Defects of signal transduction in a tumoral islet cell line

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Abstract
Introduction Most genetic defects so far identified in pancreatic islet cells concern the pathway of proinsulin biosynthesis and conversion (Chan et al., 1979 1986; Gabbay et al., 1979). The present review refers to a line of tumoral islet cells, namely RINm5F cells (Gazdar et al., 1980), in which several site-specific biochemical and functional anomalies have been identified over recent years. Anomaly in hexose transport D-glucose represents, under physiological conditions, the major, albeit not the sole, regulator of insulin release. It is currently believed that the identification of D-glucose as an insulin secretagogue is tightly and causally linked to the capacity of the hexose to be metabolized and to augment the rate of ATP generation in the pancreatic B-cell (Malaisse et al., 1979). Several rather specific features of D-glucose metabolism in normal islet cells are well suited to this glucose-sensing role. The first of these features consists of the rapid equilibration of D-glucose concentration across the B-cell plasma membrane (Hellman et al, 1971). The following findings indicate that hexose transport is perturbed in tumoral islet cells. The first indication for a deficiency of hexose transport in the RINm5F cells was obtained in a study of 3-O-methyl-D-[U-14C]glucose uptake (Malaisse et al9 1986). Results obtained at different temperatures, at various concentrations of the hexose and over different times of incubation indicated that the uptake of 3-O-methyl-D-[U-14C]glucose represents a temperature-sensitive and saturable process, so that no rapid equilibration of hexose concentrations across the plasma membrane was reached, especially at low temperature and/or high concentrations of 3-O-methyl-D-glucose.

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