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Lidiane Orlandi Programa de Pós-Graduação Multicêntrico em Ciências Fisiológicas, Universidade Federal de Alfenas, Alfenas - MG, Brazil

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Merelym K Oliveira Programa de Pós-Graduação Multicêntrico em Ciências Fisiológicas, Universidade Federal de Alfenas, Alfenas - MG, Brazil

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Fernando Vitor-Vieira Programa de Pós-Graduação Multicêntrico em Ciências Fisiológicas, Universidade Federal de Alfenas, Alfenas - MG, Brazil

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Fabiana C. Vilela Programa de Pós-Graduação em Biociências Aplicadas à Saúde, Universidade Federal de Alfenas, Alfenas – MG, Brazil

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Alexandre Giusti-Paiva Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis - SC, Brazil

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Abstract

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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László ROSIVALL (Semmelweis University, Budapest, Hungary)

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Physiology International
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