Increased body fat results in attenuated endothelium‐dependent dilation of rat aorta

Obesity is associated with high cardiovascular risk. We tested the hypothesis that obesity, independent of dietary fat content, results in vascular endothelial dysfunction. Rats were fed a high fat (HF; kcal: protein 20%; carbohydrate 20%; fat 60%), low fat (LF; kcal: 20% protein; 70% carbohydrate; 10% fat), or normal chow diet (equal to LF, but not enhanced for better taste). At 8wks of HF or LF diet, % body fat and weight were measured, and aortas excised for the assessment of acetylcholine (Ach) and sodium nitroprusside (SNP)‐induced endothelium‐dependent or independent dilation (respectively) using a wire myograph. Percent body fat (20±1.3 vs 23±1.3%, n=10) and body weight (568±12 vs. 610±17g, n=10) between LF and HF diet‐fed rats, respectively, was not significantly different, possibly due to high food consumption in both groups. However, % body fat (5.11, n=2) and weight (441±27g, n=5, p<0.05) were lower in chow‐fed rats compared to both LF and HF groups. Relaxation to Ach was not different in aortas from HF and LF rats (max % relaxation: 51±5 vs 56 ±9, respectively n=4 each), however, maximum relaxation to Ach was significantly increased in aorta from chow (76±5% n=4, p<0.05) compared to LF‐diet rats. Relaxation to SNP was not different between groups. These data suggest that increased % body fat and weight result in attenuated endothelium‐dependent vasodilation regardless of the dietary fat content. NIH: HL04346