Fasting is known to promote a shift in the conversion of thyroxine (T4), more being deiodinated to an inactive form, reverse triiodothyronine (rT3), and less to active triiodothyronine (T3). The mechanism behind this change is not known, but it has recently been demonstrated that the proportion of dietary carbohydrates influences the serum concentration of T3 and rT3. Therefore, it is possible that the deiodination of T4 is subordinated to gastroenterohepatic regulation.
To explore this possibility, we administrated glucose by the oral or the intravenous route to volunteers, who had been fasted for 48 h. It was found that glucose normalized the low fasting T3 concentrations only after oral administration. This supports the assumption that some gastro-enterohepatic factor participates in the regulation of T3 formation.