Glucagon-like peptide-1 stimulates insulin secretion by a Ca2+-independent mechanism in Zucker diabetic fatty rat islets of Langerhans

Metabolism ◽  
2000 ◽  
Vol 49 (12) ◽  
pp. 1579-1587 ◽  
Author(s):  
Seamus K. Sreenan ◽  
Anshu A. Mittal ◽  
Flora Dralyuk ◽  
William L. Pugh ◽  
Kenneth S. Polonsky ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Zucker Diabetic Fatty Rat ◽  
Rat Islets ◽  
Independent Mechanism ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Rat Islets Of Langerhans

Immunoprecipitation of a pertussis toxin substrate of the Go family from rat islets of Langerhans

1992 ◽  
Vol 12 (2) ◽  
pp. 95-100 ◽  
Author(s):  
Nicholas S. Berrow ◽  
Roger D. Hurst ◽  
Susan L. F. Chan ◽  
Noel G. Morgan
Keyword(s):  
Molecular Weight ◽  
Insulin Secretion ◽  
Adenylate Cyclase ◽  
G Protein ◽  
G Proteins ◽  
Islets Of Langerhans ◽  
Pertussis Toxin ◽  
Inhibitory Receptors ◽  
Rat Islets ◽  
Rat Islets Of Langerhans

Rat islets express a pertussis toxin sensitive G-protein involved in receptor-mediated inhibition of insulin secretion. This has been assumed previously to represent “Gi” which couples inhibitory receptors to adenylate cyclase. Incubation of islet G-proteins with32P-NAD and pertussis toxin resulted in the labelling of a band of molecular weight 40,000. This band was very broad and did not allow resolution of individual components. Incubation of the radiolabelled proteins with an anti-Go antiserum resulted in specific immunoprecipitation of a32P-labelled band. These results demonstrate that the complement of pertussis toxin sensitive G-proteins in rat islets includes Go.

scholarly journals A TRPM4 Inhibitor 9-Phenanthrol Inhibits Glucose- and Glucagon-Like Peptide 1-Induced Insulin Secretion from Rat Islets of Langerhans

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
Zuheng Ma ◽  
Anneli Björklund ◽  
Md. Shahidul Islam
Keyword(s):  
Insulin Secretion ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Monovalent Cation ◽  
Major Effect ◽  
Hyperinsulinemic Hypoglycemia ◽  
Rat Islets ◽  
Glucagon Like Peptide 1 ◽  
Transient Receptor ◽  
Rat Islets Of Langerhans

Pancreatic β-cells express several ion channels of the transient receptor potential family, which play important roles in mediating the stimulus-secretion coupling. One of these channels, the TRPM4 is a Ca2+-activated monovalent cation channel. This channel is inhibited by 9-phenanthrol, which also inhibits the TMEM16a Cl− channel, and activates the Ca2+-activated K+ channel, Kca3.1. The net effects of ion-channel modulation by 9-phenantherol on the insulin secretion remain unclear. We tested the effects of 9-phenanthrol on glucose- and GLP-1-induced insulin secretion from isolated rat islets in static incubations. When applied to the islets in the presence of 3.3 mM glucose, 9-phenanthrol caused a small increase in insulin secretion (~7% of the insulin secretion stimulated by 10 mM glucose). 10 μM 9-phenanthrol did not inhibit glucose- or GLP-1-induced insulin secretion. 20 μM and 30 μM 9-phenanthrol inhibited glucose-induced insulin secretion by ~80% and ~85%, respectively. Inhibition of the GLP-1-induced insulin secretion by 20 μM and 30 μM 9-phenanthrol was 65% and 94%, respectively. Our study shows that the major effect of 9-phenanthrol on the islets is a strong inhibition of insulin secretion, and we speculate that compounds related to 9-phenanthrol may be potentially useful in treating the pancreatogenous hyperinsulinemic hypoglycemia syndromes.

Relationships between energy level and insulin secretion in isolated rat islets of langerhans

1992 ◽  
Vol 43 (8) ◽  
pp. 1859-1864 ◽  
Author(s):  
Mitsuaki Ohta ◽  
David Nelson ◽  
Jeanne M. Wilson ◽  
Martin D. Meglasson ◽  
Maria Erecińska
Keyword(s):  
Insulin Secretion ◽  
Energy Level ◽  
Islets Of Langerhans ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

scholarly journals Studies on the role of inositol trisphosphate in the regulation of insulin secretion from isolated rat islets of Langerhans

1985 ◽  
Vol 228 (3) ◽  
pp. 713-718 ◽  
Author(s):  
N G Morgan ◽  
G M Rumford ◽  
W Montague
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Islet Cells ◽  
Inositol Trisphosphate ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat ◽  
Stimulation Of

Glucose (20 mM) and carbachol (1 mM) produced a rapid increase in [3H]inositol trisphosphate (InsP3) formation in isolated rat islets of Langerhans prelabelled with myo-[3H]inositol. The magnitude of the increase in InsP3 formation was similar when either agent was used alone and was additive when they were used together. In islets prelabelled with 45Ca2+ and treated with carbachol (1 mM), the rise in InsP3 correlated with a rapid, transient, release of 45Ca2+ from the cells, consistent with mobilization of 45Ca2+ from an intracellular pool. Under these conditions, however, insulin secretion was not increased. In contrast, islets prelabelled with 45Ca2+ and exposed to 20mM-glucose exhibited a delayed and decreased 45Ca2+ efflux, but released 7-8-fold more insulin than did those exposed to carbachol. Depletion of extracellular Ca2+ failed to modify the increase in InsP3 elicited by either glucose or carbachol, whereas it selectively inhibited the efflux of 45Ca2+ induced by glucose in preloaded islets. Under these conditions, however, glucose was still able to induce a small stimulation of the first phase of insulin secretion. These results demonstrate that polyphosphoinositide metabolism, Ca2+ mobilization and insulin release can all be dissociated in islet cells, and suggest that glucose and carbachol regulate these parameters by different mechanisms.

Effect of L-Asparaginase on Insulin Secretion from Isolated Rat Islets of Langerhans

1991 ◽  
Vol 35 (3-4) ◽  
pp. 155-160 ◽  
Author(s):  
J.M. Pou ◽  
T. Cervera ◽  
A. Perez ◽  
M.A. Ortiz ◽  
J.A. Arroyo
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat
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