tailieunhanh - Thyroid hormone metabolism in poultry

Respiratory disease complex: Under field conditions, pathogens often interact with not only the host (bird) and its environment, but also one another. For example, day-old chicks arriving infect- ed from the hatchery (vertical transmission) and remaining chroni- cally infected for life are susceptible to other respiratory diseases such as infectious bronchitis or Newcastle disease. Fine dust parti- cles in the poultry house air can then combine with superinfection by Escherichia coli bacteria contribute to additional respiratory in- sults, which will produce the (multiple) lesions that are seen at autopsy for complex respiratory disease. Field disease interactions often also involve common immunosuppressive agents, such as. | B A S E Biotechnol. Agron. Soc. Environ. 2000 4 1 13-20 Thyroid hormone metabolism in poultry Veerle M. Darras Serge Van der Geyten Eduard R. Kuhn Laboratory of Comparative Endocrinology. Zoological Institute. Katholieke Universiteit Leuven. 61 Naamsestraat B-3000 Leuven Belgium . E-mail Received 10 November1999 accepted 23 December 1999. Thyroid hormone TH receptors preferentially bind 3 5 3 -triiodothyronine T3 . Therefore the metabolism of thyroxine T4 secreted by the thyroid gland in peripheral tissues resulting in the production and degradation of receptor-active T3 plays a major role in thyroid function. The most important metabolic pathway for THs is deiodination. Another important pathway is sulfation which is a reversible pathway that has been shown to interact with TH deiodination efficiency. The enzymes catalysing TH deiodination consist of three types. Type I deiodinase D1 catalyses both outer ring ORD and inner ring deiodination IRD . Type II deiodinase D2 only catalyses ORD while type III D3 only catalyses IRD. The three chicken deiodinase cDNAs have been cloned recently. These enzymes all belong to the family of selenoproteins. Ontogenetic studies show that the availability of deiodinases is regulated in a tissue specific and developmental stage dependent way. Characteristic for the chicken is the presence of very high levels of T3 inactivating D3 enzyme in the embryonic liver. Hepatic D3 is subject to acute regulation in a number of situations. Both growth hormone and glucocorticoid injection rapidly decrease hepatic D3 levels hereby increasing plasma T3 without affecting hepatic D1 levels. The inhibition of D3 seems to be regulated mainly at the level of D3 gene transcription. The effect of growth hormone on D3 expression persists throughout life while glucocorticoids start to inhibit hepatic D1 expression in posthatch chickens. Food restriction in growing chickens increases hepatic D3 levels. This contributes to .