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Submitted on May 19, 2005
Accepted on August 29, 2005
Department of Endocrinology and Metabolism, Department of Experimental and Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam; Department of Internal Medicine, Erasmus MC, Rotterdam, the Netherlands
* To whom correspondence should be addressed. E-mail: a.boelen{at}amc.uva.nl.
During illness, changes in thyroid hormone metabolism occur, so-called Nonthyroidal Illness (NTI). NTI has been characterized by a fall of serum T3 due to decreased extrathyroidal conversion of T4 into T3 by liver type 1 deiodinase (D1), without an increase in serum TSH. Type 3 deiodinase (D3) was thought not to play an important role during NTI but recently it has been shown that D3 activity is up-regulated in liver and skeletal muscle of critically ill patients related to hypoxia. We studied D3 gene expression and activity in liver and muscle/subcutis of mice during illness, which was induced by two different stimuli; bacterial endotoxin (LPS) administration resulting in an acute systemic response, and a turpentine injection in each hindlimb resulting in a local subcutaneous abscess.
LPS induced a rapid decrease in liver D1 and D3 activity but not in skeletal muscle of hindlimb. In contrast, local inflammation induced by turpentine did not decrease liver D1 and D3 activity but increased markedly D3 activity in the muscle/subcutis sample containing the abscess, associated with strongly increased IL-1
and IL-6 mRNA expression. Inflammatory cells, surrounding the abscess showed D3 and T3-transporter MCT8 immunoreactivity while muscle cells did not show any immunoreactivity.
In conclusion, local inflammation strongly induces D3 activity in inflammatory cells, especially in invading polymorphonuclear granulocytes, suggesting enhanced local degradation of T3.
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