首都医科大学学报 ›› 2026, Vol. 47 ›› Issue (2): 338-345.doi: 10.3969/j.issn.1006-7795.2026.02.015

• 基础研究 • 上一篇    下一篇

亚临床甲状腺功能减退状态下大鼠脂肪因子与炎症因子的变化

胡亚芬1,华琳2*   

  1. 1.首都医科大学大兴教学医院内分泌科,北京 102600;2.首都医科大学生物医学工程学院智医学工程学系,北京 100069
  • 收稿日期:2025-10-09 修回日期:2025-12-07 出版日期:2026-04-21 发布日期:2026-04-21
  • 通讯作者: 华琳 E-mail:hualin7750@ccmu.edu.cn

Studies on the intrinsic mechanism of subclinical hypothyroidism

Hu Yafen1, Hua Lin2*   

  1. 1.Department of Endocrinology, Daxing Teaching Hospital, Capital Medical University, Beijing 102600, China; 2. Department of Intelligent Medical Engineering, School of Biomedical Engineering, Capital Medical University, Beijing 100069, China
  • Received:2025-10-09 Revised:2025-12-07 Online:2026-04-21 Published:2026-04-21

摘要: 目的  本研究旨在进一步探索亚临床甲状腺功能减退症(以下简称甲减)状态下大鼠脂肪因子与炎症因子的变化。方法  通过建立甲状腺摘除动物模型,模拟临床上亚临床甲减患者特点,结合分子生物学手段,研究了甲状腺生物学过程中关键分子表达变化,与脂肪和肝脏分泌的激素和炎症因子之间的关系。结果  亚临床甲减模型组血清中瘦素含量明显高于正常组(P<0.001),脂联素含量明显高于正常组(P<0.01)。此外,血清中白介素-6(interleukin-6, IL-6)含量和肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)含量均明显高于正常组(P<0.05)。肝脏中IL-6含量和TNF-α含量也均明显高于正常组(P<0.01)。脂肪组织的蛋白质印迹法(Western blotting)结果显示,亚临床甲减模型组甲状腺激素受体α亚型(thyroid hormone receptor α,TRα)、TRβ以及TR表达量均较正常组有所增加,且促甲状腺激素受体(thyrotropin receptor,TSHR)表达升高。结论  本研究初步证实,亚临床甲减状态下大鼠体内脂肪堆积与分布异常,进而引发瘦素、脂联素分泌紊乱,同时伴随IL-6、TNF-α等炎症因子水平升高;上述变化通过调控促甲状腺激素释放激素(thyrotropin-releasing hormone,TRH)、促甲状腺激素(thyroid stimulating hormone, TSH)等分泌参与局部能量代谢调节,为阐释亚临床甲减与肥胖的内在关联奠定了实验基础。

关键词: 亚临床甲状腺功能减退, 甲状腺功能减退症, 炎症因子, 瘦素, 肥胖症, 脂联素

Abstract: Objective  To explore the changes in adipokines and inflammatory factors in rats under subclinical hypothyroidism conditions. Methods  This study established an animal model of thyroidectomy to simulate the characteristics of subclinical hypothyroidism patients in clinical practice. Combined with molecular biology methods, the expression changes of key molecules in thyroid biology processes and the relationship between hormones and inflammatory factors secreted by fat and liver were investigated. Results  The results showed that the serum leptin content in the  subclinical hypothyroidism model group was significantly higher than that in the normal group (P<0.001), and the adiponectin content was significantly higher than that in the normal group (P<0.01). In addition, the levels of interleukin-6 ( IL-6 )and tumor necrosis factor-α (TNF-α) in serum were significantly higher than those in the normal group (P<0.05). The levels of IL-6 and TNF-α in the liver were significantly higher than those in the normal group (P<0.01). The Western blotting of adipose tissue showed that the expression levels of thyroid hormone receptor α(TRa), TRβ and TR in the subclinical hypothyroidism model group increased compared to the normal group, and the elevated expression of thyrotropin receptor (TSHR) was observed. Conclusion  This study preliminarily confirms that subclinical hypothyroidism leads to abnormal fat accumulation and distribution in rats, which in turn induces disorders in leptin and adiponectin secretion, accompanied by elevated levels of inflammatory factors such as IL-6 and TNF-α. These changes participate in the regulation of local energy metabolism by modulating the secretion of thyrotropin-releasing hormone (TRH) and thyroid stimulating hormone (TSH), laying an experimental foundation for elucidating the intrinsic relationship between subclinical hypothyroidism and obesity.

Key words: subclinical hypothyroidism, hypothyroidism, inflammatory factors, leptin, obesity, adiponectin

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