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缺铁大鼠的血浆甲状腺激素动力学发生改变。

Plasma thyroid hormone kinetics are altered in iron-deficient rats.

作者信息

Beard J L, Brigham D E, Kelley S K, Green M H

机构信息

Nutrition Department, The Pennsylvania State University, University Park, PA 16802, USA.

出版信息

J Nutr. 1998 Aug;128(8):1401-8. doi: 10.1093/jn/128.8.1401.

DOI:10.1093/jn/128.8.1401
PMID:9687562
Abstract

Iron deficiency anemia is associated with lower plasma thyroid hormone concentrations in rodents and, in some studies, in humans. The objective of this project was to determine if plasma triiodothyronine (T3) and thyroxine (T4) kinetics were affected by iron deficiency. Studies were done at a near-thermoneutral temperature (30 degrees C), and a cool environmental temperature (15 degrees C), to determine plasma T3 and T4 kinetics as a function of dietary iron intake and environmental need for the hormones. Weanling male Sprague-Dawley rats were fed either a low Fe diet [iron-deficient group (ID), <5 microg/g Fe] or a control diet [control group (CN), 35 microg/g Fe] at each temperature for 7 wk before the tracer kinetic studies. An additional ID group receiving exogenous thyroid hormone replacement was also used at the cooler temperature. For T4, the disposal rate was >60% lower (89 +/- 6 vs. 256 +/- 53 pmol/h, P < 0.001) in ID rats than in controls at 30 degrees C, and approximately 40% lower (192 +/- 27 vs. 372 +/- 26 pmol/h, P < 0.01) in ID rats at 15 degrees C. Exogenous T4 replacement in a cohort of ID rats at 15 degrees C normalized the T4 concentration and the disposal rate. For T3, the disposal rate was significantly lower in ID rats in a cool environment (92 +/- 11 vs. 129 +/- 11 pmol/h, P < 0.01); thyroxine replacement again normalized the T3 disposal rate (126 +/- 12 pmol/h). Neither liver nor brown fat thyroxine 5'-deiodinase activities were sufficiently different to explain the lower T3 disposal rates in iron deficiency. Thus, plasma thyroid hormone kinetics in iron deficiency anemia are corrected by simply providing more thyroxine. This suggests a central regulatory defect as the primary lesion and not peripheral alterations.

摘要

缺铁性贫血与啮齿动物以及在一些研究中与人类较低的血浆甲状腺激素浓度有关。本项目的目的是确定血浆三碘甲状腺原氨酸(T3)和甲状腺素(T4)的动力学是否受缺铁影响。研究在接近热中性温度(30摄氏度)和凉爽环境温度(15摄氏度)下进行,以确定血浆T3和T4动力学作为膳食铁摄入量和激素环境需求的函数。在示踪动力学研究前7周,将断奶雄性Sprague-Dawley大鼠在每个温度下分别喂食低铁饮食[缺铁组(ID),铁含量<5微克/克]或对照饮食[对照组(CN),铁含量35微克/克]。在较凉爽温度下还使用了一个接受外源性甲状腺激素替代的额外ID组。对于T4,在30摄氏度时,ID大鼠的处置率比对照组低>60%(89±6对256±53皮摩尔/小时,P<0.001),在15摄氏度时,ID大鼠的处置率约低40%(192±27对372±26皮摩尔/小时,P<0.01)。在15摄氏度时,一组ID大鼠接受外源性T4替代后,T4浓度和处置率恢复正常。对于T3,在凉爽环境中,ID大鼠的处置率显著较低(92±11对129±11皮摩尔/小时,P<0.01);甲状腺素替代再次使T3处置率恢复正常(126±12皮摩尔/小时)。肝脏和棕色脂肪的甲状腺素5'-脱碘酶活性差异均不足以解释缺铁时较低的T3处置率。因此,缺铁性贫血时血浆甲状腺激素动力学通过简单地提供更多甲状腺素即可得到纠正。这表明中枢调节缺陷是主要病变,而非外周改变。

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