Dexamethasone Promotes the Risk of Cardiovascular Disease in High Fructose-exposed Wistar Rats

Dyslipidemia constitutes a serious public health concern globally. It has been established that excessive fructose intake results in dyslipidemia; however, whether dexamethasone aggravates or alleviates fructose-induced dyslipidemia is unknown. Thus, we examined the effects of dexamethasone on dyslipidemia and hyperuricemia in high fructose-taking Wister rats. 

Twenty male Wister rats were randomly grouped as control (distilled water), fructose (10% fructose w/v), dexamethasone (0.2 mg/kg, PO) and fructose+dexamethasone. After a 21-day exposure, the serum and heart samples were harvested, processed and analyzed for biochemical assays.

Our findings reveal that exposure of rats to high fructose significantly increased blood glucose, elevated serum triglycerides and uric acid, activity of xanthine oxidase, and lowered high density lipoprotein cholesterol (HDL) level. However, dexamethasone administration had no significant effect on the blood glucose and did not alter the serum levels of triglycerides, uric acid and xanthine oxidase. Meanwhile, both fructose and dexamethasone treatments independently elevated the serum levels of total cholesterol (TC), low density lipoprotein cholesterol (LDL) and malondialdehyde. Further, the fructose treatment elevated the TG/HDL ratio, while both fructose and dexamethasone treatments individually and synergistically elevated TC/HDL ratio. Our study also showed that co-administration of fructose and dexamethasone aggravated the elevated serum levels of TC and LDL, while it impaired the enzymatic antioxidant systems.

Dexamethasone, though slightly reduced fructose-induced hyperglycemia, impaired the antioxidant enzymes and escalated dyslipidemia during fructose intake. Hence, our study suggests that dexamethasone administration may increase the risk of CVD in animals with excessive intake of fructose.