A fish oil-rich diet leads to lower adiposity and serum triglycerides but increases liver lipid peroxidation in fructose-fed rats

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.

Metabolic Effects of Coconut Oil on Fatty Liver and Oxidative Stress Induced by a High-fat Diet in Rats

“…Among the liver diseases, nonalcoholic fatty liver disease (NAFLD) is characterized by the hepatic accumulation of lipids, mainly in the form of triglycerides, which, due to progressive inflammatory activity, can evolve into a more severe form, nonalcoholic steatohepatitis. 1,2 NAFLD and nonalcoholic steatohepatitis are associated with insulin resistance, type 2 diabetes mellitus, obesity, hyperlipidemia, hypertension, and metabolic syndrome as well as extrahepatic manifestations, such as sleep apnea, chronic kidney disease, and cardiovascular disease. 1,3 Also, it is believed that the first event necessary for fat accumulation originates from insulin resistance, resulting in altering lipid and apolipoprotein metabolisms.…”