The levels of insulin-like growth factors (IGF), two somatomedin-like polypeptides of human serum and of their carrier protein were determined in sera of patients with various metabolic disorders. IGF was measured by 4 different methods (fat pad and fat cell assay and competitive protein binding assay measuring total IGF, and a radioimmunoassay for IGF I) after extraction by acidic gel filtration on Sephadex G-50. This procedure is necessary to separate IGF from the carrier protein, which interferes with all of these assays.
1) In normal serum, immunoreactive IGF I accounts for one third of total IGF determined by the fat pad assay, but only for one fifth to one sixth of immunoreactive IGF I + II.
2) In acromegalics total IGF was increased 1.5- (protein binding and fat cell assay) to 2-fold (fat pad assay), but the increase was solely due to immunoreactive IGF I, which was ∼ 5-times above normal. The IGF binding activity was not elevated. Total IGF and IGF binding were decreased in hypopituitarism, Laron-type dwarfism and in liver cirrhosis. Immunoreactive IGF I was more drastically reduced in these diseases than total IGF. Apparently, only IGF I is under growth hormone control. The liver seems to be involved in the production of IGF.
3) No elevation of total IGF was found in patients with extrapancreatic tumour hypoglycaemia, but IGF binding was reduced. Immunoreactive IGF I was decreased in 5 of 10 patients. These results suggest that tumour hypoglycaemia in our patients is unlikely to be caused by increased IGF levels.
4) In patients with hyperprolactinaemia neither total IGF nor immunoreactive IGF I were elevated, and IGF binding was unchanged.
5) In newly detected insulin-deficient juvenile diabetics total IGF and immunoreactive IGF I levels were within the normal range, although the variation was greater than in normal subjects. However, IGF binding was markedly decreased.