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首页> 外文期刊>The Journal of Endocrinology: The Journal of the Society for Endocrinology >Effects of maternal nicotine exposure on thyroid hormone metabolism and function in adult rat progeny
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Effects of maternal nicotine exposure on thyroid hormone metabolism and function in adult rat progeny

机译：母体尼古丁暴露对成年大鼠子代甲状腺激素代谢和功能的影响

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Postnatal nicotine exposure leads to obesity and hypothyroidism in adulthood. We studied the effects of maternal nicotine exposure during lactation on thyroid hormone (TH) metabolism and function in adult offspring. Lactating rats received implants of osmotic minipumps releasing nicotine (NIC, 6?mg/kg per day s.c.) or saline (control) from postnatal days 2 to 16. Offspring were killed at 180 days. We measured types 1 and 2 deiodinase activity and mRNA, mitochondrial α-glycerol-3-phosphate dehydrogenase (mGPD) activity, TH receptor (TR), uncoupling protein 1 (UCP1), hypothalamic TRH, pituitary TSH, and in vitro TRH-stimulated TSH secretion. Expression of deiodinase mRNAs followed the same profile as that of the enzymatic activity. NIC exposure caused lower 5′-D1 and mGPD activities; lower TRβ1 content in liver as well as lower 5′-D1 activity in muscle; and higher 5′-D2 activity in brown adipose tissue (BAT), heart, and testis, which are in accordance with hypothyroidism. Although deiodinase activities were not changed in the hypothalamus, pituitary, and thyroid of NIC offspring, UCP1 expression was lower in BAT. Levels of both TRH and TSH were lower in offspring exposed to NIC, which presented higher basal in vitro TSH secretion, which was not increased in response to TRH. Thus, the hypothyroidism in NIC offspring at adulthood was caused, in part, by in vivo TRH–TSH suppression and lower sensitivity to TRH. Despite the hypothyroid status of peripheral tissues, these animals seem to develop an adaptive mechanism to preserve thyroxine to triiodothyronine conversion in central tissues.
机译：产后尼古丁暴露会导致肥胖和甲状腺功能减退。我们研究了哺乳期间母体尼古丁暴露对成年后代甲状腺激素（TH）代谢和功能的影响。哺乳期的大鼠接受了从出生后第2天到第16天释放尼古丁（NIC，每天皮下剂量为6？mg / kg）或生理盐水（对照组）的渗透性微型泵的植入，其后代在180天被杀死。我们测量了1型和2型脱碘酶活性和mRNA，线粒体α-甘油-3-磷酸脱氢酶（mGPD）活性，TH受体（TR），解偶联蛋白1（UCP1），下丘脑TRH，垂体TSH和体外TRH刺激TSH分泌。脱碘酶mRNA的表达遵循与酶活性相同的谱。 NIC暴露引起较低的5'-D1和mGPD活性;降低肝脏中的TRβ1含量，降低肌肉中的5'-D1活性;与甲状腺功能减退症相关的棕色脂肪组织（BAT），心脏和睾丸中5'-D2活性较高。尽管在NIC后代的下丘脑，垂体和甲状腺中脱碘酶活性没有变化，但BAT中UCP1表达较低。在暴露于NIC的后代中，TRH和TSH的水平均较低，这表示基础TSH的体外分泌较高，而对TRH的响应并未增加。因此，成年后NIC后代甲状腺功能减退的部分原因是体内TRH–TSH抑制和对TRH敏感性降低。尽管周围组织的甲状腺功能低下，这些动物似乎仍发展出一种适应性机制，可以在中央组织中保持甲状腺素向三碘甲状腺素的转化。

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