IS BODY FATNESS OR ITS DISTRIBUTION RELATED TO ENDOTHELIAL FUNCTION IN OLDER PERSONS?

Abstract

Increased fatness, and in particular central obesity, has been linked to a higher risk of atherosclerosis. However, the relationships of body fat and its distribution to endothelial dysfunction, a marker of early atherosclerosis have not been established. In this study, we evaluated mildly hypertensive but otherwise healthy men (n = 14) and women (n = 22), aged 55 to 75 years (mean 62.9 ± 5.2). As a marker of endothelial function, we used ultrasound to measure endothelium-dependent flow-mediated vasodilatation (FMD) as the percent change of brachial artery diameter at 1-minute of reactive hyperemia. We evaluated fatness and its distribution using anthropometric measures (BMI, waist/hip ratio, sum of 7 skinfolds); dual energy X-ray absorptiometry for percent body fat; and magnetic resonance imaging for abdominal total, subcutaneous, and visceral fat. Using bivariate analysis, we found that FMD was inversely related to key measures of central obesity including the waist-to-hip ratio (r = −0.37, p ≤ 0.02); visceral-to-total abdominal fat ratio (r = −0.36, p ≤ 0.03); and visceral-to-subcutaneous abdominal fat ratio (r = −0.35, p ≤ 0.04). Total percent body fat was positively related to FMD, r = 0.34, p ≤ 0.04. However, this association of FMD and percent body fat did not persist in multivariate analysis and was explained by the finding that individuals with the least percent body fat had the most abdominal visceral fat. No other measure of total body fatness or total abdominal or abdominal subcutaneous fat was associated with FMD. Thus, in older persons, the amounts of visceral adipose tissue and the waist-hip-ratio, the hallmark indices of central obesity, are predictive of endothelium-dependent flow-mediated vasodilatation whereas parameters of total fatness show little association. Whether the cause-effect relationship between vascular endothelial function and central obesity involves metabolic (lipids and lipoproteins, glucose, insulin) and hormonal (leptin, cortisol, growth hormone) alterations related to visceral fat remains to be determined. Supported by NIH 1R01HL59164 and 5M01RR02719