Substance P ◽  
Blood Vessels ◽  
Vasoactive Intestinal Polypeptide ◽  
Pancreatic Blood Flow ◽  
Major Site ◽  
Site Of Action ◽  
Immunocytochemical Studies ◽  
Intestinal Polypeptide

Immunocytochemical studies habe shown that many peptides which profoundly affect the endocrine and exocrine functions of the pancreas are localized to neurons. In the cat, such peptidergic nerves appear to innervate ganglia, islets and blood vessels of the pancreas, whereas their contributions to exocrine cells are minor. Our studies suggest that pancreatic ganglia represent one major site of action of the peptides and that, in addition, nerves containing the vasoactive intestinal polypeptide and gastrin/CCK-related peptides profoundly affect pancreatic blood flow and insulin secretion, respectively.

Mechanism of fat-induced attenuation of glucose-induced insulin secretion from mouse pancreatic islets

1999 ◽  
Vol 36 (3) ◽  
pp. 119-125 ◽  
Author(s):  
K. Capito ◽  
R. Reinsmark ◽  
P. Thams
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Mouse Pancreatic Islets

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.

Effect of vasoactive intestinal polypeptide infused intrapancreatically on glucagon and insulin secretion

Metabolism ◽  
1977 ◽  
Vol 26 (7) ◽  
pp. 781-786 ◽  
Author(s):  
Akio Kaneto ◽  
Toshio Kaneko ◽  
Hiroshi Kajinuma ◽  
Kinori Kosaka
Keyword(s):  
Insulin Secretion ◽  
Vasoactive Intestinal Polypeptide ◽  
Glucagon And Insulin ◽  
Intestinal Polypeptide
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