肥胖对甲状腺功能的影响在一个代谢健康的高脂肪,高碳水化合物饮食诱导的肥胖大鼠模型中
Reveshni Pather1, Andile Khathi1, Phikelelani Ngubane1
1Department of Human Physiology, School of Laboratory Medicine and Medical Science, University of KwaZulu-Natal, Durban, South Africa.
Frontiers in endocrinology
|May 7, 2025
概括
这项研究表明,高脂肪,高碳水化合物饮食可以诱导大鼠的代谢健康肥胖,导致甲状腺功能障碍. 这种模型有助于理解甲状腺在肥胖中的变化,而没有胰岛素抵抗.
科学领域:
- 内分泌学 在内分泌学.
- 代谢障碍 代谢障碍 代谢障碍
- 甲状腺研究 甲状腺研究
背景情况:
- 肥胖会加剧甲状腺功能障碍,主要研究的是具有胰岛素耐药性的代谢不健康肥胖症 (MUO).
- 在缺乏胰岛素抵抗的代谢健康肥胖 (MHO) 模型中,对甲状腺功能障碍的研究有限.
研究的目的:
- 为了研究甲状腺功能障碍和肥胖之间的关联,在一个代谢健康的高脂肪,高碳水化合物饮食诱导的肥胖大鼠模型中.
- 建立和利用一个MHO大鼠模型来研究甲状腺平衡.
主要方法:
- 雄性Sprague Dawley大鼠在12个月内接受了对照或高脂肪,高碳水化合物 (HFHC) 饮食.
- 每个月监测身体质量指数 (BMI),热量摄入量和禁食血糖 (FBG).
- 甲状腺功能,葡萄糖平衡和炎症标志物被评估为终端.
主要成果:
- 在HFHC饮食组中,肥胖症发生,BMI,热量摄入量,FBG,胰岛素,HOMA-IR,Hb1Ac,瘦素和IL-6都增加了.
- 在HFHC组中观察到甲状腺刺激激素 (TSH),自由三甲状腺素 (fT3) 和自由甲状腺素 (fT4) 的水平明显升高.
- 尽管甲状腺乱,HFHC组满足了MHO,而不是MUO的标准.
结论:
- 一种高脂肪,高碳水化合物饮食在老鼠中成功诱导了代谢健康的肥胖状态.
- 这种MHO大鼠模型适用于调查甲状腺平衡变化.
- 使用该模型进行进一步的研究可能会揭示防止MUO进展的预防策略.
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