Andrea Győrffy

Effects of energy restriction on thyroid hormone metabolism in chickens

Energy restriction induces changes in thyroid hormone economy in the form of a complex adaptation mechanism, in order to conserve energy storage and protein reserves. In the present work, thyroid hormone serum concentrations, hepatic deiodinase enzyme activities and hepatic deiodinase mRNA expression were examined after feed restriction and fasting. We demonstrate that during energy restriction, T 3 concentration is lowered due to a decreased T 4 activation and increased T 3 inactivation. We show that hepatic type-I deiodinase (D1) is not affected by energy restriction, however, hepatic D2 is decreased on both transcriptional and enzyme activity levels. Furthermore, hepatic D3 is increased after feed restriction in the liver. We also show that the hypothalamic feedback is not involved in the changes in serum T 3 and T 4 concentrations. Our data indicate that D2 enzyme contributes to the special hormone-exporting role of the chicken liver and this enzyme can be modulated by feed restriction.

LIGAND-INDUCED CHANGES IN OESTROGEN AND THYROID HORMONE RECEPTOR EXPRESSION IN THE DEVELOPING RAT CEREBELLUM: A COMPARATIVE QUANTITATIVE PCR AND WESTERN BLOT STUDY

Oestrogen (E2) and thyroid hormones (THs) are key regulators of cerebellar development. Recent reports implicate a complex mechanism through which E2 and THs influence the expression levels of each others receptors (ERs and TRs) to precisely mediate developmental signals and modulate signal strength. We examined the modulating effects of E2 and THs on the expression levels of their receptor mRNAs and proteins in cultured cerebellar cells obtained from 7-day-old rat pups. Cerebellar granule cell cultures were treated with either E2, THs or a combination of these hormones, and resulting receptor expression levels were determined by quantitative PCR and Western blot techniques. The results were compared to non-treated controls and to samples obtained from 14-day-old in situ cerebella. Additionally, we determined the glial effects on the regulation of ER-TR expression levels. The results show that (i) ER and TR expression depends on the combined presence of E2 and THs; (ii) glial cells mediate the hormonal regulation of neuronal ER-TR expression and (iii) loss of tissue integrity results in characteristic changes in ER-TR expression levels. These observations suggest that both E2 and THs, in adequate amounts, are required for the precise orchestration of cerebellar development and that alterations in the ratio of E2/THs may influence signalling mechanisms involved in neurodevelopment. Comparison of data from in vitro and in situ samples revealed a shift in receptor expression levels after loss of tissue integrity, suggesting that such adjusting/regenerative mechanisms may function after cerebellar tissue injury as well.

Glycogenic induction of thyroid hormone conversion and leptin system activation in the liver of postpartum dairy cows

In the regulation of energy metabolism, the liver plays an important role in the reinforcement of energy production. In periparturient cows the energy homeostasis turns into a negative energy balance that may shift the physiological regulation of energy balance towards pathological processes. Propylene glycol (PG), as a complementary source of energy used in the nutrition of dairy cows, alters systemic thyroid hormone economy; however, the exact mechanism through which highly glycogenic feed supplements impact liver metabolism is little known. Previous studies showed that only leptin receptors are expressed in the liver of cows, and now we report that leptin mRNA is expressed in the liver of cows as well. The present results show that the mRNA of leptin and its receptors are differentially modulated by the increased energy content of the feed consumed. Simultaneous changes in hepatic type I deiodinase activity suggest that hepatic modulation of the leptin system by PG supplementation may be mediated by an increased local thyroxine-triiodothyronine conversion. Since PG supplementation with simultaneous T4-T3 turnover and increased hepatic leptin- and short-form leptin receptor mRNA were not associated with a significant change in hepatic total lipid levels, it is suggested that the leptin system, directly or indirectly modulated by thyroid hormones, may represent a local defence mechanism to prevent fatty liver formation.