Stimulation of insulin release from rat pancreatic islets induced by cyclosporine

1989 ◽  
Vol 17 (2) ◽  
pp. 351-352 ◽  
Author(s):  
M. E. FERRERO ◽  
A. MARNI ◽  
G. GAJA
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Rat Pancreatic Islets ◽  
Stimulation Of

Mechanisms of synergism between glucose and cAMP on stimulation of insulin release

1984 ◽  
Vol 247 (6) ◽  
pp. E701-E708 ◽  
Author(s):  
W. Phang ◽  
L. Domboski ◽  
Y. Krausz ◽  
G. W. Sharp
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Ringer Solution ◽  
Intracellular Camp ◽  
Cyclic Monophosphate ◽  
Rat Pancreatic Islets ◽  
Individual Effects ◽  
The Individual ◽  
Isolated Rat ◽  
Stimulation Of

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.

scholarly journals Cerulenin, an inhibitor of protein acylation, selectively attenuates nutrient stimulation of insulin release: a study in rat pancreatic islets

Diabetes ◽  
2000 ◽  
Vol 49 (5) ◽  
pp. 712-717 ◽  
Author(s):  
H. Yajima ◽  
M. Komatsu ◽  
S. Yamada ◽  
S. G. Straub ◽  
T. Kaneko ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Rat Pancreatic Islets ◽  
Protein Acylation ◽  
Stimulation Of

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets

1990 ◽  
Vol 258 (6) ◽  
pp. E975-E984 ◽  
Author(s):  
G. Z. Fadda ◽  
M. Akmal ◽  
L. G. Lipson ◽  
S. G. Massry
Keyword(s):  
Insulin Secretion ◽  
Parathyroid Hormone ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Direct Effect ◽  
Indirect Evidence ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Stimulation Of

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

Sensitivity to Cd2+ but resistance to Ni2+ of Ca2+ inflow into rat pancreatic islets

1990 ◽  
Vol 258 (3) ◽  
pp. E529-E533 ◽  
Author(s):  
P. O. Plasman ◽  
M. Hermann ◽  
A. Herchuelz ◽  
P. Lebrun
Keyword(s):  
Pancreatic Islets ◽  
Insulin Release ◽  
Islet Cells ◽  
Excitable Cells ◽  
45Ca Uptake ◽  
Rat Pancreatic Islets ◽  
Cell Plasma ◽  
Different Types ◽  
45Ca Efflux ◽  
Ca2 Channels

The presence of different types [long lasting (L) and transient (T)] of active voltage-operated Ca2+ channels in islet cells was investigated by comparing the effects of Cd2+, Ni2+, and 1,4-dihydropyridines on 45Ca uptake, 45Ca efflux, and insulin release in intact rat pancreatic islets. In several other excitable cells the L-channel has been shown to be modulated by 1,4-dihydropyridines and Cd2+, whereas the T-channel was reported to be sensitive to Ni2+. Nifedipine and Cd2+ inhibited whereas BAY K 8644 enhanced the glucose (11.1, 22.2 mM)-stimulated short-term 45Ca uptake, 45Ca efflux, and insulin release. In contrast, the stimulatory effects of glucose (11.1, 22.2 mM) on 45Ca uptake, 45Ca efflux, and insulin release were unaffected by Ni2+. These findings confirm that glucose provokes Ca2+ entry mainly by activating voltage-sensitive Ca2+ channels of the L-type and suggest that the B-cell plasma membrane is not equipped with active T-type Ca2+ channels.

Sign in / Sign up

Export Citation Format

Share Document