Diarra A, Lefauconnier J M, Valens M, Georges P, Gripois D
Laboratoire d'Endocrinologie, Université Paris-Sud, Orsay, France.
Arch Int Physiol Biochim. 1989 Oct;97(5):317-32. doi: 10.3109/13813458909104543.
The influence of neonatal hypo- and hyperthyroidism on different aspects of tyrosine metabolism in the hypothalamus, striatum, brainstem, adrenal glands, heart and brown adipose tissue (BAT) were studied in 14-day old rats. The synthesis rate of catecholamines (CA) was also determined in vivo after the injection of labelled tyrosine. Hypothyroidism increases tyrosinaemia and endogenous tyrosine concentration in the hypothalamus and BAT. Hyperthyroidism decreases tyrosinaemia and endogenous tyrosine levels in the striatum, adrenals and heart. The accumulation rate of tyrosine determined 30 min after an intravenous injection of the labelled amino acid has been determined in the organs, together with the influx of the amino acid, determined within 20s. Hypothyroidism increases tyrosine accumulation rate in all the organs studied, and tyrosine clearance is decreased in the striatum and brainstem; together with an increased tyrosinaemia, this leads to a normal influx. The influx of tyrosine is increased in the hypothalamus. Hyperthyroidism decreases tyrosine accumulation rate in all the organs except the adrenals. These results indicate that the thyroid status of the young rat can influence tyrosine uptake mechanisms, without modifying an organ's tyrosine content. The fact that hypothyroidism increases tyrosine influx in the hypothalamus without modifying it in the brainstem and striatum reflects an heterogeneous reactivity to the lack of thyroid hormones in different brain structures. Neonatal hypothyroidism decreases the CA synthesis rate in the striatum, the heart and the interscapular brown adipose tissue, while synthesis was enhanced in the brainstem and the adrenals. It is likely that these variations in CA synthesis are due to thyroid hormone modulation of tyrosine hydroxylase activity, the enzyme which catalyses the rate limiting step in CA biosynthesis.
在14日龄大鼠中研究了新生儿甲状腺功能减退和亢进对下丘脑、纹状体、脑干、肾上腺、心脏和棕色脂肪组织（BAT）中酪氨酸代谢不同方面的影响。在注射标记酪氨酸后还测定了体内儿茶酚胺（CA）的合成速率。甲状腺功能减退会增加下丘脑和BAT中的酪氨酸血症和内源性酪氨酸浓度。甲状腺功能亢进会降低纹状体、肾上腺和心脏中的酪氨酸血症和内源性酪氨酸水平。在静脉注射标记氨基酸30分钟后测定了各器官中酪氨酸的积累速率，同时在20秒内测定了氨基酸的流入量。甲状腺功能减退会增加所有研究器官中的酪氨酸积累速率，纹状体和脑干中的酪氨酸清除率降低；连同酪氨酸血症增加，这导致正常的流入量。下丘脑的酪氨酸流入量增加。甲状腺功能亢进会降低除肾上腺外所有器官中的酪氨酸积累速率。这些结果表明幼鼠的甲状腺状态可以影响酪氨酸摄取机制，而不改变器官的酪氨酸含量。甲状腺功能减退增加下丘脑的酪氨酸流入量而不改变脑干和纹状体中的流入量这一事实反映了不同脑结构对甲状腺激素缺乏的异质性反应。新生儿甲状腺功能减退会降低纹状体、心脏和肩胛间棕色脂肪组织中的CA合成速率，而脑干和肾上腺中的合成则增强。CA合成的这些变化可能是由于甲状腺激素对酪氨酸羟化酶活性的调节，该酶催化CA生物合成中的限速步骤。
