scholarly journals Regulation of insulin secretion from islets of Langerhans rendered permeable by electric discharge

1982 ◽  
Vol 206 (1) ◽  
pp. 81-87 ◽  
Author(s):  
M. Adel Yaseen ◽  
Kevin C. Pedley ◽  
Simon L. Howell
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Electric Discharge ◽  
Significant Inhibition ◽  
Marker Enzyme ◽  
Ultrastructural Studies ◽  
Isolated Islets Of Langerhans ◽  
Vinblastine Sulphate

1. High-voltage electric discharge has been used to increase the permeability of B-cells of isolated islets of Langerhans to facilitate studies of the effects of normally impermeable substances on insulin secretion. 2. The application of an intense electric field increased the [14C]sucrose space of the islets from 37.8±3.1% to 86.2±5.2% of their total volume as assessed by 3H2O content. The cells remained permeable for at least 40min. 3. Ultrastructural studies showed no deleterious changes in the structure of the B-cells after discharge. 4. Insulin secretion from normal islets was unaffected by increasing the medium [Ca2+] from 10nm to 10μm. In the islets that had been rendered permeable by discharge, insulin secretion was significantly increased under these conditions, without any alteration in the release of lactate dehydrogenase, a cytoplasmic marker enzyme. 5. Studies of the dynamics of insulin release during perifusion showed that the response to increased (10μm) Ca2+ concentration was rapid and sustained over a period of at least 13min. 6. Secretion responses to Ca2+ in perifusion established that maximum release in permeabilized islets occurs at approx. 1μm-Ca2+ and half-maximum release occurs at approx. 0.6μm-Ca2+. 7. The study of the effect of agents that interfere with the microtubular microfilamentous system in B-cells using a perifusion system revealed that cytochalasin B caused a considerable increase, whereas vinblastine sulphate caused a significant inhibition, in insulin release in response to 1μm-Ca2+. 8. This technique should facilitate the study of the role of normally impermeable ions and metabolic intermediates in the regulation of insulin secretion.

scholarly journals A species difference in nucleoside phosphorylase activity and inosine-stimulated insulin secretion in isolated islets of Langerhans

1977 ◽  
Vol 168 (3) ◽  
pp. 591-593 ◽  
Author(s):  
I L Campbell ◽  
K W Taylor
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Species Differences ◽  
Species Difference ◽  
Isolated Islets ◽  
Phosphorylase Activity ◽  
Nucleoside Phosphorylase ◽  
Isolated Islets Of Langerhans

Inosine is a potent simulant of insulin release from rat but not from rabbit islets of Langerhans. Further investigation showed that nucleoside phosphorylase activity is exceptionally low in rabbit islets. The ability of inosine to promote insulin release seems to be related to islet nucleoside phosphorylase activity, which can display marked species differences.

scholarly journals Nitric oxide inhibits, and carbon monoxide activates, islet acid α-glucoside hydrolase activities in parallel with glucose-stimulated insulin secretion

2006 ◽  
Vol 190 (3) ◽  
pp. 681-693 ◽  
Author(s):  
Henrik Mosén ◽  
Albert Salehi ◽  
Ragnar Henningsson ◽  
Ingmar Lundquist
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Insulin Secretion ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Direct Effect ◽  
Appreciable Effect ◽  
Intact Mouse ◽  
Glucose Stimulated Insulin Secretion ◽  
Glucoside Hydrolases

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.

Insulin secretion in Walker 256 tumor cachexia

1990 ◽  
Vol 258 (6) ◽  
pp. E1033-E1036 ◽  
Author(s):  
L. C. Fernandes ◽  
U. F. Machado ◽  
C. R. Nogueira ◽  
A. R. Carpinelli ◽  
R. Curi
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Adult Male ◽  
Male Rats ◽  
Control Group ◽  
Tumor Bearing ◽  
Isolated Islets Of Langerhans ◽  
Outflow Rate ◽  
Walker 256 ◽  
Walker 256 Tumor

The effect of cachexia on insulin secretion was examined in adult male rats. Isolated islets of Langerhans from Walker 256 tumor-bearing rats secreted less insulin by glucose stimuli as compared with the control group; this was accompanied by significant change in 45Ca2+ outflow rate. Reduced insulin secretion to glucose stimuli in tumor-bearing rats probably led to low insulinemia (one-third). These findings indicate that reduced insulin secretion is probably an important factor for the development of cachexia in Walker 256 tumor-bearing rats.

scholarly journals The possible mechanisms by which phanoside stimulates insulin secretion from rat islets

2007 ◽  
Vol 192 (2) ◽  
pp. 389-394 ◽  
Author(s):  
Nguyen Khanh Hoa ◽  
Åke Norberg ◽  
Rannar Sillard ◽  
Dao Van Phan ◽  
Nguyen Duy Thuan ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
B Cells ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Pertussis Toxin ◽  
Insulin Response ◽  
Gk Rat ◽  
Isolated Pancreatic Islets ◽  
Gk Rats ◽  
Rat Islets

We recently showed that phanoside, a gypenoside isolated from the plant Gynostemma pentaphyllum, stimulates insulin secretion from rat pancreatic islets. To study the mechanisms by which phanoside stimulates insulin secretion. Isolated pancreatic islets of normal Wistar (W) rats and spontaneously diabetic Goto-Kakizaki (GK) rats were batch incubated or perifused. At both 3.3 and 16.7 mM glucose, phanoside stimulated insulin secretion several fold in both W and diabetic GK rat islets. In perifusion of W islets, phanoside (75 and 150 μM) dose dependently increased insulin secretion that returned to basal levels when phanoside was omitted. When W rat islets were incubated at 3.3 mM glucose with 150 μM phanoside and 0.25 mM diazoxide to keep K-ATP channels open, insulin secretion was similar to that in islets incubated in 150 μM phanoside alone. At 16.7 mM glucose, phanoside-stimulated insulin secretion was reduced in the presence of 0.25 mM diazoxide (P<0.01). In W islets depolarized by 50 mM KCl and with diazoxide, phanoside stimulated insulin release twofold at 3.3 mM glucose but did not further increase the release at 16.7 mM glucose. When using nimodipine to block L-type Ca2+ channels in B-cells, phanoside-induced insulin secretion was unaffected at 3.3 mM glucose but decreased at 16.7 mM glucose (P<0.01). Pretreatment of islets with pertussis toxin to inhibit exocytotic Ge-protein did not affect insulin response to 150 μM phanoside. Phanoside stimulated insulin secretion from Wand GK rat islets. This effect seems to be exerted distal to K-ATP channels and L-type Ca2+ channels, which is on the exocytotic machinery of the B-cells.

Insulin release from isolated islets of Langerhans of the rat in organ culture

1973 ◽  
Vol 29 (7) ◽  
pp. 881-882 ◽  
Author(s):  
Brigitte Ziegler ◽  
R. Butter ◽  
H. -J. Hahn ◽  
R. Mehling ◽  
H. Fiedler
Keyword(s):  
Organ Culture ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Isolated Islets ◽  
Isolated Islets Of Langerhans

scholarly journals Chromium-induced inhibition of insulin secretion from isolated Islets of Langerhans

Diabetologia ◽  
1980 ◽  
Vol 18 (3) ◽  
pp. 229-232 ◽  
Author(s):  
T. Ghafghazi ◽  
M. L. McDaniel ◽  
P. E. Lacy
Keyword(s):  
Insulin Secretion ◽  
Islets Of Langerhans ◽  
Isolated Islets ◽  
Isolated Islets Of Langerhans
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