Mice with hepatocyte-specific deficiency of type 3 deiodinase have intact liver regeneration and accelerated recovery from nonthyroidal illness after toxin-induced hepatonecrosis.

Abstract:

: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.

journal_name

Endocrinology

journal_title

Endocrinology

authors

Castroneves LA,Jugo RH,Maynard MA,Lee JS,Wassner AJ,Dorfman D,Bronson RT,Ukomadu C,Agoston AT,Ding L,Luongo C,Guo C,Song H,Demchev V,Lee NY,Feldman HA,Vella KR,Peake RW,Hartigan C,Kellogg MD,Desai A,Salvatore D

doi

10.1210/en.2013-2028

subject

Has Abstract

pub_date

2014-10-01 00:00:00

pages

4061-8

issue

10

eissn

0013-7227

issn

1945-7170

journal_volume

155

pub_type

杂志文章