期刊
NATURE CLINICAL PRACTICE ENDOCRINOLOGY & METABOLISM
卷 4, 期 3, 页码 148-155出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncpendmet0727
关键词
critical illness; D3; deiodinase; euthyroid sick syndrome; low-T-3 syndrome
资金
- NIDDK NIH HHS [R01 DK076099, DK76099, R56 DK058538, DK65055, R01 DK065055-03, R01 DK065055, R01 DK077148, R01 DK077148-01, DK58538, R01 DK058538, DK77148, R01 DK058538-10] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK077148, R01DK058538, R01DK065055, R01DK076099] Funding Source: NIH RePORTER
Thyroid hormones influence gene expression in virtually all vertebrate tissues. Precise regulation of the active endogenous ligand, 3,5,3'-triiodothyronine (T-3), is achieved by the sequential removal of iodine moieties from the thyroid hormone molecule. Type III iodothyronine deiodinase (D3) is the major inactivating enzyme terminating the action of T-3 and preventing activation of the prohormone, thyroxine (T-4). Recent studies have revealed the induction of high D3 activity in diverse animal models of tissue injury including starvation, cryolesion, cardiac hypertrophy, infarction, and chronic inflammation. By analyzing serum and tissues taken from hospitalized patients at the time of death, investigators have also documented the robust induction of D3 activity in several human tissues that normally have none, including the liver and skeletal muscle, and shown clinically relevant consequences to systemic thyroid status. These studies reveal a novel role of D3 in the tissue response to injury and in the derangement of thyroid hormone homeostasis commonly observed during critical illness.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据