首页> 外文期刊>Endocrine journal >Leptin Regulation of the Thyroids: Negative Regulation on Thyroid Hormone Levels in Euthyroid Subjects and Inhibitory Effects on Iodide Uptake and Na(+)/I(-) Symporter mRNA Expression in Rat FRTL-5 Cells.
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Leptin Regulation of the Thyroids: Negative Regulation on Thyroid Hormone Levels in Euthyroid Subjects and Inhibitory Effects on Iodide Uptake and Na(+)/I(-) Symporter mRNA Expression in Rat FRTL-5 Cells.

机译:甲状腺的瘦蛋白调节:甲状腺激素水平的负调节和对​​大鼠FRTL-5细胞中碘摄取和Na(+)/ I(-)转运蛋白mRNA表达的抑制作用。

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Leptin receptors are distributed throughout the body and leptin has been shown to have various effects. As we have recently demonstrated a positive correlation between serum leptin levels and TSH in euthyroid subjects, we investigated the effect of leptin on the thyroids. It was observed that serum leptin levels were negatively correlated with free thyroxine/TSH ratios in the serum of euthyroid female subjects. This suggests that leptin may modulate TSH effects. RT-PCR for leptin receptor expression revealed that FRTL-5 cells possess the gene transcript to the long cytoplasmic form of the receptor. Leptin actually appeared to induce an increase in c-fos mRNA expression. However, it inhibited iodide uptake typically induced by both TSH and dibutyryl cAMP, while leptin did not inhibit TSH-induced cAMP production or TSH-stimulated DNA synthesis in 4H medium (in the absence of insulin and TSH). Leptin also was observed to inhibit TSH- and dibutyryl cAMP-induced Na(+)/I(-) symporter and thyroglobulin mRNA expression. Lastly, leptin was seen to inhibit TSH-stimulated thymidine incorporation in 5H medium. Taken together, these results suggest that leptin suppresses TSH-induced thyroid function. Therefore, we hypothesized that leptin may be one of the regulators of thyroid function in obese patients.
机译:瘦素受体分布在全身,瘦素已显示出多种作用。由于我们最近证明了甲状腺素正常患者血清瘦素水平与TSH之间呈正相关,因此我们研究了瘦素对甲状腺的影响。观察到血清瘦素水平与正常甲状腺女性受试者血清中的游离甲状腺素/ TSH比值呈负相关。这表明瘦素可以调节TSH作用。瘦素受体表达的RT-PCR表明FRTL-5细胞具有该受体长细胞质形式的基因转录本。瘦素实际上似乎诱导了c-fos mRNA表达的增加。但是,它抑制了通常由TSH和二丁酰cAMP共同诱导的碘摄取,而瘦素在4H培养基中(没有胰岛素和TSH的情况下)没有抑制TSH诱导的cAMP产生或TSH刺激的DNA合成。还观察到瘦素抑制TSH和二丁酰基cAMP诱导的Na(+)/ I(-)转运蛋白和甲状腺球蛋白mRNA表达。最后,瘦蛋白被认为抑制了5H培养基中TSH刺激的胸苷的掺入。综上所述,这些结果表明瘦素可抑制TSH诱导的甲状腺功能。因此,我们假设瘦素可能是肥胖患者甲状腺功能的调节剂之一。

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