scholarly journals Insulin release from the perifused isolated rat langerhans islets under a slow-rise glucose stimulation.

1977 ◽  
Vol 25 (8) ◽  
pp. 2112-2116 ◽  
Author(s):  
KUNIO KOBAYASHI ◽  
YOKO TSUMURA ◽  
HISAYO ISE ◽  
SHOHEI KAGAWA ◽  
AKIRA MATSUOKA
1977 ◽  
Vol 24 (5) ◽  
pp. 451-456
Author(s):  
KUNIO KOBAYASHI ◽  
YOKO TSUMURA ◽  
HISAYO ISE ◽  
SHOHEI KAGAWA ◽  
AKIRA MATSUOKA

1979 ◽  
Vol 27 (9) ◽  
pp. 2198-2202 ◽  
Author(s):  
KUNIO KOBAYASHI ◽  
SHOHEI KAGAWA ◽  
YOKO TSUMURA ◽  
HISAYO ISE ◽  
KEIKO YOSHIDA ◽  
...  

1983 ◽  
Vol 245 (6) ◽  
pp. E591-E597 ◽  
Author(s):  
D. Giugliano ◽  
P. Di Pinto ◽  
R. Torella ◽  
N. Frascolla ◽  
F. Saccomanno ◽  
...  

These studies were undertaken to evaluate in humans the possible physiological role of prostaglandins of the E series (PGE) in modulating insulin release and to assess whether endogenous PGE synthesis may account for the biphasic pattern of insulin secretion. We used a square-wave glucose stimulation previously determined to give maximal biphasic insulin release. Infusion of lysine acetylsalicylate to block the synthesis of endogenous PGE increased by twofold total insulin response to glucose and also converted insulin release to a multiphasic pattern. The infusion of exogenous PGE1 (0.2 microgram X kg-1 X min-1) or PGE2 (10 micrograms/min) in addition to lysine acetylsalicylate restored the typical biphasic pattern of insulin release and also decreased total insulin release to values similar to those of control studies. Infusion of either PGE1 or PGE2 in the absence of lysine acetylsalicylate reset insulin secretion to a lower level without altering the kinetics of release. On the basis of these results, it is hypothesized that endogenous PGE released in response to glucose stimulation exert an inhibiting effect on insulin release that becomes biphasic in appearance.


1984 ◽  
Vol 247 (6) ◽  
pp. E701-E708 ◽  
Author(s):  
W. Phang ◽  
L. Domboski ◽  
Y. Krausz ◽  
G. W. Sharp

The mechanism of synergism between glucose and adenosine 3',5'-cyclic monophosphate (cAMP) on insulin release has been studied. Synergism may result from 1) inhibition of Na+-Ca2+ exchange by glucose and 2) a cAMP-induced sensitization of the release machinery to Ca2+. To distinguish between these two possibilities, isolated rat pancreatic islets were perifused with agents that raise intracellular levels of cAMP [3-isobutyl-1-methylxanthine (IBMX) and forskolin] and others that increase intracellular concentrations of Ca2+ either by blocking Na2+-Ca2+ exchange (ouabain and choline-Ringer solution) or by causing increased Ca2+ influx (KCl, carbachol, and 10 mM Ca2+). The results indicate that both the combination of cAMP and increased Ca2+ influx or blocked Na2-Ca2+ exchange and increased Ca2+ influx potentiated insulin release. When the relative potentiating abilities of cAMP and blocked Na2+-Ca2+ exchange were compared by determining the individual effects of IBMX and 1 mM ouabain (a concentration that causes similar inhibition of 45C2+ efflux as 16.7 mM glucose) in the presence of carbachol, cAMP was only 1.4 times more potent as a potentiating agent than blocked Na+-Ca2+ exchange. The greatest potentiation of insulin release was observed when Na+-Ca2+ exchange was blocked in the presence of increased levels of intracellular cAMP.


1986 ◽  
Vol 233 (1) ◽  
pp. 287-289 ◽  
Author(s):  
C S Hii ◽  
J Stutchfield ◽  
S L Howell

The phorbol ester 4 beta-phorbol 12-myristate 13-acetate (PMA), at concentrations of 0.1 microM and above, stimulated secretion of glucagon and of insulin from isolated rat islets of Langerhans incubated in the presence of 5.5 mM-glucose. Stimulation of secretion of both hormones by 1 microM-PMA persisted in the absence of external Ca2+, and could be abolished by incubating the islets at 4 degrees C. These findings suggest a role of protein kinase C in the alpha-cell (and beta-cell) secretory mechanism.


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