| Autor: |
Schröder-van der Elst, Janny P, van der Heide, Daan, DiStefano, Joe J, van der Bent, Chris, Kaptein, Ellen, Visser, Theo J |
| Zdroj: |
European Journal of Endocrinology; March 1997, Vol. 136 Issue: 3 p324-329, 6p |
| Abstrakt: |
Treatment of rats with phenytoin (DPH), an anti-epileptic drug, results in lower tissue thyroid hormone (TH) levels and interferes with the metabolic pathway of TH. To test the hypothesis that DPH affects the enterohepatic cycle of TH and, thus, the kinetics of TH turnover, we performed a kinetic experiment (three-compartment analysis) and a steady-state, double-isotope equilibrium experiment in rats treated for 3 weeks with DPH (50 mg/kg body weight per day) and in untreated controls. This included measurements of TH and TH metabolite levels, as well as the activities of enzymes involved in the TH metabolic pathway.DPH treatment resulted in a decrease in the production of thyroxine (T4) (by 25%) and triiodothyronine (T3) (by 37%), a decrease in the T3concentration in all three pools, and a redistribution of T4from the fast to the slow pool. The amount of T4increased in intestinal contents and feces by 66% and 71% respectively. Expressed as a fraction of daily TH disposal, fecal loss of T4was enhanced from 10 to 23% and that of T3from 16 to 21%. An increase in T4and T3UDP-glucuronyltransferase activities was observed, suggesting that the increased fecal loss of T4and T3is secondary to an increased biliary output of their glucuronides. The reduced secretion of TH and increased fecal clearance during DPH treatment can lead in the long run to depletion of TH stores.European Journal of Endocrinology136324–329 |
| Databáze: |
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