A fish oil-rich diet leads to lower adiposity and serum triglycerides but increases liver lipid peroxidation in fructose
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ORIGINAL RESEARCH ARTICLE
Egyptian Liver Journal
Open Access
A fish oil-rich diet leads to lower adiposity and serum triglycerides but increases liver lipid peroxidation in fructose-fed rats Gabriel Perri Esteves1* , Camila Sanches Manca1, Hellen Paraguassú Veida-Silva2, Paula Payão Ovidio1, Héric Holland1, Flávia Sayuri Matsuo3, Mariana Kiomy Osako3 and Alceu Afonso Jordao1
Abstract Background: Consumption of refined carbohydrates has risen in recent years alongside chronic diseases such as type 2 diabetes mellitus, dyslipidemia, obesity, and non-alcoholic fatty liver disease (NAFLD). Fructose is a monosaccharide made widely available in industrialized products, capable of inducing excessive weight gain and liver steatosis in animal models, while omega-3 fatty acids, present in foods such as fatty fish and fish oil, have shown to inhibit genes related to lipogenesis and decrease cardiovascular risk. Therefore, our objective was to evaluate the impact of a high-fructose diet on weight gain, biochemical and oxidative stress parameters, and liver histology and investigate fish oil’s potential protective role. Thirty male Wistar rats were divided into 3 groups: regular chow diet (CT), regular chow diet plus 20% fructose in drinking water (Fr), and a diet containing 10% fish oil plus 20% fructose in drinking water (FOFr). After 12 weeks, tissues of interest were collected for biochemical and histological analyses. Results: Although fructose consumption did not lead to increased hepatic fat, it caused a significant increase in weight gain, white adipose tissue, and serum triglycerides in the Fr group, while fish oil promoted normalized serum triglycerides and even reduced adiposity in the FOFr group. Additionally, the inclusion of fish oil in the FOFr diet led to increased liver lipid peroxidation in the form of increased hepatic MDA. Conclusions: It is concluded that fish oil can prevent important metabolic alterations caused by fructose consumption, but its dosage must be taken into account to prevent oxidative stress and potential liver damage. Keywords: Oxidative stress, Lipid peroxidation, Omega-3 fatty acids, Fish oil, NAFLD, Fructose, Obesity
Background The alarming increase in obesity prevalence around the world is a public health concern [1]. This pathological expansion of adipose tissue is accompanied by an inflammatory state and many comorbidities, such as type 2 diabetes (T2D), dyslipidemia, cardiovascular diseases (CVD), and non-alcoholic fatty liver disease (NAFLD) [2]. The latter is currently considered the most prevalent liver disease in the world, characterized by a higher than * Correspondence: [email protected] 1 Department of Health Sciences, Ribeirao Preto Medical School, University of Sao Paulo, São Paulo, Brazil Full list of author information is available at the end of the article
5% fat deposition in the liver of individuals with no history of excessive alcohol intake. It is believed NAFLD progression occurs initially through increased lipid accumulation in the liver (the first “h
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