Abstract. A method based on the principle of gel separation followed by antibody extraction (GSAE) has been developed for isolation of radioactive thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2), 3',5'-diiodothyronine (3',5'-T2) and 3'-monoiodothyronine (3'-T1) in serum. This method was used for the estimation of the metabolic clearance rate (MCR) of the iodothyronines using the single injection, non-compartmental approach, and was compared to the conventional trichloroacetic acid precipitation/ethanol extraction (TCA-E) technique. The GSAE method excluded the co-determination of radioactive iodine and iodoproteins, whereas the co-determination of radiolabelled daughter iodothyronines was found negligible. The relative difference of duplicate estimations of MCR was approximately 10%. Using the TCA-E method for isolation of tracer, the MCR of T4, T3 and rT3 was underestimated to a minor degree (20%), whereas the MCRs of 3,3'-T2, 3',5'-T2 and 3'-T1 were 20–40% of those estimated by the GSAE method. In conclusion the GSAE method was found suitable for kinetic studies of iodothyronines, whereas the TCA-E method cannot be used for turnover studies of 3,3'-T2, 3',5'-T2 or 3'-T1.

A new method for the estimation of the bioavailability of thyroxine (T4) and 3,5,3\m='\-triiodothyronine (T3) is described based on gel separation followed by antibody extraction of labelled T4 and T3 from serum, and using the area under the curve of disappearance of the tracer (AUC) for the calculations. The peak serum concentrations of radioactive labelled T4 and T3 were reached approximately 90 min after oral administration of both tracers. The relative difference of duplicate estimations was below 10% (n = 3). The bioavailability of T4 in 6 euthyroid controls was in median 65% (range 64\p=n-\75%),and it was significantly increased both in hyperthyroidism (88% (75\p=n-\99%), n = 6, P < 0.01) and hypothyroidism (84% (67\p=n-\100%), n = 6, P<0.02).The bioavailability of T3 in 6 euthyroid controls was in median 78% (69\p=n-\99%) and significantly greater than that of T4 (P < 0.02). The bioavailability was unaffected by hyperthyroidism (79% (61\p=n-\98%), n = 9) and hypothyroidism (77% (66\p=n-\97%), n = 7). No significant difference between T4 and T3 bioavailabilities was found in hyper-or hypothyroidism. The clinical implication of the present study is that the bioavailability of T4 and T3 is almost identical and approximately 80% in patients with severe hypothyroidism.Most previous studies on the bioavailability of thy¬ roxine (T4) and 3,5,3'-triiodothyronine (T3) have used the double isotope technique as introduced by Hays (Hays 1968(Hays , 1970Read et al. 1970;Wenzel & Kirschsieper 1977). The bioavailability was calcu¬ lated from the ratio between 125I and 131I labelled iodothyronine as estimated at a time when equilibrium between iv and orally administrated iodo¬ thyronine was assumed. Radioactive labelled iodo¬ thyronine was measured as the total serum radio¬ activity which comprises inorganic iodine, iodoproteins, T4 and T3, and their metabolites. This approach resulted in a considerable variation of individual T4 bioavailability, which was apparently only partly explained by the dose of T4 given, its form of preparation, and whether or not the subjects were fasting (Hays 1968; Wenzel & Kirsch¬ sieper 1977). Only one study had dealt with the bioavailability of T3 and although it generally was found to be high it seemed to decrease from 95 to 79%, 4 and 24 h, respectively, after the administra¬ tion of T3 (Hays 1970).In patients with hyperthyroidism and hypothy¬ roidism T4 bioavailability is comparable to that in controls (Hays 1968;Read et al. 1970) whereas no data are available on the bioavailability of T3 in thyroid disorders.We have evaluated the bioavailability of T4 and T3 in normal subjects and in patients with un¬ treated hyper-and hypothyroidism by estimating the total area under the curve of disappearance (AUC) of radioactive labelled T4 and T3 after simultaneous oral and iv administration. Further¬ more we have isolated the tracers in serum from radioactive iodine, iodoproteins and daughter iodothyronines by means of a technique based on gel separation followed by antibody extraction (Faber et a...

Abstract. The C-peptide and insulin secretory responses to increasing doses of iv glucagon (1, 2, 5, 10 μg/kg body weight and I mg (only diabetics)) were investigated in six lean non-insulin-dependent diabetic patients and six normal subjects, matched for body weight and fasting blood glucose concentrations. A well defined relationship between glucagon dose and the C-peptide/insulin response was observed in both groups. The course of the dose-response curves was significantly different in diabetics. The maximal obtainable C-peptide response (E-max) was reduced to 53% of the response in normal subjects (P = 0.037), and the insulin response was reduced to 52% (P = 0.014). E-max was reached in diabetics with only 10 μg/kg of glucagon, whereas higher doses seem to be needed in the control group. However, the glucagon dose causing 50% of E-max (ed50) was not significantly higher. Thus, the widely accepted use of 1 mg of glucagon to test residual beta cell function secures a maximal response of both insulin and C-peptide in non-insulin-dependent diabetic subjects. In addition, our data support the theory that beta cell deficiency is a basic feature of non-insulin-dependent diabetes.