2026-04-14T02:34:05Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1194532025-12-04T22:54:55Zcom_2072_1057col_2072_478782col_2072_478903col_2072_478917

00925njm 22002777a 4500 dc Alcalá, Martín author Calderón Domínguez, María author Serra i Cucurull, Dolors author Herrero Rodríguez, Laura author Ramos, Maria P. author Viana Arribas, Marta author 2018-01-31T13:26:14Z 2018-01-31T13:26:14Z 2017-10-13 2018-01-31T13:26:14Z Objectives The use of antioxidant therapy in the treatment of oxidative stress-related diseases such as cardiovascular disease, diabetes or obesity remains controversial. Our aim is to demonstrate that antioxidant supplementation may promote negative effects if used before the establishment of oxidative stress due to a reduced ROS generation under physiological levels, in a mice model of obesity. Methods C57BL/6J mice were fed with a high-fat diet for 14 weeks, with (OE group) or without (O group) vitamin E supplementation. Results O mice developed a mild degree of obesity, which was not enough to induce metabolic alterations or oxidative stress. These animals exhibited a healthy expansion of retroperitoneal white adipose tissue (rpWAT) and the liver showed no signs of lipotoxicity. Interestingly, despite achieving a similar body weight, OE mice were insulin resistant. In the rpWAT they presented a reduced generation of ROS, even below physiological levels (C: 1651.0 ± 212.0; O: 3113 ± 284.7; OE: 917.6 ±104.4 RFU/mg protein. C vs OE p< 0.01). ROS decay may impair their action as second messengers, which could account for the reduced adipocyte differentiation, lipid transport and adipogenesis compared to the O group. Together, these processes limited the expansion of this fat pad and as a consequence, lipid flux shifted towards the liver, causing steatosis and hepatomegaly, which may contribute to the marked insulin resistance. Conclusions This study provides in vivo evidence for the role of ROS as second messengers in adipogenesis, lipid metabolism and insulin signaling. Reducing ROS generation below physiological levels when the oxidative process has not yet been established may be the cause of the controversial results obtained by antioxidant therapy. Teixit adipós Resistència a la insulina Vitamina E Malalties del fetge Transducció de senyal cel·lular Obesitat Adipose tissues Insulin resistance Vitamin E Liver diseases Cellular signal transduction Obesity Short-term vitamin E treatment impairs reactive oxygen species signaling required for adipose tissue expansion, resulting in fatty liver and insulin resistance in obese mice