Effect of tormentic acid on insulin secretion in isolated rat islets of langerhans

1989 ◽  
Vol 3 (4) ◽  
pp. 145-147 ◽  
Author(s):  
M. D. Ivorra ◽  
M. Paya ◽  
A. Villar
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Tormentic Acid ◽  
Isolated Rat

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

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

1991 ◽  
Vol 42 (3) ◽  
pp. 593-598 ◽  
Author(s):  
Ohta Mitsuaki ◽  
David Nelson ◽  
June Nelson ◽  
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

Effects of noradrenaline on 45Ca2+ efflux from isolated rat islets of Langerhans

1985 ◽  
Vol 5 (12) ◽  
pp. 1053-1060 ◽  
Author(s):  
Noel G. Morgan ◽  
Gwyneth M. Rumford ◽  
William Montague
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Choline Chloride ◽  
Muscarinic Agonist ◽  
Primary Role ◽  
Dibutyryl Camp ◽  
Rat Islets ◽  
Isolated Rat Islets ◽  
Rat Islets Of Langerhans ◽  
Isolated Rat

Noradrenaline caused a prompt but transient increase in the rate of45Ca2+ efflux from isolated rat islets of Langerhans perifused in Ca2+ depleted medium. The response was modest in size and was unaffected by isosmotic replacement of NaCl with choline chloride or by inclusion of 0.5 mM dibutyryl cAMP in the perifusion medium, suggesting that it was not mediated by Na+: Ca2+ exchange nor by lowered cAMP. Despite its effect on45Ca2+ efflux, noradrenaline treatment did not alter the kinetics of45Ca2+ efflux in response to the muscarinic agonist, carbamylcholine, nor did it change the magnitude of the response to this agent. Simultaneous introduction of 20 mM glucose with noradrenaline prevented a rise in45Ca2+ efflux and indeed resulted in inhibition of45Ca2+ efflux. The data suggest that noradrenaline does not directly activate the mechanisms which regulate Ca2+ extrusion from islets cells, and they do not support a primary role for the Ca2+ efflux response in mediating adrenergic inhibition of insulin secretion.

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