Increased consumption of fat and soft drinks rich in fructose is closely associated with a higher prevalence of metabolic syndrome. The major pathogenesis of metabolic syndrome is the development of insulin resistance caused by the accumulation of visceral fat, which promotes the elevation of blood pressure, dyslipidemia, and dysregulation of glucose metabolism. Expression of all components of the renin–angiotensin–aldosterone–system (RAAS) has been shown in adipose tissue of human and rodent models. The present work aimed at studying the effects of inhibition of angiotensin converting enzyme, blocking angiotensin II type 1 receptor, and blocking aldosterone receptor on high fat fructose diet (HFFD) feeding induced-changes in body weight, insulin resistance, and hepatic steatosis in male albino rats. Fifty adult male albino rats were included in this study, divided into five equal groups. Each group contained 10 rats with equal average body weights: Group I: control rats fed standard chow (SC) , Group II: high fat-fructose fed rats (HFFD), Group III: HFFD rats treated with angiotensin-converting enzyme inhibitor(Captopril), Group IV: HFFD rats treated with angiotensin receptor-1 blocker (Losartan) and Group V : HFFD rats treated with aldosterone receptor blocker (Spironolactone) . Our results showed that feeding rats with HFFD for 10 weeks resulted in significant increase in body weight together with increased both absolute and relative epididymal fat weight, elevation of systolic blood pressure, significant increase in fasting serum glucose, serum insulin and insulin resistance as indicated by HOMA index compared to control group. Concerning circulating lipids, HFFD- fed rats showed significant elevation in serum triglycerides, serum free fatty acids, total cholesterol and low HDL-cholesterol. Both absolute and relative liver weight increased as well. Histological examination revealed accumulation of lipid droplets in the hepatocytes indicating development of hepatic steatosis. Moreover, non alcoholic steatohepatitis (NAS) score and fibrotic changes significantly increased compared to control group with increased gene expression of SREBP1c, while gene expression of ChoREBP decreases. Moreover, the expression of genes encoding the synthesis of two key inflammatory mediators TNF and IL-6 significantly increased compared to normal chow fed rats. Treatment with ACE inhibitor (Captopril), AT1 receptor blocker (Losartan), or aldosterone receptor blocker (Spironolactone) demonstrated significant decrease in the body weight gain compared to untreated rats fed HFFD, significant decrease in insulin resistance as indicated by decreased fasting serum glucose level, insulin level and HOMA index, reduction of serum levels of triglycerides, cholesterol, FFA and elevation of serum level of HDL-cholesterol, reduction of systolic blood pressure, decrease the development of hepatic steatohepatitis and fibrosis compared to HFFD-fed untreated rats, with decreased gene expression of SREBP1c, IL-6, TNF-alpha, and increased expression of ChoREBP compared to HFFD-fed untreated rats.