Hepatic and biochemical repercussions of a polyunsaturated fat-rich hypercaloric and hyperlipidic diet in Wistar rats

Abstract

-Context -Non-alcoholic fatty liver disease is characterized by lipid deposits in the hepatocytes and has been associated with obesity, dyslipidemia and type-2 diabetes. It is considered a hepatic manifestation of the metabolic syndrome, of which the main component is insulin resistance leading to hyperinsulinemia and increased production of inflammatory cytokines. Saturated fat promotes hypertriglyceridemia and hyperinsulinemia, reduces levels of high-density cholesterol and increases levels of low-density cholesterol, while polyunsaturated fat is associated with hypolipidemic, antiinflammatory and imunoregulating action. ObjectiveTo evaluate the hepatic and biochemical repercussions of a polyunsaturated fat-rich diet in Wistar rats. Methods -Twenty-two rats were distributed equally in two groups: GI -standard diet (Biobase Bio-tec Ratos e Camundongos ® ) providing 3.000 kcal/kg and GII -hypercaloric and hyperlipidic diet providing 4.250 kcal/kg (ω-6:ω-3 = 3:1). The animals were euthanized after 23 weeks of experiment. The weight, biochemical parameters and hepatohistological changes were registered. Results -Findings were submitted to variance analysis with the level of statistical significance at 5%. The average weight did not differ significantly between the groups at baseline (P = 0.711), but was greater in Group II by the end of the experiment (P = 0.000). The levels of triglycerides (P = 0.039), total cholesterol (P = 0.015) and HDL (P = 0.005) were higher in Group I than in Group II. Macrovesicular steatosis was significantly more common in Group II than in Group I (P = 0.03). Conclusion -Hypercaloric and hyperlipidic diet rich in polyunsaturated fat promotes weight gain and favors the development of hepatic steatosis while reducing serum levels of triglycerides, total cholesterol and HDL.

Eicosapentaenoic acid/docosahexaenoic acid 1:1 ratio improves histological alterations in obese rats with metabolic syndrome

“…Various studies have shown that both the excess and the total absence of omega 3 PUFA in experimental animals have given rise to hepatic steatosis [19,20]. This could be explained by the nature of the PUFA n-3, which is fat.…”

Physical training at sub-threshold intensity reduces the prevalence of hepatic steatosis after high-fat diet in rats

“…It is important to emphasize that there is difference in the composition of lipids (4.24% lower in Baru diet) and calories (5.04Kcal/100g higher in Cafeteria diet) between the experimental diets; nevertheless, this reduction in the lipids supply occurred only after the diet-induced obesity model. Therefore, the harm to health was expected (i.e., consumption of unsaturated fat), as aforementioned (Burlamaqui et al, 2011;De Souza et al, 2005;Macedo et al, 2012). Even with this reduction, this diet can be considered as both high-fat and high-calorie (Reeves, Nielsen, & Fahey, 1993).…”

“…Diets rich in Omega3 improve the control of triglyceride concentrations in the liver, the hepatic oxidation of lipids and diminish the lipogenic capacity (Neschen et al, 2002;Valenzuela & Videla, 2011). But, it is not sufficient to prevent NAFLD if the diet used is high-fat in experiments with sedentary animals (Burlamaqui et al, 2011).…”

“…Baru has a nutritional composition that is more favorable to health in comparison with products extensively used industrially, such as the Brazil nut, cashew nut, peanut, almonds and fat liver accumulation (Burlamaqui et al, 2011;De Souza et al, 2005). Cafeteria diet is known to promote obesity, to increase adipose tissue and plasma levels of leptin, triglycerides and total cholesterol (Macedo et al, 2012).…”

Sweet swell of burning fat: emerging role of high-density lipoprotein in energy homeostasis

“…The evidence about the effect of hypercaloric diets (>3000 kcal/day) on HDL comes mostly from animal studies and appears contradictory. Said effect depends on the type of diet (high fat vs. high carbohydrate vs. high protein) [4,5]. Regarding recent evidence, in a controlled feeding study which involved a single human participant, both HDL-C and apo A-I increased after 5 days of a ketogenic hypercaloric diet [6 ▪ ].…”