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Mono A14-[125I]-iodoinsulin was incubated with cultured endothelial cells derived from bovine pulmonary arteries at physiologic conditions. The processing of the cell-bound A14-[125I]-iodoinsulin was evaluated by trichloroacetic acid precipitation, gel filtration and high performance liquid chromatography. In contrast to insulin processing in many other cell types, approximately 95% of cell bound insulin was dissociated from the cells in less than 15 minutes, and biologically intact insulin rapidly passed through the endothelial cells. The unique location of endothelial cells coupled with the ability of rapid transport of intact insulin are consistent with an endothelial role for either the transport of insulin out of the bloodstream or as an extra-pancreatic storage area for insulin.

The erythrocyte (RBC) has received recent interest as a cell model to examine insulin receptor status in humans. In the present study we have compared the insulin receptors on mature RBCs and monocytes of four hyperinsulinemic obese patients in the fed state and after a 14-day fast (less than 50 cal/day). Insulin binding in the basal (fed) state was described in RBC and monocytes due predominantly to a decrease in the receptor concentration in both cell types. After a 14-day fast, insulin binding to both RBCs and monocytes increased significantly in each patient. Maximal binding of [125I]iodoinsulin to RBCs increased by 29% (range, 20-46%), and binding to monocytes increased by 116% (range, 46-321%). In response to the fast, the concentration of insulin needed to inhibit binding by 50% decreased from 5 to 2 ng/ml in RBC and from 3 to 1 ng/ml in monocytes. Conventional and computer-fitted Scatchard analyses demonstrated no change in the receptor concentration of RBCs of any patient, whereas the receptor concentration of monocytes increased by more than 50% in two of the four patients and by 40% for the group. Thus, in response to the fast, the direction of the change in insulin binding was similar in the RBCs and monocytes, whereas the magnitude and, in certain patients, the mechanism of the binding increase differed.