The results from the work of Krenning and Docter in our laboratory, as discussed in previous sections, led to the hypothesis that inhibition of transmembraneous transport of iodothyronines, could be a major factor in inducing the hormonal changes in the low T 3 syndrome. A three-pool model of distribution and metabolism ofT 4, T 3 and rT 3 was used for kinetic analysis. Two conditions in which a low T 3 syndrome is known to originate, were studied: caloric deprivation and oral administration of propranolol. Chapter 2 deals with alterations in kinetic parameters during caloric deprivation in 10 obese subjects. The same parameters were assessed in six normal non-obese L-T4 replaced male students before and during D- propranolol treatment. The results obtained in this latter group are presented in chapter 3. In chapter 4 early serum disappearance and computed liver uptake of thyroxine in humans during caloric deprivation and D-propranolol administration are discussed. In addition, both parameters were assessed immediately after intravenous administration of fructose, a manoeuvre by which a prompt and significant fall in liver A TP is induced. In chapter 5 the results from the above mentioned sections are summarized.

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Erasmus University Rotterdam
G. Hennemann (George)
hdl.handle.net/1765/51063
Erasmus MC: University Medical Center Rotterdam

van der Heyden, J. T. M. (1988, October 19). Cellular mechanisms in the generation of the low T3 syndrome. Retrieved from http://hdl.handle.net/1765/51063