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Canadian Journal of Gastroenterology
Volume 14, Issue 5, Pages 389-396
Original Article

Insulin Induces Cation Fluxes and Increases Intracellular Calcium in the HTC Rat Hepatoma Cell Line

Laurence Mathé,1 Diane Vallerand,1 and Pierre S Haddad1,2

1Groupe de Recherche en Transport Membranaire et Départements de pharmacologie, Université de Montréal, Montréal, Québec, Canada
2Groupe de Recherche en Transport Membranaire et Départements de physiologie, Université de Montréal, Montréal, Québec, Canada

Received 5 January 2000; Revised 20 March 2000

Copyright © 2000 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


BACKGROUND/AIMS: Rat hepatoma HTC cells were used to study conductive pathways implicated in insulin-induced cation and calcium influx into liver cells.

METHODS: Membrane potentials and currents were measured by whole-cell patch clamp. Cytosolic calcium was measured using FURA-2 fluorescence.

RESULTS: Insulin induced a gradual and reversible depolarization of 5.7±0.8 mV. Insulin-induced currents showed a linear slope conductance of 663 pS and a reversal potential of  -17.9 mV. Ion substitution experiments showed that these currents were composed mainly of a nonselective cation component. In FURA-2 experiments, insulin caused a slow monophasic rise in HTC cell calcium, which depended on the presence of extracellular calcium. Insulin also induced significant increases of 1.58- and 1.54-fold in basal calcium influx when studied by external calcium withdrawal and readmission, or by the manganese quench method, respectively. Using the latter approach, we found that 100 µM gadolinium and 10 µM SKF96365 blocked the rise of  the basal manganese quench rate induced by insulin whereas 100 µM verapamil was without effect.

CONCLUSIONS: Insulin induces inward cation currents that depolarize HTC cell membrane potentials and participate in increased calcium influx.