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Lipogenesis and hepatic CD36 expression in the response to cafeteria and high-fructose diet

Selecting an adequate experimental model for metabolic syndrome can be rather challenging due to its multifactorial nature. The most used experimental models have been high fructose and cafeteria diets. The aim of our investigation was to determine possible differences between these two models in the hepatic expression of CD36 and the fatty acid profile of total lipids. Additionally, we tested sex as a variable in both models of metabolic syndrome. Wistar rats (15 male and 15 female) were divided into control group (CON), high fructose group (HF, 15% of fructose in the drinking water) and cafeteria diet group (CAF, basal diet and cafeteria diet in the 1:1 ratio). The experiment lasted 16 weeks. The analysis of hepatic fatty acid composition was performed by using gas chromatography. The lipid peroxidation was determined by MDA-TBARS method using high performance liquid chromatography. Liver triglyceride content was measured by colorimetric quantification kit. The expression of CD36 gene was assessed by qPCR. The statistical analysis was performed using the GraphPad 8 statistical software. Data were compared by the analysis of variance and Tukey post hoc test. The fatty acid profile of the liver fatty acids was significantly different between CAF and HF diets. The most significant differences were a decrease in the EPA content and an increase in the content of n6 DPA in the CAF diet versus the HF diet. An increase in the n6 DPA content was also higher in the female rats compared to the male rats. Lipid peroxidation expressed as MDA-TBARS, was significantly higher in the CAF group compared to the CON and HF groups. Both experimental diets led to the accumulation of triglycerides in the liver. The expression of CD36 gene was significantly increased in the male and female rats fed with the CAF diet. The results showed that the experimental models of metabolic syndrome differ significantly in lipid metabolism and lipid peroxidation. Moreover, male and female rats respond differently to experimental diets.

Metabolic syndrome ; CD-36 ; Lipids ; Fructose

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