The influence of K+-induced membrane depolarization on insulin secretion in islets of lean and obese (ob/ob) mice

1990 ◽  
Vol 68 (1) ◽  
pp. 243-248 ◽  
Author(s):  
Linda A. Fournier ◽  
H. M. C. Heick ◽  
Nicole Bégin-Heick
Keyword(s):  
Insulin Secretion ◽  
Membrane Potential ◽  
Glucose Metabolism ◽  
Pertussis Toxin ◽  
Similar Response ◽  
Obese Mice ◽  
Induced Membrane ◽  
Voltage Dependent ◽  
Insulin Secretory Response ◽  
Altered Sensitivity

The present study was undertaken to determine whether factors that affect K+ permeability produce differences in insulin secretion in the islets of obese versus lean mice. At basal glucose (3 mM), the obese islets secreted more insulin for a given increment in depolarizing K+ concentration and responded to a wider range of K+ concentrations (5–45 mM) than the lean islets (5–25 mM). In contrast, the membrane potential changes induced by increments in pK+ were not significantly different in the two types of islets. The islets of lean and obese mice treated with pertussis toxin showed a qualitatively similar response to glucose and to epinephrine, but only the control and pertussis toxin treated obese islets responded to K+ depolarization when deprived of calcium. Abnormal responses to quinine and apamin were identified in the islets of obese mice. These findings show that the abnormal insulin secretory response of the obese islet is due, at least in part, to a defect independent of glucose metabolism. This is best explained by an altered sensitivity of voltage-dependent events, most likely the result of differential effects of an intracellular element acting on ATP-sensitive and Ca2+-activated K+ channels, both of which are implicated in membrane repolarization.Key words: pertussis toxin, voltage-activated Ca2+ channels, ATP-sensitive K+ channels, membrane potential.

scholarly journals Anoctamin 1 (Ano1) is required for glucose-induced membrane potential oscillations and insulin secretion by murine β-cells

2015 ◽  
Vol 468 (4) ◽  
pp. 573-591 ◽  
Author(s):  
Raphaël Crutzen ◽  
Myrna Virreira ◽  
Nicolas Markadieu ◽  
Vadim Shlyonsky ◽  
Abdullah Sener ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Membrane Potential ◽  
Β Cells ◽  
Anoctamin 1 ◽  
Potential Oscillations ◽  
Induced Membrane ◽  
Membrane Potential Oscillations

Intermittent protein–calorie malnutrition in the young rat causes long-term impairment of the insulin secretory response to glucose in vitro

1988 ◽  
Vol 118 (2) ◽  
pp. 295-302 ◽  
Author(s):  
I. Swenne ◽  
C. J. Crace ◽  
L. Jansson
Keyword(s):  
Insulin Secretion ◽  
Glucose Concentration ◽  
Secretory Response ◽  
Similar Response ◽  
Protein Calorie Malnutrition ◽  
Early Protein ◽  
Low Glucose ◽  
Old Rats ◽  
C And N ◽  
Insulin Secretory Response

ABSTRACT The effect of a limited period of protein–calorie malnutrition in young rats on insulin secretion in the adult has been studied. Three-week-old rats were weaned onto diets containing 5% protein (low protein; LP) or 15% protein (control; C) and maintained for 3 weeks on their respective diets. A third experimental group was weaned onto standard rat chow (18% protein; normal diet; N). From 6 weeks of age onwards all rats were fed the standard rat chow. Pancreatic islets were isolated from rats aged 3, 6 and 12 weeks and their insulin secretory response to glucose or arginine was tested. At 12 weeks the effects of the secretagogues were also tested using perfusion of isolated pancreatic glands. In islets from 6-week-old LP rats the glucose-stimulated insulin release was only 25% of that of C and N rats of the same age. Islets from C and N rats responded to arginine in the presence of a low glucose concentration with a small increase in insulin secretion, whereas no such response could be demonstrated in islets from 6-week-old LP rats. Islets from 6- and 12-week-old N rats responded to glucose and arginine. Islets from 12-week-old C rats had a similar response to glucose but did not respond to arginine in the presence of a low glucose concentration. In islets from 12-week-old LP rats the secretory response to glucose remained only 40% that of C and N rats and there was no response to arginine in the presence of a low glucose concentration. The observations on the secretory response of isolated islets from 12-week-old rats were paralleled by similar findings with the perfused, isolated pancreas. It is concluded that protein–calorie malnutrition early in life persistently impairs the insulin secretory response of the B cell. The individual may, as a consequence, have a lowered ability to respond to nutritional and diabetogenic challenges and it is thus possible that early protein–calorie malnutrition predisposes for diabetes. J. Endocr. (1988) 118, 295–302

scholarly journals Different insulin-secretory responses to calcium-channel blockers in islets of lean and obese (ob/ob) mice

1988 ◽  
Vol 249 (2) ◽  
pp. 401-407 ◽  
Author(s):  
M A Black ◽  
L A Fournier ◽  
H M Heick ◽  
N Bégin-Heick
Keyword(s):  
Insulin Secretion ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Potent Inhibitor ◽  
Secretory Activity ◽  
Obese Mouse ◽  
Channel Blockers ◽  
Obese Mice ◽  
Voltage Dependent ◽  
Glucose Stimulated Insulin Secretion

The purpose of these experiments was to determine whether the activity of the voltage-dependent Ca2+ channel was modulated in the same manner in islets of the ob/ob mouse as in islets of homozygous lean mice of the same strain. The effect of agents that are known to alter the concentrations and movements of intracellular Ca2+ were investigated in relation to glucose-stimulated insulin secretion and in relation to the effect of forskolin. In islets of obese mice, verapamil and nifedipine both inhibited glucose-induced insulin release, nifedipine being the more potent inhibitor. Forskolin-stimulated secretion was inhibited either not at all (verapamil) or much less (nifedipine) in islets of the ob/ob mouse compared with those of lean mice. At basal glucose concentrations, verapamil initiated insulin secretion in islets of the ob/ob mouse and acted synergistically with forskolin to evoke a secretory activity that was 3-fold greater than that evoked by 20 mM-glucose. Nifedipine also initiated secretion at basal glucose concentrations and acted synergistically with forskolin, but its effect was considerably smaller than that of verapamil. A comparison of the effect of forskolin in the presence of Ca2+-channel blockers and in the absence of Ca2+ suggests that, in the obese mouse, the operation of the voltage-dependent Ca2+ channel is impaired.

