Significance of ionic fluxes and changes in membrane potential for stimulus-secretion coupling in pancreatic B-cells

1984 ◽  
Vol 40 (10) ◽  
pp. 1043-1052 ◽  
Author(s):  
J. C. Henquin ◽  
H. P. Meissner
Keyword(s):  
Membrane Potential ◽  
B Cells ◽  
Ionic Fluxes ◽  
Pancreatic B Cells ◽  
Stimulus Secretion Coupling

scholarly journals Two sites of glucose control of insulin release with distinct dependence on the energy state in pancreatic B-cells

1994 ◽  
Vol 297 (3) ◽  
pp. 455-461 ◽  
Author(s):  
P Detimary ◽  
P Gilon ◽  
M Nenquin ◽  
J C Henquin
Keyword(s):  
Membrane Potential ◽  
B Cells ◽  
Insulin Release ◽  
Cell Function ◽  
Energy State ◽  
Secretory Process ◽  
High K ◽  
Pancreatic B Cells ◽  
Stimulus Secretion Coupling ◽  
Intracellular Targets

The energy state of pancreatic B-cells may influence insulin release at several steps of stimulus-secretion coupling. By closing ATP-sensitive K+ channels (K(+)-ATP channels), a rise in the ATP/ADP ratio may regulate the membrane potential, and hence Ca2+ influx. It may also modulate the effectiveness of Ca2+ on its intracellular targets. To assess the existence of these two roles and determine their relative importance for insulin release, we tested the effects of azide, a mitochondrial poison, on mouse B-cell function under various conditions. During stimulation by glucose alone, when K(+)-ATP channels are controlled by cellular metabolism, azide caused parallel, concentration-dependent (0.5-5 mM), membrane repolarization, decrease in cytosolic Ca2+ concentration [Ca2+]i and inhibition of insulin release. When K(+)-ATP channels were closed pharmacologically (by tolbutamide in high glucose), azide did not repolarize the membrane or decrease [Ca2+]i, and was much less effective in inhibiting insulin release. A similar resistance to azide was observed when K(+)-ATP channels were opened by diazoxide, and high K+ was used to depolarize the membrane and raise [Ca2+]i. In contrast, azide similarly decreased ATP levels and increased ADP levels, thereby lowering the ATP/ADP ratio under all conditions. In conclusion, lowering the ATP/ADP ratio in B-cells can inhibit insulin release even when [Ca2+]i remains high. However, this distal step is much more resistant to a decrease in the energy state of B-cells than is the control of membrane potential by K(+)-ATP channels. Generation of the signal triggering insulin release, high [Ca2+]i, through metabolic control of membrane potential requires a higher global ATP/ADP ratio than does activation of the secretory process itself.

Effects of Phe-Met-Arg-Phe-NH2 (FMRFa)-Related Peptides on Na-Ca Exchange and Ionic Fluxes in Rat Pancreatic B Cells

1996 ◽  
Vol 779 (1) ◽  
pp. 288-289
Author(s):  
F. EYLEN ◽  
P. GOURLET ◽  
A. VANDERMEERS ◽  
P. LEBRUN ◽  
A. HERCHUELZ
Keyword(s):  
B Cells ◽  
Ionic Fluxes ◽  
Pancreatic B Cells

scholarly journals Potassium dependence of the membrane potential of pancreatic B-cells

FEBS Letters ◽  
1978 ◽  
Vol 94 (1) ◽  
pp. 87-89 ◽  
Author(s):  
H.P. Meissner ◽  
J.C. Henquin ◽  
M. Preissler
Keyword(s):  
Membrane Potential ◽  
B Cells ◽  
Pancreatic B Cells

The effects of nitric oxide on the membrane potential and ionic currents of mouse pancreatic B cells.

Endocrinology ◽  
1995 ◽  
Vol 136 (12) ◽  
pp. 5363-5369 ◽  
Author(s):  
P Krippeit-Drews ◽  
K D Kröncke ◽  
S Welker ◽  
G Zempel ◽  
M Roenfeldt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Membrane Potential ◽  
B Cells ◽  
Ionic Currents ◽  
Pancreatic B Cells
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