Using the adjacent histologically normal tissues obtained from the same patients as controls, six human lung tumors were studied for the activities of epidermal growth factor (EGF) receptor binding, and receptor autophosphorylation. There was a 1.2- to 2.8-fold increase in EGF receptor activities in lung tumors due to an increase in the number of receptors without changes in their affinity. The increase had no direct correlation with the degree of differentiation or the type of lung tumors. The elevated expression of EGF receptor may be one of the characteristics in lung tumors. Epidermal growth factor and its receptor also may play a role in the regulatory mechanisms during tumorigenesis.

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Triton X-100 strongly affects the receptor binding and autophosphorylation of insulin and epidermal growth factor (EGF) in rat liver Golgi fractions and partially purified microsomal receptors. At concentration 0.05% Triton X-100 decreased the insulin receptor binding by 15% and the EGF receptor binding by 70% as compared to controls. In contrast, 0.05% Triton X-100 increased insulin-stimulated receptor autophosphorylation by more than 370% as compared to 87% in the control. Similarly, the same concentration of Triton X-100 increased the EGF-stimulated receptor phosphorylation by 65% as compared to 14% in the control. EGF receptor binding was more sensitive to the treatment of Triton. At Triton concentrations 0.2% or more, the EGF receptor binding was totally abolished while the insulin receptor binding was decreased by 50%. On the other hand, the activity of ligand-stimulated receptor phosphorylation of both insulin and EGF receptors was only slightly decreased in the presence of 0.2% Triton.

In rats, a moderately hepatotoxic single dose of diethylnitrosamine (DEN) 100 mg/kg causing depletion of liver glycogen, elevation of aspartate aminotransferase and decreased liver uptake of 3-O-methylglucose, resulted in substantial changes in insulin and glucagon balance. Two days after DEN, insulin binding to liver membranes and insulin removal by the liver were sharply reduced whereas its binding to muscle and adipocyte membranes remained unaltered. Serum insulin (random and after an overnight fast) remained normal. Intravenous (I.V.) insulin (10 U/kg) caused the usual degree of hypoglycemia that, however, lasted longer than in the control animals. Removal of glucagon by liver was also depressed in spite of its normal binding to hepatocytes, and peripheral serum glucagon was increased three-fold. I.V. glucagon (40 micrograms/kg) resulted in a blunted response of plasma glucose. I.V. glucose tolerance test (1 g/kg) remained normal in spite of the insulin increase to a level twice as high as in the controls, and in spite of nonsuppressed glucagon. These changes were still present after 1-3 months, but disappeared by 6 months. The results demonstrate remarkable ability of homeostatic mechanisms to preserve normal plasma glucose and glucose tolerance in spite of dramatic changes in insulin and glucagon.