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Insulinlike growth factors bind to specific receptors in isolated pancreatic acini
Recently we have demonstrated the existence of specific receptors for insulin on pancreatic acini. Employing 125I-labeled insulinlike growth factors (IGFs) and insulin, we report the existence of distinct receptors for IGF-I and IGF-II on mouse pancreatic acini. Insulin competes with 125I-IGF-I with 1,000-fold less potency. By contrast, insulin increases the binding of 125I-IGF-II to its receptor. IGF in turn inhibits 125I-insulin binding to its receptor but with 250-fold less potency. Thus, distinct receptors exist on acini for IGF-I, IGF-II, and insulin. Moreover, IGF, like insulin, stimulates sugar transport by acini. The mechanism of IGF stimulation may be similar to insulin, as the effect of maximal concentrations of the two peptides when added together is not additive. These results raise the possibility, therefore, that IGFs may be a new class of physiological regulators of pancreatic acinar cell function.
Recently we have demonstrated the existence of specific receptors for insulin on pancreatic acini. Employing 125I-labeled insulinlike growth factors (IGFs) and insulin, we report the existence of distinct receptors for IGF-I and IGF-II on mouse pancreatic acini. Insulin competes with 125I-IGF-I with 1,000-fold less potency. By contrast, insulin increases the binding of 125I-IGF-II to its receptor. IGF in turn inhibits 125I-insulin binding to its receptor but with 250-fold less potency. Thus, distinct receptors exist on acini for IGF-I, IGF-II, and insulin. Moreover, IGF, like insulin, stimulates sugar transport by acini. The mechanism of IGF stimulation may be similar to insulin, as the effect of maximal concentrations of the two peptides when added together is not additive. These results raise the possibility, therefore, that IGFs may be a new class of physiological regulators of pancreatic acinar cell function.