Abstract
Recent data suggest that bone marrow derived endothelial progenitor cells contribute to endothelial repair after damage. We investigated whether obesity modulates the number and function of progenitor cells, and whether lifestyle intervention with a healthy diet influences this effect. We hypothesized that obesity-mediated vascular injury stimulates progenitor cell mobilization. Methods Peripheral blood mononuclear cells were cultured on fibronectin plates for 7 days and the number of colony forming units (CFUs) with endothelial-type cells at their periphery were counted. 28 lean healthy subjects were compared with 30 overweight/obese age-and sex-matched non-smokers on a high saturated fat (> 10%) American style diet. Twenty obese subjects were then randomized to receive either a Mediterranean-style (MED) diet (n=11) or the control regular American diet (n=9) for 2 months. Endothelium-dependent and -independent function was measured by brachial reactivity testing at baseline, 1 and 2 months. Results CFUs were significantly higher in overweight/obese compared to lean subjects (74±42 vs 23±10, p<0.001), even after adjustment for other risk factors. When overweight/obese subjects were treated with a MED diet, CFUs reduced significantly, a change that was not observed in the controls (Table ). There was a simultaneous improvement in brachial flow-mediated vasodilation but not endothelium-independent function in the MED group. No changes were observed in controls(Table ). Conclusion Endothelial precursors are stimulated in obese compared to lean subjects. Dietary alteration to a MED diet resulted in improvement in endothelial function and reduced mobilization of endothelial precursors. These observations suggest that endothelial injury in obesity provokes a compensatory mobilization of endothelial progenitor cell population that may help repair damage to the endothelial lining.
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