A high-fat, high-fructose diet induced hepatic steatosis, renal lesions, dyslipidemia, and hyperuricemia in non-obese rats

Excessive consumption of fat and sugar is associated with various chronic diseases. However, the variation of fat and sugar content in the diet greatly affected the outcome. In this study, a high-fat, high-fructose diet (HFHFD) formula was made with a composition of 31.99% carbohydrate, 40.7% fat, 11.8% protein, and an additional 30% fructose drink to confirm the effects of HFHFD on metabolic health and pathological changes in organs, especially the liver, kidneys, pancreas, muscles, and spleen. A total of 24 male Wistar rats aged 8–12 weeks were divided into four groups: standard chow (SC), HFHFD, SC þ carbon tetrachloride (CCl4), and HFHFD þ CCl4. After eight weeks of dietary intervention, body mass index, obesity index, lipid profiles, liver function tests, fasting blood glucose, serum uric acid and urea levels, and tissue histopathology were examined. HFHFD with the main un- saturated fatty acids of linoleic acid (14.57%) and palmitoleic acid (8.28%), the main saturated fatty acids of stearic acid (13.62%) and myristic acid (10.09%), and a low trans-fatty acids content, did not promote the rats to become obese. However, liver histology examination showed severe hepatic steatosis (78.33%), leading to steatohepatitis accompanied by an increase in serum ALP (p < 0.01), triglyceride (p < 0.001), total cholesterol (p < 0.05), and uric acid (p < 0.001) levels. Other histological features showed moderate lesions (45%) of the kidney, slight vacuolization of the pancreas, and a mild increase of inflammatory cells in the spleen and muscle. So, this study found that although HFHFD did not promote obesity within 8 weeks of administration, it induced hepatic and renal lesions, dyslipidemia, and hyperuricemia as a metabolic consequence of excessive fatty acids and fructose.