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首页> 外文会议>European Congress of Pharmacology >Transient Exposition to Neonatal Hypothyroidism Increases Hepatic Gene Expression of Suppressors of Cytokine Signaling (SOCS) During Catch-Up Growth and in Adulthood
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Transient Exposition to Neonatal Hypothyroidism Increases Hepatic Gene Expression of Suppressors of Cytokine Signaling (SOCS) During Catch-Up Growth and in Adulthood

机译：新生儿甲状腺功能减退症的瞬态阐述增加了在追赶生长和成年期间细胞因子信号传导（SOC）抑制剂的肝基因表达

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Thyroid hormones (TH) are required for normal postnatal growth development in mammals. Thephysiological importance of TH becomes evident under the conditions of congenital-neonatal hypothyroidism(CH). If not treated immediately, CH has a profound impact on physiology and can permanently imprintneurological and endocrine systems, which, in turn, led to mental retardation, growth arrest, and metabolicdisturbances. A delayed growth development or long-lasting influence of CH on liver physiology could berelated with an state of Growth Hormone (GH) resistance. GH resistance has been shown in rat models of sepsis,uremia or in small rats for gestational age. In these models, GH resistance has been associated with increasedexpression of SOCS proteins which contribute to impair GH-JAK2-STAT5 signaling. Here, we studiedexpression of SOCS genes in liver from rats previously exposed to CH. Pregnant rats were given anti-thyroiddrug methimazole (MMI) from Gestational Day 12 until postnatal day (PND)30 to induce CH in male offspring.Growth defects due to CH were evident as a reduction in body weight and tail length from the second week oflife. Once the growth inhibiting condition (i.e., MMI) was discontinued on PND30, significant catch-up growthwas evident in CH rats. On PND80, significant reduction in body mass, tail length, and circulating IGF-Iremained in CH rats. Serum levels of TH, cholesterol, and triglycerides showed no significant differences.However, we observed down-regulation of female predominant (e.g., CYP2C7) together with induction of malepredominantgenes (e.g., CYP2C11) which suggested that a male pattern of gene expression was enhanced in CHrat liver. Finally, we observed an impaired somatic growth followed by catch-up growth in rats previouslyexposed to CH that was associated with increased expression of SOCS2 and CIS. In the present study, weprovide in vivo evidences that exposure to CH alters postnatal development which influences liver transcriptionalprogram in adulthood.
机译：甲状腺激素（Th）是哺乳动物中正常的产后生长发育所必需的。在先天性新生甲状腺功能亢进（CH）的条件下，Th的体内重要性变得明显。如果没有立即治疗，CH对生理学产生深远的影响，可永久性地造成了脑内和内分泌系统，这反过来又导致了精神发育迟滞，生长逮捕和代谢。 CH对肝脏生理学的延迟的生长发育或持久的影响可能与生长激素（GH）抵抗力的状态偏离。败血症，尿毒症或小鼠胎龄的大鼠大鼠模型已显示GH抗性。在这些模型中，GH抗性与SOCS蛋白的表达增加有关，其有助于损害GH-JAK2-STAT5信号传导。在此，我们研究了先前暴露于CH的大鼠肝脏的SOCS基因。从妊娠第12天给予妊娠大鼠抗甲状腺甲咪唑（MMI）直至产后日（PND）30，以诱导雄性后代的CH诱导CH。由于CH引起的缺陷是显而易见的，因为在第二周的第二周的体重和尾长的减少。一旦生长抑制条件（即，MMI）在PND30上停药，就在CH大鼠中显着的追赶增长。在PND80上，体重显着降低，尾部长度和CH大鼠中的IGF-IREMINATION。无论如何，胆固醇和甘油三酯的血清水平没有显着的差异。然而，我们观察到雌性母导致（例如，CYP2C7）的诱导诱导男性预测（例如，CYP2C11），这表明增强了基因表达的男性模式在克拉特肝脏。最后，我们观察到体细胞增长受损，然后通过与SOCS2和CIS的表达增加相关的CH相关的大鼠追加大鼠的生长。在目前的研究中，Weprovide在体内证据中，暴露于CH改变后期发育，其在成年期地影响肝脏转录的肝癌。

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