Research Article High-Fat Diet Induces Oxidative Stress and MPK2 and HSP83 Gene Expression in Drosophila melanogaster Mariane Trindade de Paula, 1 Márcia Rósula Poetini Silva, 1 Stífani Machado Araujo, 1 Vandreza Cardoso Bortolotto, 1 Luana Barreto Meichtry, 1 Ana Paula Pegoraro Zemolin, 2 Gabriel L. Wallau, 3 Cristiano Ricardo Jesse, 1 Jeferson Luís Franco, 3 Thaís Posser, 3 and Marina Prigol 1 1 Laborat´ orio de Avaliac ¸˜ oes Farmacol´ ogicas e Toxicol´ ogicas Aplicadas ` as Mol´ eculas Bioativas, Universidade Federal do Pampa (Unipampa), Campus Itaqui, 97650-000 Itaqui, RS, Brazil 2 Programa de P´ os Graduac ¸˜ ao em Ciˆ encias Biol´ ogicas: Bioqu´ ımica Toxicol´ ogica, Departamento de Qu´ ımica, Centro de Ciˆ encias Naturais e Exatas, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil 3 Centro Interdisciplinar de Pesquisa em Biotecnologia (CIP/BIOTEC), Universidade Federal do Pampa, Campus S˜ ao Gabriel, 97300 000 S˜ ao Gabriel, RS, Brazil Correspondence should be addressed to Marina Prigol; marinaprigol@gmail.com Received 14 May 2016; Revised 26 June 2016; Accepted 30 June 2016 Academic Editor: Silvana Hrelia Copyright © 2016 Mariane Trindade de Paula et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Te consumption of a high-fat diet (HFD) causes alteration in normal metabolism afecting lifespan of fies; however molecular mechanism associated with this damage in fies is not well known. Tis study evaluates the efects of ingestion of a diet supplemented with 10% and 20% of coconut oil, which is rich in saturated fatty acids, on oxidative stress and cells stress signaling pathways. Afer exposure to the diet for seven days, cellular and mitochondrial viability, lipid peroxidation and antioxidant enzymes SOD and CAT activity, and mRNA expression of antioxidant enzymes HSP83 and MPK2 were analyzed. To confrm the damage efect of diet on fies, survival and lifespan were investigated. Te results revealed that the HFD augmented the rate of lipid peroxidation and SOD and CAT activity and induced a higher expression of HSP83 and MPK2 mRNA. In parallel, levels of enzymes involved in lipid metabolism (ACSL1 and ACeCS1) were increased. Our data demonstrate that association among metabolic changes, oxidative stress, and protein signalization might be involved in shortening the lifespan of fies fed with a HFD. 1. Introduction Obesity is a chronic multifactorial disease, result of positive energy balance, where food intake is greater than energy expenditure. Tis overweight predisposes the organism to a series of diseases such as cardiovascular problems, diabetes, and sleep apnea [1, 2]. Given that, excessive food intake is ofen directly linked to the consumption of foods rich in fat and the increase in the amount of fatty acids in the diet causes an imbalance in the metabolism [3]. A high-fat diet (HFD) causes damage at the cellular and molecular levels, and it triggers an oxidative stress process. Studies have demonstrated that this oxidative stress process generates diferent responses such as the activation of signal- ing pathways implicated in protecting cells against oxidative damage, such as heat shock proteins (HSP) and mitogen- activated protein kinase (MAPK) [3], peroxidation of lipids and modifcation of proteins [4, 5], and insulin resistance [6, 7]. Moreover, a HFD promotes an increased supply of triglycerides and fatty acids and consequently it results in an increase of fatty acids oxidation in order to produce energy. Terefore, the study of biochemical mechanisms involved in the cellular responses to changes in the diet requires close attention to several metabolic pathways, given the complexity of the organism, since in cellular signaling pathways the interaction between genes and protein expression changes Hindawi Publishing Corporation Oxidative Medicine and Cellular Longevity Volume 2016, Article ID 4018157, 12 pages http://dx.doi.org/10.1155/2016/4018157