The uptakes of thyroablative doses of 131I by postoperative thyroid remnants and/or thyroid carcinoma metastases following diagnostic surveys with 131I or 123I were retrospectively compared by visual inspection. Only those patients with a diagnostic scan demonstrating functioning tissue, remnant, and/or metastasis, following thyroidectomy for differentiated thyroid carcinoma, were evaluated. The 131I survey group (n = 26) had received a diagnostic dose of 3 to 10 mCi of 131I. The 123I group (n = 14) had received the usual diagnostic dose of 300 microCi of 123I. The age, sex, and tumor type in the two groups were not statistically different. The uptake of the ensuing thyroablative dose of 131I appeared, by visual inspection, to be impaired in 20 of 26 patients in the 131I group and in none of the 14 patients in the 123I group (p < 0.00003). In the 131I group there was suggestion of a dose-response, that is, the higher the administered activity of 131I for the diagnostic scan, the more reduced was the subsequent apparent uptake of the thyroablative dose (p = 0.0007). Thyroid remnants or cervical lymph node metastases appeared to be affected more frequently than were the distant (pulmonary or skeletal) metastases (p = 0.004). This study suggests that iodine uptake function may be suppressed by the absorbed radiation from the 3 to 10 mCi "diagnostic" scanning dose of 131I. In this regard, 123I may be a better initial diagnostic agent to be used prior to radioablation therapy.

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Several compounds known to alter receptor-mediated endocytosis were tested for their effect on insulin action in isolated rat hepatocytes. Dansylcadaverine blocked the inhibitory effect of insulin on hepatic protein degradation, but was without effect on the inhibition produced by high concentrations of amino acids. Dansylcadaverine also was without effect on the stimulatory action of insulin on glucose incorporation into glycogen, but totally blocked the insulin stimulation of alanine uptake. No inhibition of basal or (Bu)2cAMP-stimulated alanine uptake was observed with dansylcadaverine. These results indicate that dansylcadaverine has selective effects on some but not all of insulin's actions. Methylamine also blocked insulin stimulation of alanine transport, although at higher doses, methylamine decreased basal and (Bu)2cAMP-stimulated uptake due to cellular toxicity. Chloroquine, an inhibitor of intracellular insulin processing, had no effect on insulin-stimulated alanine transport. To examine the site of action of dansylcadaverine on insulin processing, the binding (cell-associated radioactivity) and degradation of [125I]iodoinsulin by hepatocytes were examined in the presence and absence of dansylcadaverine. Dansylcadaverine delayed the time required to achieve maximal insulin binding and produced a dose-dependent decrease in cell-mediated insulin degradation. Acid dissociation and proteolytic digestion methods were used to differentiate between [125I]iodoinsulin bound to the cell surface vs. that which had been internalized. Dansylcadaverine did not block internalization as measured by either of these criteria, but did block the increase in cell-associated radioactivity produced by chloroquine, suggesting that dansylcadaverine blocks insulin processing after internalization but before the chloroquine-sensitive step. These data show that some of the hepatic actions of insulin, namely inhibition of protein degradation and stimulation of alanine transport, are blocked by certain inhibitors of cellular hormone processing, suggesting that these actions of insulin may require postreceptor events involving insulin metabolism.

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