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A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
Published on: July 16, 2016
Insulin-like growth factors in patients with nonislet cell tumors and hypoglycemia
Insulin-like growth factors (IGF) in serum from 3 patients with nonislet cell tumors and hypoglycemia were measured by radioimmunoassay and by means of a rat liver membrane assay (specific for IGF II). The concentration of IGF II by receptor assay was greater than normal when the samples were initially assayed, but subsequently decreased 48% to 80% over the next 8 to 15 weeks. In the same serum samples, concentrations of both IGF I and IGF II by radioimmunoassay were consistently less than normal. In all 3 patients growth hormone (GH) responses to intravenous arginine were depressed and in 2 of the 3 patients, a GH-dependent 150 K serum protein carrier of IGF was absent. None of these abnormalities were seen in 7 patients with insulinomas and chronic hypoglycemia. The data suggest that some patients with nonislet cell tumors and hypoglycemia produce a receptor-active, nonimmunoreactive IGF-II-like material. This material appears (a) more labile than normal IGF II and (b) capable of inhibiting GH secretion. The latter effect may decrease immunoreactive IGF I and II, as well as decrease the GH-dependent 150 K protein carrier of these factors. The extreme lability of the IGF-II-like material produced by tumors probably explains the previous contradictory reports on this topic.
Insulin-like growth factors (IGF) in serum from 3 patients with nonislet cell tumors and hypoglycemia were measured by radioimmunoassay and by means of a rat liver membrane assay (specific for IGF II). The concentration of IGF II by receptor assay was greater than normal when the samples were initially assayed, but subsequently decreased 48% to 80% over the next 8 to 15 weeks. In the same serum samples, concentrations of both IGF I and IGF II by radioimmunoassay were consistently less than normal. In all 3 patients growth hormone (GH) responses to intravenous arginine were depressed and in 2 of the 3 patients, a GH-dependent 150 K serum protein carrier of IGF was absent. None of these abnormalities were seen in 7 patients with insulinomas and chronic hypoglycemia. The data suggest that some patients with nonislet cell tumors and hypoglycemia produce a receptor-active, nonimmunoreactive IGF-II-like material. This material appears (a) more labile than normal IGF II and (b) capable of inhibiting GH secretion. The latter effect may decrease immunoreactive IGF I and II, as well as decrease the GH-dependent 150 K protein carrier of these factors. The extreme lability of the IGF-II-like material produced by tumors probably explains the previous contradictory reports on this topic.
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