果糖饮食会加剧代谢紊乱大鼠的外周炎症性痛感。

IF 2.2 4区 医学 Q3 PHYSIOLOGY
Physiology international Pub Date : 2024-05-31 Print Date: 2024-06-19 DOI:10.1556/2060.2024.00376
Lidiane Orlandi, Merelym K Oliveira, Fernando Vitor-Vieira, Fabiana C Vilela, Alexandre Giusti-Paiva
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引用次数: 0

摘要

本研究探讨了果糖诱导的肥胖和代谢紊乱对外周炎症性痛觉过敏的影响,采用了von Frey试验进行定量感觉测试,并测量爪水肿以评估炎症反应。研究人员给 Wistar 大鼠喂食水或 10% 的果糖溶液,连续喂食 5 周。在跖内注射角叉菜胶(1 毫克/爪)、脂多糖(LPS;100 微克/爪)或前列腺素 E2(PGE2,100 纳克/爪)等炎症因子后,我们进行了机械痛觉试验和爪水肿评估。与对照组动物相比,果糖饮食导致血脂异常、胰岛素和瘦素血浆水平升高、胰岛素抵抗以及附睾和腹膜后脂肪增加。在炎症反应中,果糖组的外周痛觉明显增强,爪水肿更明显。我们的研究结果表明,果糖不仅会导致肥胖和代谢紊乱,还会通过提高前列腺素敏感性而加剧外周炎症性疼痛反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Peripheral inflammatory hyperalgesia is exacerbated in rats with metabolic disorders induced by a fructose diet.

This study explored the effects of fructose-induced obesity and metabolic disorders on peripheral inflammatory hyperalgesia, employing quantitative sensory testing with the von Frey test and measuring paw edema to assess inflammatory responses. Wistar rats were administered water or 10% fructose solution ad libitum over a period of 5 weeks. After intraplantar administration of inflammatory agents such as carrageenan (1 mg/paw), lipopolysaccharide (LPS; 100 µg/paw), or prostaglandin E2 (PGE2, 100 ng/paw), we conducted mechanical hyperalgesia tests and paw edema evaluations. The fructose diet resulted in dyslipidemia, elevated insulin and leptin plasma levels, insulin resistance, and increased epididymal and retroperitoneal adiposity compared to control animals. In response to inflammatory agents, the fructose group displayed significantly enhanced peripheral hyperalgesia and more pronounced paw edema. Our results demonstrate that fructose not only contributes to the development of obesity and metabolic disorder but also exacerbates peripheral inflammatory pain responses by enhancing prostaglandin sensitivity.

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来源期刊
Physiology international
Physiology international Medicine-Physiology (medical)
CiteScore
3.40
自引率
0.00%
发文量
37
期刊介绍: The journal provides a forum for important new research papers written by eminent scientists on experimental medical sciences. Papers reporting on both original work and review articles in the fields of basic and clinical physiology, pathophysiology (from the subcellular organization level up to the oranizmic one), as well as related disciplines, including history of physiological sciences, are accepted.
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