Mechanism of Action of Growth-Hormone-Releasing Hormone in Stimulating Insulin Secretion in vitro from Isolated Rat Islets and Dispersed Islet Cells

1990 ◽  
Vol 33 (5) ◽  
pp. 199-204 ◽  
Author(s):  
I.C. Green ◽  
C. Southern ◽  
K. Ray
Endocrine ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 91-102 ◽  
Author(s):  
Hilda Martínez-Coria ◽  
L Javier López-Rosales ◽  
Martha Carranza ◽  
Laura Berumen ◽  
Maricela Luna ◽  
...  

1985 ◽  
Vol 228 (3) ◽  
pp. 713-718 ◽  
Author(s):  
N G Morgan ◽  
G M Rumford ◽  
W Montague

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.


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