Endocrinology, Vol 126, 1527-1533, Copyright © 1990 by Endocrine Society

ARTICLES

Inhibitors of glucose uptake stimulate the production of insulin-like growth factor-binding protein (IGFBP-1) by human fetal liver

MS Lewitt and RC Baxter
Department of Medicine, University of Sydney, New South Wales, Australia.

Cultured human fetal hepatic explants were used to study the role of hexose uptake in regulating production of the GH-independent insulin- like growth factor-binding protein (IGFBP-1). Cytochalasin B (100 microM), but not cytochalasin E, inhibited 2-deoxyglucose uptake by fetal liver explants and increased production of IGFBP-1 2-fold. Two agents which stimulate cyclic nucleotide-dependent pathways, cholera toxin and theophylline, also inhibited 2-deoxyglucose uptake in this system and both stimulated IGFBP-1 production. When added to a maximally inhibiting concentration of cytochalasin B (250 microM), hexose uptake was not further inhibited by theophylline (5 mM) or cholera toxin (10 micrograms/ml), suggesting that the three substances interact with the same hexose transport mechanism. However, the stimulatory effect of theophylline (5 mM) or cholera toxin (10 micrograms/ml) on IGFBP-1 production was additive to the effect of 250 microM cytochalasin B, suggesting that another pathway, possibly involving cyclic nucleotide accumulation, could further stimulate IGFBP- 1 above the effect of blocking glucose transport. Insulin (300 nM) had no effect on hexose uptake by human fetal liver explants but inhibited IGFBP-1 production, both basally and when stimulated by cytochalasin B (100 microM) or cholera toxin (1 microgram/ml). These results are consistent with the conclusion that a cyclic nucleotide-dependent pathway, activated by blocking hexose transport and inhibited by insulin, is involved in the regulation of IGFBP-1 synthesis.

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