Measurement of Intracellular T3 and T3 disposal in normal subjects.
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Biomedical subjects
Publications and source records attributed to R Docter.
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Binding of 125I-labelled triiodothyronine (T3) to rat liver and kidney cytosol was examined. In both organs a very similar binding protein was detected. The apparent equilibrium association constants amounted to 4.8 X 10(7) M-1 for the liver protein and to 1.8 X 10(7) M-1 for the kidney protein. In the two organs a high capacity for T3 binding was observed: maximal binding capacities of respectively 4.3 and 33.2 pmol per mg total cytosol protein. Displacement studies using thyroid hormone analogues showed that the binding exhibited similar specificity.
Three groups of patients who had undergone subtotal thyroidectomy for Graves's disease, toxic multinodular goitre, or euthyroid multinodular goitre 12 to 15 years before and in whom a normal serum thyroxine (T-4) level was found were each divided into two subgroups on the basis of a normal or a raised serum thyrotrophin concentration. There was no difference in mean serum T-4 concentration between patients with normal and those with raised serum thyrotrophin concentrations, and the values were similar to the mean T-4 values of the normal population. The mean serum triiodothyronine values of all groups were higher than normal, but the mean values of the groups with a normal and a raised serum thyrotrophin were similar. After thyroidectomy a mildly raised serum thyrotrophin does not in itself indicate the presence of hypothyroidism.
A highly specific radioimmunoassay for the measurement of pGlu-His-Pro-OH (TRH-OH), a compound proposed to be a metabolite of pGlu-His-Pro-NH2 (TRH) has been developed. Using this assay experiments have been performed to study the inactivation of TRH and TRH-OH by serum. The results show that TRH-OH is inactivated in a fashion resembling the inactivation of TRH as has been described by others. Support for the deamidation mechanism as the main pathway for TRH degradation could not be achieved.
LATS was measured with the double isotope technique in IgG serum concentrates of 23 patients with Graves' disease before treatment and of 18 patients during treatment with carbimazole and triiodothyronine. LATS activity was present in 18 out of 23 patients before treatment (78%). When the second measurement was taken into account the incidence did increase to 95%. No difference could be found in the mean values of total thyroxine, thyroid 131-I uptake and thyroid weight of the group of LATS positive and LATS negative patients before treatment. Also no relation could be established between LATS activity and suppressibility of thyroid 131-I uptake during treatment. It was found that LATS positive patients who suppress during therapy have lower initial LATS blood levels than LATS positive patients who remain unsuppressed. It is concluded that it is more likely that LATS is a "marker" of Graves' disease rather than the cause of the hyperthyroidism.
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