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三碘甲状腺原氨酸对正常大鼠白色脂肪组织脂联素表达和瘦素释放的影响。

Effect of triiodothyronine on adiponectin expression and leptin release by white adipose tissue of normal rats.

机构信息

Laboratório de Endocrinologia Molecular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.

出版信息

Horm Metab Res. 2010 Apr;42(4):254-60. doi: 10.1055/s-0029-1246118. Epub 2010 Jan 21.

Abstract

Previous studies have shown that alterations in thyroid status may lead to changes in serum leptin and adiponectin, both in humans and rodents. The mechanisms, especially for adiponectin, are unclear. In the present study, we investigated the effect of triiodothyronine (T3) on the expression of adiponectin mRNA and the release of leptin and adiponectin by white adipose tissue (WAT) explants obtained from epididymal (visceral) or inguinal (subcutaneous) depots from normal rats. We also analyzed the effects of other known regulators of adiponectin and leptin release, such as rosiglitazone and dexamethasone. T3 acted directly at rat WAT explants in a depot-specific manner and in a unique fashion to each hormone. T3 was able to inhibit leptin release only by epididymal explants, and to reduce adiponectin mRNA expression only in inguinal explants. However, T3 was incapable of modifying adiponectin release by both explants. Additionally, rosiglitazone exhibited an inhibitory effect on adiponectin release by both WAT explants, even though adiponectin mRNA was importantly upregulated only in inguinal explants. Rosiglitazone acted as an inhibitor of leptin release by both studied fat depots, while only epididymal explants responded to the stimulatory effect of dexamethasone on leptin release. Therefore, the present model of isolated rat white adipose tissue explants highlights the fact that the regulation of hormonal production by white adipose tissue depends on the type of depot and its anatomical location. In this context, our results show for the first time a potential inhibitory effect of T3 on adiponectin mRNA expression specifically on WAT from a subcutaneous depot.

摘要

先前的研究表明,甲状腺状态的改变可能导致瘦素和脂联素的变化,这在人类和啮齿动物中均有体现。但具体的机制,特别是脂联素,仍不清楚。在本研究中,我们研究了三碘甲状腺原氨酸(T3)对正常大鼠附睾(内脏)或腹股沟(皮下)脂肪组织(WAT)外植体中脂联素 mRNA 表达和瘦素及脂联素分泌的影响。我们还分析了其他已知的脂联素和瘦素分泌调节剂,如罗格列酮和地塞米松的影响。T3 以组织特异性和独特的方式直接作用于大鼠 WAT 外植体,对每种激素均有影响。T3 仅能通过附睾外植体抑制瘦素的释放,仅能降低腹股沟外植体中脂联素 mRNA 的表达。然而,T3 并不能改变两种外植体的脂联素释放。此外,罗格列酮对两种 WAT 外植体的脂联素释放均表现出抑制作用,尽管脂联素 mRNA 仅在腹股沟外植体中显著上调。罗格列酮对两种研究脂肪组织的瘦素释放均表现出抑制作用,而只有附睾外植体对地塞米松刺激瘦素释放有反应。因此,本孤立大鼠白色脂肪组织外植体模型强调了一个事实,即白色脂肪组织对激素产生的调节取决于脂肪组织的类型及其解剖位置。在这种情况下,我们的研究结果首次显示 T3 对来自皮下脂肪组织的 WAT 中脂联素 mRNA 表达具有潜在的抑制作用。

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