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首页> 外文期刊>Endocrinology >Fasting-Induced Changes in Hepatic Thyroid Hormone Metabolism in Male Rats Are Independent of Autonomic Nervous Input to the Liver
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Fasting-Induced Changes in Hepatic Thyroid Hormone Metabolism in Male Rats Are Independent of Autonomic Nervous Input to the Liver

机译：空腹诱导的雄性大鼠肝甲状腺激素代谢变化与自主神经输入肝脏无关

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摘要

During fasting, profound changes in the regulation of the hypothalamus-pituitary-thyroid axis occur in order to save energy and limit catabolism. In this setting, serum T-3 and T-4 are decreased without an appropriate TSH and TRH response reflecting central down-regulation of the hypothalamus- pituitary-thyroid axis. Hepatic thyroid hormone (TH) metabolism is also affected by fasting, because type 3 deiodinase (D3) is increased, which is mediated by serum leptin concentrations. Arecent study showed that fasting-induced changes in liver THsulfotransferases (Sults) and uridine 5=-diphospho-glucuronosyltransferase (Ugts) depend on a functional melanocortin system in the hypothalamus. However, the pathways connecting the hypothalamus and the liver that induce these changes are currently unknown. In the present study, we investigated in rats whether the fasting-induced changes in hepatic TH metabolism are regulated by the autonomic nervous system. We selectively cut either the sympathetic or the parasympathetic input to the liver. Serum and liver TH concentrations, deiodinase expression, and activity and Sult and Ugt expression were measured in rats that had been fasted for 36 hours or were fed ad libitum. Fasting decreased serum T-3 and T-4 concentrations, whereas intrahepatic TH concentrations remained unchanged. D3 expression and activity increased, as was the expression of constitutive androstane receptor, Sult1b1, and Ugt1a1, whereas liver D1 was unaffected. Neither sympathetic nor parasympathetic denervation affected the fasting-induced alterations. We conclude that fasting-induced changes in liver TH metabolism are not regulated via the hepatic autonomic input in a major way and more likely reflect a direct effect of humoral factors on the hepatocyte.
机译：禁食期间，下丘脑-垂体-甲状腺轴的调节发生了深刻变化，以节省能量并限制分解代谢。在这种情况下，血清T-3和T-4降低而没有适当的TSH和TRH反应，反映了下丘脑-垂体-甲状腺轴的中央下调。禁食也会影响肝甲状腺激素（TH）的代谢，因为3型脱碘酶（D3）升高，这是由血清瘦素浓度介导的。 Arecent研究表明，空腹诱导的肝脏TH磺基转移酶（Sults）和尿苷5 =-二磷酸-葡萄糖醛酸糖基转移酶（Ugts）的变化取决于下丘脑中功能性的黑皮质素系统。但是，目前尚不知道连接下丘脑和肝脏的诱导这些变化的途径。在本研究中，我们调查了大鼠中空腹诱导的肝脏TH代谢变化是否受自主神经系统调节。我们有选择地切断了交感神经或副交感神经的输入。在禁食36小时或随意进食的大鼠中，测量其血清和肝脏TH浓度，脱碘酶表达，活性以及Sult和Ugt表达。空腹降低血清T-3和T-4浓度，而肝内TH浓度保持不变。 D3的表达和活性增加，组成型雄烷受体，Sult1b1和Ugt1a1的表达也增加，而肝脏D1则不受影响。交感神经和副交感神经都不影响空腹诱导的改变。我们得出的结论是，空腹诱导的肝脏TH代谢变化主要不是通过肝脏自主神经输入调节的，更可能反映出体液因子对肝细胞的直接影响。

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