Thyroid hormones are of crucial importance for the functioning of nearly every 
organ. Remarkably, disturbances of thyroid hormone synthesis and function are 
among the most common endocrine disorders affecting approximately one third of 
the working German population. Over the last ten years our understanding of 
biosynthesis and functioning of these hormones has increased tremendously. This 
includes the identification of proteins involved in thyroid hormone biosynthesis 
like Thox2 and Dehal where mutations in these genes are responsible for certain 
degrees of hypothyroidism. One of the most important findings was the 
identification of a specific transporter for triiodothyronine (T3), the 
monocarboxylate transporter 8 (MCT8) responsible for directed transport of T3 
into target cells and for export of thyroid hormones out of thyroid epithelial 
cells. Genetic disturbances of MCT8 in patients result in a biochemical 
constellation of high T3 levels in combination with low or normal TSH and 
thyroxine levels leading to a new syndrome of severe X-linked mental 
retardation. Importantly mice lacking MCT8 presented only with a mild phenotype, 
indicating that compensatory mechanisms exist in mice. Moreover, it has become 
clear that not only genomic actions of T3 exist. T3 is also capable to activate 
adhesion receptors and it signals via activation of PI3K and MAPK pathways. Most 
recently, thyroid hormone derivatives were identified, the thyronamines which 
are decarboxylated thyroid hormones initiating physiological actions like 
lowering body temperature and heart rate, thereby acting in opposite direction 
to the classical thyroid hormones. So far it is believed that thyronamines 
function via the activation of a G-protein coupled receptor, TAAR1. The 
objective of this review is to summarise the recent findings in thyroid hormone 
synthesis and action and to discuss their implications for diagnosis of thyroid 
disease and for treatment of patients.