Abstract

The intracellular thyroid hormone (TH) availability is influenced by different metabolic pathways. Some of the changes in intracellular TH availability can be linked to changes in local deiodination and sulfation capacities. The secretion of the chicken thyroid consists predominantly of thyroxine (T 4). TH receptors (TRs) preferentially bind 3,5,3′-triiodothyronine (T 3). Therefore, the metabolism of T 4 secreted by the thyroid gland in peripheral tissues, resulting in the production and degradation of receptor-active T 3, plays a major role in thyroid function. Food restriction in growing chickens increases hepatic type III deiodinase (D3) levels but decreases growth hormone (GH)-dependent variables such as plasma insulin-like growth factor-I (IGF-I) and T 3 concentrations. Refeeding restores hepatic D3 and plasma T 3 to control levels within a few hours. It can be concluded that the tissue and time dependent regulation of the balance between TH activating and inactivating enzymes plays an essential role in the control of local T 3 availability and hence in TH activity. Two separate genes encode multiple TR isoforms, i.e. TRα and TRβ. These TRs consist of a DNA-binding domain, a ligand-binding domain, a hinge region and an amino-terminal (A/B) domain. TRs mediate their effects on transcription by binding as homodimers or heterodimers to the TH response elements (TREs). Also, unliganded TRs can bind to TREs and may so modulate transcription of target genes.

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