Insulin induces cation fluxes and increases intracellular calcium in the HTC rat hepatoma cell line
Cell surface tyrosine kinase-linked receptors mediate the cellular response to certain hormones, with insulin being a common example. In liver cells, the primary physiological role of insulin is to participate in the control of carbohydrate, lipid and protein metabolism. In addition, insulin induces a slow depolarization of membrane potential in primary cultured rat hepatocytes and antagonizes glucagon-evoked hyperpolarization in the isolated perfused rat liver. Insulin also promotes cation influx into liver cells by unspecified mechanisms, and this effect is important for its metabolic actions. The action of insulin on cytosolic calcium, on the other hand, is more controversial. The hormone increases cytosolic calcium in vascular smooth muscle cells and has no effect on intracellular calcium in a skeletal muscle cell line, whereas contradictory results have been reported in adipocytes. Finally, recent results from our laboratory have shown that insulin increases steady state intracellular calcium in primary cultured rat hepatocytes by promoting an influx of the ion from the extracellular milieu. However, the mechanisms by which insulin triggers membrane potential change and calcium influx in liver cells remain unclear.
The pathway(s) of calcium entry into liver cells is still an area of active investigation. In hepatocytes, there is no evidence for the presence of voltage-activated calcium channels, whether by functional experiments or at the mRNA level. Recent studies have demonstrated the presence of nonselective cation channels (NSCC) on the surface of isolated rat hepatocytes and of the HTC model liver cell line. The channels exhibit slope conductances of 18 and 28 pS, can use sodium, potassium or calcium ions equally well as charge carriers, and their open probability depends on the cytosolic calcium concentration but not on membrane voltage. Under physiological conditions, these channels are thought to mediate largely sodium and calcium influx into liver cells. A previous report using HTC cells also demonstrated that NSCCs are inhibited by nickel and SKF96365 but not by verapamil, properties that correspond to store depletion-triggered calcium influx in primary rat hepatocytes. However, the conductive pathways responsible for the cation influx induced by insulin into liver cells have not been explored.
The present study aimed to determine the mechanisms by which insulin modulates hepatocellular electrophysio- logical membrane properties and influences intracellular calcium.
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