(searched for: doi:10.5530/ptb.2016.2.5)
Veterinary world; https://doi.org/10.14202/vetworld.2021.1774-1783
Metabolic syndrome (MetS) has become a global problem. With the increasing prevalence of MetS worldwide, understanding its pathogenesis and treatment modalities are essential. Animal models should allow an appropriate representation of the clinical manifestations of human conditions. Rats are the most commonly used experimental animals for the study. The development of a proper MetS model using rats will contribute to the successful application of research findings to the clinical setting. Various intervention methods are used to induce MetS through diet induction with various compositions, chemicals, or a combination of both. This review will provide a comprehensive overview of several studies on the development of rat MetS models, along with the characteristics of the clinical manifestations resulting from each study.
Egyptian Liver Journal, Volume 10, pp 1-9; https://doi.org/10.1186/s43066-020-00045-9
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.