Physiological effects of nutrients on insulin release by pancreatic beta cells

2021 ◽  
Author(s):  
Monica Losada-Barragán
Keyword(s):  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Physiological Effects

Tetraethylammonium modifies gap junctions between pancreatic beta-cells

1981 ◽  
Vol 240 (3) ◽  
pp. C116-C120 ◽  
Author(s):  
M. S. Sheppard ◽  
P. Meda
Keyword(s):  
Beta Cell ◽  
Gap Junctions ◽  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Freeze Fracture ◽  
Potassium Conductance ◽  
Median Number ◽  
Rat Islets Of Langerhans ◽  
Gap Junctional

Gap junctions between pancreatic beta-cells were quantitatively assessed in freeze-fracture replicas of isolated rat islets of Langerhans incubated for 90 min with or without the potassium conductance blocker tetraethylammonium (TEA). The results show that TEA increases the median number of particles per beta-cell gap junction but not the frequency of gap junctions at both nonstimulating and threshold-stimulating concentrations of glucose. TEA increased the relative gap junctional area at both concentrations of glucose. TEA had no effect on insulin release at a basal concentration of glucose but potentiated that release at the threshold glucose level. Thus TEA modifies beta-cell gap junctions independently of its effect on insulin release. However, the junctional changes observed were greater when insulin release was also elevated.

2089268 Ultrasound Stimulation of Insulin Release From Pancreatic Beta Cells

2015 ◽  
Vol 41 (4) ◽  
pp. S65 ◽  
Author(s):  
Ivan Mauricio Suarez Castellanos ◽  
Aleksandar Jeremic ◽  
Vesna Zderic
Keyword(s):  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Ultrasound Stimulation ◽  
Stimulation Of

scholarly journals Ablation of AMP-activated protein kinase α1 and α2 from mouse pancreatic beta cells and RIP2.Cre neurons suppresses insulin release in vivo

Diabetologia ◽  
2010 ◽  
Vol 53 (5) ◽  
pp. 924-936 ◽  
Author(s):  
G. Sun ◽  
A. I. Tarasov ◽  
J. McGinty ◽  
A. McDonald ◽  
G. da Silva Xavier ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Amp Activated Protein Kinase

scholarly journals Glucose induces oscillatory Ca2+ signalling and insulin release in human pancreatic beta cells

Diabetologia ◽  
1994 ◽  
Vol 37 (S2) ◽  
pp. S11-S20 ◽  
Author(s):  
B. Hellman ◽  
E. Gylfe ◽  
P. Bergsten ◽  
E. Grapengiesser ◽  
P. E. Lund ◽  
...  
Keyword(s):  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells

Furosemide reduces insulin release by inhibition of Cl- and Ca2+ fluxes in beta-cells

1988 ◽  
Vol 255 (5) ◽  
pp. E591-E596 ◽  
Author(s):  
P. E. Sandstrom ◽  
J. Sehlin
Keyword(s):  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Calcium Uptake ◽  
Influx Rate ◽  
Low Concentrations ◽  
Reduced Gradient ◽  
36Cl Fluxes ◽  
High Doses ◽  
Equilibrium Content

The effect of furosemide on insulin release, glucose oxidation, 36Cl- fluxes, and 45Ca2+ uptake was studied in isolated, beta-cell-rich pancreatic islets from ob/ob mice. Low concentrations of furosemide (0.01-0.1 mM) reduced the glucose-induced insulin release, whereas high doses (1-10 mM) increased basal and glucose-induced release. Furosemide at concentrations that reduced glucose-induced insulin release (0.01-0.1 mM) did not affect the islet production of 14CO2 from D-[U-14C]glucose. The influx rate and equilibrium content of 36Cl- were reduced by furosemide, whereas the basal and glucose-stimulated 36Cl- efflux rates were unaffected. The glucose-induced (10 mM) uptake of 45Ca2+ was inhibited by furosemide. It is suggested that the diabetogenic action of furosemide may be due, at least in part, to direct inhibition of insulin release from the pancreatic beta-cells. This may be caused primarily by inhibition of an inwardly directed Cl- pump, leading to a reduced transmembrane electrochemical gradient for chloride in the beta-cells. This reduced gradient in combination with unaltered Cl- permeability may lead to decreased total outward Cl- transport, a factor associated with stimulated calcium uptake and insulin release.

Sign in / Sign up

Export Citation Format

Share Document