RESUMEN
Thyroid hormones (TH) and somatotropin (ST) play critical role in lactation. One explanation of their multiple physiological actions is based on the functional interrelationships among ST, TH, and thyroxin deiodinase (5'D). This enzyme is present in the mammary tissue, milk cellular components, and whole milk and is responsible for intramammary production of triiodothyronine (T3). In rats in which the 5'D isozymes in the mammary gland and in the liver are similarly of type I (5'D-I), an enhancement of mammary 5'D-I causes a reduction of hepatic 5'D-I activities. This opposite rearrangement in the mammary and hepatic deiodinating activities is thought to be a factor of a homeorhetic response characterized by an increased and compartmentalized energy expenditure of the mammary gland. In the cow, the mammary 5'D is the type II (5'D-II) deiodinase. The 5'D-II, owing to its high catalytic efficiency, secures T3 production, making tissues relatively independent from the circulatory levels of TH and from variations in the hepatic 5'D-I activity. No significant alterations of 5'D-II isozymes were found during a low T3 syndrome. Location of tissue deiodinases in the cow, the 5'D-II in the mammary gland, and the 5'D-I in the liver make it so that T3 production in these two tissues can be dissociated in time to secure better local requirement for T3 supporting lactation. To date, attempts to evidence that the alterations in iodothyronines blood levels and in tissues' 5'Ds activity during lactation are due to ST action have not received clear experimental support in either cows or rats.