Fekete Csaba, Sarkar Sumit, Christoffolete Marcelo A, Emerson Charles H, Bianco Antonio C, Lechan Ronald M
Tupper Research Institute and Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Tufts-New England Medical Center, 750 Washington St., Boston, MA 02111, USA.
Brain Res. 2005 Sep 14;1056(1):97-9. doi: 10.1016/j.brainres.2005.07.021.
By administration of bacterial lipopolysaccharide (LPS) to intact and T4-replaced thyroidectomized rats, we demonstrate that in contrast to the cortex and anterior pituitary, there is a persistent increase in type 2 iodothyronine deiodinase (D2) activity in the mediobasal hypothalamus (MBH). We propose that endotoxin-induced D2 activation in the MBH is independent of circulating levels of thyroid hormone and that this mechanism may contribute to central hypothyroidism associated with infection.
通过对完整大鼠和接受T4替代的甲状腺切除大鼠注射细菌脂多糖（LPS），我们证明，与皮质和垂体前叶不同，中基底下丘脑（MBH）中2型碘甲状腺原氨酸脱碘酶（D2）的活性持续增加。我们提出，MBH中内毒素诱导的D2激活独立于甲状腺激素的循环水平，并且该机制可能导致与感染相关的中枢性甲状腺功能减退。
