High-fructose diet initially promotes increased aortic wall thickness, liver steatosis, and cardiac histopathology deterioration, but does not increase body fat index.

Abstract

Background: Dietary fats and fructose have been responsible for inducing obesity and body tissues damage due to the consequence of metabolic syndrome through several mechanisms. The body fat index (BFI) is one of the anthropometric measures used to detect obesity in rats. This study aims to examine the correlation between high-fat high-fructose diet and liver steatosis cell count, early atherosclerosis characteristics, and body fat index (BFI) in Sprague Dawley rats.Design and methods: This was an experimental design using 2 groups of 12-weeks-old Sprague Dawley (SD) rats. The control group received a standard diet and tap water beverages for 17 weeks. The intervention group was fed with high-fat diet from modified AIN 93-M and additional 30% fructose drink. We analyzed the foam cell count, aortic wall thickness, cardiac histopathology, and liver steatosis cell count after the sacrifice process.Results: The rats in the intervention group had a higher aortic wall thickness, liver steatosis, and foam cell count (+125%, p<0.01; +317%, p<0.01 and +165%, p<0.01 respectively) compared to the control group. The intervention group also showed higher mononuclear inflammatory and hypertrophic cell count. A significant positive correlation was found between dietary fructose with premature atherosclerosis by increasing foam cell count (r=0.66) and aortic wall thickness (r=0.68). In addition, 30% dietary fructose increased liver steatosis (r=0.69) and mononuclear inflammatory cardiac cell count (r=0.61). Interestingly, the intervention had no effect on the body fat index (p>0.5; r=0.13).Conclusions: Dietary fat and fructose consumption for 17 weeks promotes atherosclerosis, liver steatosis, and cardiac histopathology alteration without increasing BFI.Significance for public healthObesity is a major health problem that is a powerful inducer of non-communicable disease (NCD) both in the national and global level of the human population age groups. Based on this study, consumption of fructose also poses an increased risk in developing metabolic syndrome, which differs from the current understanding of dominantly caused by excessive intake of fat. Furthermore, high fructose consumption promotes early signs of cardiovascular and liver disease without significant manifestation in anthropometry characteristics. It is believed that these results are important and will give readers a broader view on combating obesity epidemics from a dietary and nutritional perspective, which may also contain additional reference for nutrition education or dietary advice for the prevention of obesity.