T3 Binding Capacity Research Articles

Role of thyroxine-binding globulin in the early distribution of thyroxine and triiodothyronine.

ABSTRACT The thyroxine (T4)-binding capacity of the T4-binding globulin (TBG) affects the distribution within the body and the rate of disappearance from plasma of both labeled T4 and triiodothyronine (T3). Thus, estrogens, which increase T4-binding by TBG, reduce the hepatic incorporation, hepatic volume of distribution (VL) and hepatic clearance (CL) of both hormones in normal adults without altering the extrahepatic fractions of T4 or T3. Conversely, in 2 brothers who lack TBG, the hepatic uptake, VL and CL were much greater than in normals. We infer that increased T4-binding capacity is responsible for the reduced VL and CL produced by estrogens in normal subjects. The qualitatively similar effects of estrogens on the hepatic incorporation and VL of T3 show that TBG also influences the distribution of T3. Comparison of the rates of plasma disappearances of T3 and T4 with the rates of hepatic uptake suggests that the period of time from 20 to 50 min after injection reflects principally hepatic uptake o...

Effect of norethandrolone on the metabolism of 125-I-labeled thyroxine-binding prealbumin.

The effect of norethandrolone on the metabolism of 125I-labeled thyroxine (T4)- binding prealbumin (TBPA) has been assessed in 5 patients. Norethandrolone greatly increased the T4-binding capacity, and presumably the concentration, of TBPA in serum. This change was unaccompanied by any significant alteration in the volume of distribution, fractional rate of turnover, or rate of peripheral clearance of the labeled protein. Hence, the absolute rate of TBPA disposal was greatly increased, suggesting that the increased concentration induced by norethandrolone is the result of enhanced synthesis of the protein. Norethandrolone also decreased significantly the serum BEI and increased the proportion of free T4, changes which can be ascribed to the decrease in the T4-binding activity of TBG which norethandrolone induces. The possibility that the synthesis of TBG and TBPA are reciprocally regulated is discussed.

Effects of norethandrolone on the transport in serum and peripheral turnover of thyroxine.

The effects of the androgenicanabolic steroid, norethandrolone, on the binding of thyroxine (T4) in serum and on its peripheral metabolism in vivo have been studied in a total of 19 patients. In doses of 40 or 50 mg daily, norethandrolone decreased the T4-binding capacity of the thyroxine-binding globulin (TBG) and increased the binding capacity of the thyroxinebinding prealbumin (TBPA). The latter change was observed even when control values of the T4-binding capacity of TBPA were subnormal. Values for the serum PBI were also decreased by this agent. In 11 patients, norethandrolone increased the fractional rate of peripheral turnover of T4 and T4 clearance rate, but, because of the decrease in PBI, total daily T4 disposal was not significantly changed.

Polyacrylamide gel electrophoretic study on the effect of estrogen on human thyroxine-binding prealbumin.

Ethinyl estradiol was administered orally in a daily dose of 0.18-0.3mg for seven days to subjects with normal and abnormal thyroid function, and the changes of several parameters of the thyroid function during estrogen administration were investigated. The concentration and maximum T4 binding capacity of thyroxine-binding prealbumin (TBPA) were estimated by polyacrylamide gel electrophoresis. Estrogen increased the serum PBI value and the binding capacity of thyroxinebinding globulin (TBG), while it lowered Triosorb test value, elutable fraction and the concentration and binding capacity of TBPA. However, free T4 value, BMR, thyroidal 24-hour uptake of 131I and thyroidal effective half-life of 131I did not change. T4 half-life in serum was prolonged. These results show that ethinyl estradiol may have an effect at first on the metabolism of thyroxine-binding proteins. The concentration and binding capacity of thyroxine-binding proteins may increase as a whole. The fact that T4 half-life is prolonged and free T4 level stays as before in spite of the rise of PBI in estrogen administration might be due to suppressed decomposition of free T4. These results are observed equally in subjects with intact and abnormal thyroid functions, and it is concluded that these phenomena have no relation to the pituitary-thyroid system.