Bofutsushosan Improves Gut Barrier Function with a Bloom of Akkermansia Muciniphila and Improves Glucose Metabolism in Diet-Induced Obese Mice

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1990-P ◽  
Author(s):  
SHIHO FUJISAKA ◽  
ISAO USUI ◽  
ALLAH NAWAZ ◽  
YOSHIKO IGARASHI ◽  
TOMONOBU KADO ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Barrier Function ◽  
Obese Mice ◽  
Gut Barrier ◽  
Akkermansia Muciniphila ◽  
Gut Barrier Function

Effect of multiple doses of cadmium on glucose metabolism and insulin secretion in the rat

1975 ◽  
Vol 31 (1) ◽  
pp. 143-149 ◽  
Author(s):  
Dionyssis S. Ithakissios ◽  
Taghi Ghafghazi ◽  
John H. Mennear ◽  
Wayne V. Kessler
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Multiple Doses

Effects of ouabain on background and voltage-dependent currents in canine colonic myocytes

1990 ◽  
Vol 259 (3) ◽  
pp. C402-C408 ◽  
Author(s):  
E. P. Burke ◽  
K. M. Sanders
Keyword(s):  
Membrane Potential ◽  
Potential Gradient ◽  
Circular Muscle ◽  
Input Resistance ◽  
Pump Current ◽  
Muscle Layer ◽  
Membrane Properties ◽  
Resting Potential ◽  
Voltage Dependent ◽  
In Cells

Previous studies have suggested that the membrane potential gradient across the circular muscle layer of the canine proximal colon is due to a gradient in the contribution of the Na(+)-K(+)-ATPase. Cells at the submucosal border generate approximately 35 mV of pump potential, whereas at the myenteric border the pump contributes very little to resting potential. Results from experiments in intact muscles in which the pump is blocked are somewhat difficult to interpret because of possible effects of pump inhibitors on membrane conductances. Therefore, we studied isolated colonic myocytes to test the effects of ouabain on passive membrane properties and voltage-dependent currents. Ouabain (10(-5) M) depolarized cells and decreased input resistance from 0.487 +/- 0.060 to 0.292 +/- 0.040 G omega. The decrease in resistance was attributed to an increase in K+ conductance. Studies were also performed to measure the ouabain-dependent current. At 37 degrees C, in cells dialyzed with 19 mM intracellular Na+ concentration [( Na+]i), ouabain caused an inward current averaging 71.06 +/- 7.49 pA, which was attributed to blockade of pump current. At 24 degrees C or in cells dialyzed with low [Na+]i (11 mM), ouabain caused little change in holding current. With the input resistance of colonic cells, pump current appears capable of generating at least 35 mV. Thus an electrogenic Na+ pump could contribute significantly to membrane potential.

The Effects of Sevoflurane Anesthesia on Insulin Secretion and Glucose Metabolism in Pigs

1997 ◽  
Vol 84 (6) ◽  
pp. 1359-1365 ◽  
Author(s):  
Shozo Saho ◽  
Yoshitami Kadota ◽  
Teruko Sameshima ◽  
Junko Miyao ◽  
Takeshi Tsurumaru ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Sevoflurane Anesthesia

Magnesium requirement for somatostatin inhibition of insulin secretion

1984 ◽  
Vol 105 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Donald L. Curry ◽  
Leslie L. Bennett
Keyword(s):  
Insulin Secretion ◽  
Calcium Concentration ◽  
Inhibitory Effect ◽  
Secretory Process ◽  
Magnesium Ion ◽  
Second Phase ◽  
Intracellular Membrane ◽  
Calcium Magnesium ◽  
First Phase Insulin Secretion ◽  
Insulin Secretory Response

Abstract. Rat pancreas perfusions were performed using a perfusate with a fixed calcium concentration of 5 mEq/l and magnesium varying from 0 to 0.6 mEq/dl. Insulin secretion was stimulated by a constant glucose infusion of 300 mg/dl. This glucose concentration produces the typical biphasic insulin secretory response. We observed that in the absence of magnesium, somatostatin concentrations of 0.5 and 2.0 ng/ml were without effect on first phase insulin secretion. However, these same somatostatin levels produced 50% or more inhibition of insulin secretion in the presence of magnesium at 0.3 or 0.6 mEq/l. Similarly, in the absence of magnesium, somatostatin at 50 ng/ml failed to inhibit second phase insulin secretion, whereas this same somatostatin level produced about 50% inhibition of insulin secretion in the presence of magnesium at 0.3 mEq/l. Thus, altering perfusate magnesium concentrations without changing calcium is an important determinant of the degree of inhibition of secretion produced by somatostatin. In particular, in the absence of magnesium ion, somatostatin concentrations which would 'normally' produce 50% inhibition of secretion (ID50) are without effect. Therefore, magnesium ion is necessary for the full inhibitory effect of somatostatin to occur. These results suggest that inhibitors, as well as potentiators, of the insulin secretory process may act by altering intracellular/membrane calcium-magnesium ratios, but in opposite directions.

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