Santos-Ledo Adrián, Luxán-Delgado Beatriz de, Caballero Beatriz, Potes Yaiza, Rodríguez-González Susana, Boga José Antonio, Coto-Montes Ana, García-Macia Marina
Institute of Neurosciences of Castilla y León-INCYL, Institute of Biomedical Research of Salamanca-IBSAL, Cell Biology and Pathology, University of Salamanca, 37007 Salamanca, Spain.
Centre for Tumour Biology, Barts Cancer Institute-Queen Mary, University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
Antioxidants (Basel). 2021 May 18;10(5):796. doi: 10.3390/antiox10050796.
Metabolic syndrome is a global health problem in adults and its prevalence among children and adolescents is rising. It is strongly linked to a lifestyle with high-caloric food, which causes obesity and lipid metabolism anomalies. Molecular damage due to excessive oxidative stress plays a major role during the development of metabolic syndrome complications. Among the different hormones, melatonin presents strong antioxidant properties, and it is used to treat metabolic diseases. However, there is not a consensus about its use as a metabolic syndrome treatment. The aim of this study was to identify melatonin effects in a metabolic syndrome model. Golden hamsters were fed with 60% fructose-enriched food to induce metabolic syndrome and were compared to hamsters fed with regular chow diet. Both groups were also treated with melatonin. Fructose-fed hamsters showed altered blood lipid levels (increased cholesterol and LDL) and phenotypes restored with the melatonin treatment. The Harderian gland (HG), which is an ideal model to study autophagy modulation through oxidative stress, was the organ that was most affected by a fructose diet. Redox balance was altered in fructose-fed HG, inducing autophagic activation. However, since LC3-II was not increased, the impairment must be in the last steps of autophagy. Lipophagy HG markers were also disturbed, contributing to the dyslipidemia. Melatonin treatment improved possible oxidative homeostasis through autophagic induction. All these results point to melatonin as a possible treatment of the metabolic syndrome.
代谢综合征是成年人面临的全球性健康问题，其在儿童和青少年中的患病率正在上升。它与高热量食物的生活方式密切相关，高热量食物会导致肥胖和脂质代谢异常。在代谢综合征并发症的发展过程中，过度氧化应激引起的分子损伤起主要作用。在不同的激素中，褪黑素具有强大的抗氧化特性，可用于治疗代谢性疾病。然而，对于其作为代谢综合征治疗方法的使用尚无共识。本研究的目的是确定褪黑素在代谢综合征模型中的作用。给金黄仓鼠喂食富含60%果糖的食物以诱导代谢综合征，并与喂食常规饲料的仓鼠进行比较。两组仓鼠也都接受了褪黑素治疗。喂食果糖的仓鼠血脂水平发生改变（胆固醇和低密度脂蛋白升高），而褪黑素治疗使表型恢复。哈德氏腺（HG）是通过氧化应激研究自噬调节的理想模型，是受果糖饮食影响最大的器官。喂食果糖的HG中的氧化还原平衡发生改变，诱导自噬激活。然而，由于LC3-II没有增加，损伤一定发生在自噬的最后步骤。脂质自噬HG标志物也受到干扰，导致血脂异常。褪黑素治疗通过自噬诱导改善了可能的氧化稳态。所有这些结果表明褪黑素可能是治疗代谢综合征的一种方法。
