scholarly journals Effect of potassium ions on insulin release in the rat from the perifused islets of Langerhans with slow-rise glucose stimulation.

1979 ◽  
Vol 27 (9) ◽  
pp. 2198-2202 ◽  
Author(s):  
KUNIO KOBAYASHI ◽  
SHOHEI KAGAWA ◽  
YOKO TSUMURA ◽  
HISAYO ISE ◽  
KEIKO YOSHIDA ◽  
...  
1968 ◽  
Vol 108 (1) ◽  
pp. 17-24 ◽  
Author(s):  
S. L. Howell ◽  
K W Taylor

1. A method was devised for the isolation of islets of Langerhans from rabbit pancreas by collagenase digestion in order to study the influx and efflux of K+ in islets during insulin secretion. 2. Glucose-induced insulin release was accompanied by an increased rate of uptake of 42K+ by the islets of Langerhans, though this was not the case for secretion in response to tolbutamide. Ouabain significantly inhibited the uptake of 42K+ by islet tissue. 3. No significant increase in the rate of efflux of 42K+ was demonstrated during active insulin secretion. 4. Slices of rabbit pancreas were incubated in media of different K+ content, and rates of insulin release were determined. Alteration of the K+ concentration of the medium between 3 and 8mm had no effect on the rate of insulin release by pancreas slices. However, decrease of the K+ concentration to 1mm resulted in inhibition of secretion in response to both glucose and to tolbutamide. Conversely, an increase in K+ concentration increased rates of insulin release in response to both these stimuli. 5. It is concluded that, though unphysiological concentrations of K+ may influence the secretion of insulin, fluxes of K+ in the islets do not appear to be important in the initiation of insulin secretion.


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

1975 ◽  
Vol 78 (3) ◽  
pp. 524-530 ◽  
Author(s):  
O. García Hermida ◽  
J. Gómez-Acebo

ABSTRACT The insulin components released from normal and tolbutamide treated islets of the rat were studied in a perifusion system. The treated islets showed diminished quantities of insulin secreted as compared to the controls and an increase in the proportions of "big insulin" secreted during the second phase of this release. On the other hand, the main component of insulin released during the first phase was "little insulin". These studies confirm that the subtotally degranulated islets are less efficient than the controls in producing insulin release.


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

Diabetes ◽  
1979 ◽  
Vol 28 (3) ◽  
pp. 204-207 ◽  
Author(s):  
P. Schauder ◽  
C. McIntosh ◽  
J. Arends ◽  
H. Frerichs

2006 ◽  
Vol 190 (3) ◽  
pp. 681-693 ◽  
Author(s):  
Henrik Mosén ◽  
Albert Salehi ◽  
Ragnar Henningsson ◽  
Ingmar Lundquist

We have studied the influence of nitric oxide (NO) and carbon monoxide (CO), putative messenger molecules in the brain as well as in the islets of Langerhans, on glucose-stimulated insulin secretion and on the activities of the acid α-glucoside hydrolases, enzymes which we previously have shown to be implicated in the insulin release process. We have shown here that exogenous NO gas inhibits, while CO gas amplifies glucose-stimulated insulin secretion in intact mouse islets concomitant with a marked inhibition (NO) and a marked activation (CO) of the activities of the lysosomal/vacuolar enzymes acid glucan-1,4-α-glucosidase and acid α-glucosidase (acid α-glucoside hydrolases). Furthermore, CO dose-dependently potentiated glucose-stimulated insulin secretion in the range 0.1–1000 μM. In intact islets, the heme oxygenase substrate hemin markedly amplified glucose-stimulated insulin release, an effect which was accompanied by an increased activity of the acid α-glucoside hydrolases. These effects were partially suppressed by the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one. Hemin also inhibited inducible NO synthase (iNOS)-derived NO production probably through a direct effect of CO on the NOS enzyme. Further, exogenous CO raised the content of both cGMP and cAMP in parallel with a marked amplification of glucose-stimulated insulin release, while exogenous NO suppressed insulin release and cAMP, leaving cGMP unaffected. Emiglitate, a selective inhibitor of α-glucoside hydrolase activities, was able to markedly inhibit the stimulatory effect of exogenous CO on both glucose-stimulated insulin secretion and the activityof acid glucan-1,4-α-glucosidase and acid α-glucosidase, while no appreciable effect on the activities of other lysosomal enzyme activities measured was found. We propose that CO and NO, both produced in significant quantities in the islets of Langerhans, have interacting regulatory roles on glucose-stimulated insulin secretion. This regulation is, at least in part, transduced through the activity of cGMP and the lysosomal/vacuolar system and the associated acid α-glucoside hydrolases, but probably also through a direct effect on the cAMP system.


1973 ◽  
Vol 29 (7) ◽  
pp. 881-882 ◽  
Author(s):  
Brigitte Ziegler ◽  
R. Butter ◽  
H. -J. Hahn ◽  
R. Mehling ◽  
H. Fiedler

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