Document Detail

Mice with hepatocyte-specific deficiency of type 3 deiodinase have intact liver regeneration and accelerated recovery from nonthyroidal illness after toxin-induced hepatonecrosis.
MedLine Citation:
PMID:  25004090     Owner:  NLM     Status:  Publisher    
Type 3 deiodinase (D3), the physiologic inactivator of thyroid hormones, is induced during tissue injury and regeneration. This has led to the hypotheses that D3 impacts injury tolerance by reducing local T3 signaling and contributes to the fall in serum triiodothyronine (T3) observed in up to 75 of sick patients (termed the low T3 syndrome). Here we show that a novel mutant mouse with hepatocyte-specific D3 deficiency has normal local responses to toxin-induced hepatonecrosis, including normal degrees of tissue necrosis and intact regeneration, but accelerated systemic recovery from illness-induced hypothyroxinemia and hypotriiodothyroninemia, demonstrating that peripheral D3 expression is a key modulator of the low T3 syndrome.
Luciana A Castroneves; Rebecca H Jugo; Michelle A Maynard; Jennifer S Lee; Ari J Wassner; David Dorfman; Roderick T Bronson; Chinweike Ukomadu; Agoston T Agoston; Lai Ding; Cristina Luongo; Cuicui Guo; Huaidong Song; Valeriy Demchev; Nicholas Y Lee; Henry A Feldman; Kristen R Vella; Roy W Peake; Christina Hartigan; Mark D Kellogg; Anal Desai; Domenico Salvatore; Monica Dentice; Stephen A Huang
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-7-8
Journal Detail:
Title:  Endocrinology     Volume:  -     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2014 Jul 
Date Detail:
Created Date:  2014-7-8     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  en20132028     Citation Subset:  -    
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