Abstract
Aims This study was designed to reveal the effect of probiotics and omega-3 fatty acids in a fatty liver model in rats induced by high-fructose corn syrup (HFCS). Methods In the study, 40 male Wistar Albino rats were used, and these rats were divided into five groups. HFCS was added to the drinking water (30% solution) of four groups (Groups 2, 3, 4, and 5) for three weeks, and the animals were fed ad libitum. At the end of three weeks, the rats in Groups 3, 4, and 5 were administered omega-3 fatty acids (400 mg/kg) and probiotics (1.5 × 109 cfu/mL/day) with the gavage method for four weeks. The body weights of rats were weighed and recorded before starting the experiment, at the end of the third week, and before the animals were sacrificed at the last week, all at the same hour. By subtracting the remaining amount of food and water from the daily food and water amount, the amount of food and water consumed was calculated. These values were recorded for seven weeks. At the end of the seven weeks, the rats were sacrificed after blood specimens and tissues were taken. Results Analyzing the changes in the food intake of each group within itself throughout the experiment, it was observed that there was an increase in the food intake in the control group; from the starting week to the last week, the food intake amount of the HFCS group began to decrease particularly after the second week; and it began to decrease after the third week in the groups that were administered probiotics and omega-3 fatty acids. The changes in the sacrifice weights in the HFCS + omega-3 fatty acid, HFCS + probiotic, and HFCS + probiotic + omega-3 fatty acid groups were found to be lower than that in the HFCS group. The maximum levels of glucose, ALT, ALP, serum cholesterol, triglyceride and AST were found to be in the HFCS group. It was determined that the minimum mean steatosis level was in the control group, while the maximum steatosis level was in the HFCS group. Conclusions As a result, there was a protective effect of probiotic and omega-3 fatty acid.
Highlights
Fatty liver, known as hepatic steatosis, is a condition defined by excessive fat accumulation in the liver (>5% by weight) and by all clinical pictures where the diagnosis of steatosis is made due to any condition induced by alcohol or nonalcoholic factors [1]. e incidence and prevalence of nonalcoholic fatty liver disease (NAFLD) increase all around the world
Analyzing the changes in the food intake of each group within itself during the experiment, an increase in the food intake in the control group was observed from the starting week to the last week. e increase in the amount of food intake seen in the control group in the periods of weeks 3-4, weeks 4-5, and weeks 5-6 was found significant (p ≤ 0.05). e amount of food intake in the high-fructose corn syrup (HFCS) group began to decrease especially after the second week, while the reduction in the amount of food intake between weeks 1 and 2 was found to be significant (p ≤ 0.05)
In the high-fructose diet model, these supplements were found to have a useful effect on some serum parameters and appetite control that are important in fatty liver disease. e interaction between the gut-liver axis, dietary factors, microbiota and intestinal barrier integrity, and a high-fructose diet and an omega-3 fatty acids-deficient diet are thought to play an important role in the development of NAFLD
Summary
Known as hepatic steatosis, is a condition defined by excessive fat accumulation in the liver (>5% by weight) and by all clinical pictures where the diagnosis of steatosis is made due to any condition induced by alcohol or nonalcoholic factors [1]. e incidence and prevalence of nonalcoholic fatty liver disease (NAFLD) increase all around the world. E incidence and prevalence of nonalcoholic fatty liver disease (NAFLD) increase all around the world. In animal experiments, it has been shown that high-fructose diets, compared to glucose, result in increased hepatic triglyceride content. The pathogenesis of the nonalcoholic fatty liver disease remains poorly understood, it is thought to be a multifactorial process involving genetic and environmental elements [3]. E first hit during the process of the disease which results in steatosis is insulin resistance Cellular mechanisms, such as oxidative stress, mitochondrial dysfunction, and tumor necrosis factor-α (TNFα), and hormones, such as adiponectin and leptin, play a role in the second hit that involves inflammation and fibrosis [4]. Perfusion studies show that fructose can stimulate the liver to produce higher levels of triglycerides in comparison to glucose [3]
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