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In recent tracer studies utilizing I131 labeled insulin, in vivo and in vitro metabolic degradation of the labeled insulin has generally been presumed to parallel the disappearance of protein precipitable radioactivity and the appearance of non-precipitable radioactivity (1, 2). The present investigations were prompted by the paucity of data on the metabolic fate of insulin in human subjects and the need for a more specific identification of insulin-I'13 in blood and tissues than has heretofore been employed. The methods developed during this study have permitted quantitative evaluation of the rate of insulin-I'13 metabolism and have led to the discovery of an insulin-transporting globulin in the blood of insulin treated subjects. Regular crystalline insulin 4 was iodinated by the method of Pressman and Eisen (3) (Method A) or by Newerly's modification of their method as previously described (4) (Method B). Insulin-I13. supplied by Abbott Laboratories was also employed in some experiments. The insulin-I.3. solutions prepared in our laboratory were dialyzed against distilled water with frequent changes for 24 to 72 hours, acidified to pH 3.0 with HCl, maintained sterile by the addition of phenol and cultured before use. These lots of insulin-I.3. contained an average of 0.1 to 1.0 iodine atoms per molecule, 12,000 molecular weight, insulin. As deduced from the blood sugar responses in fasting rabbits following intravenous administration of labeled and unlabeled insulin, there was no obvious loss in hypoglycemic potency as a result of the

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In normal subjects, hypoglycemia produces an abrupt and sustained rise in levels of human growth hormone in plasma. This effect is independent of insulin, glucagon, or epinephrine. Prolonged fasting is accompanied by a rise in the hormone level in plasma. Measurement of this hormone after induced hypoglycemia is a specific test for pituitary somatotropic function.