The impairment of flow-mediated vasodilatation in obese men with visceral fat accumulation.

BACKGROUND

Obesity has been reported to be associated with coronary artery disease and other atherosclerotic diseases. Recently, evidence has accumulated indicating that intra-abdominal visceral fat accumulation contributes to atherogenesis; however, the mechanism underlying this remains to be determined. This study was undertaken to elucidate whether intra-abdominal visceral fat accumulation impairs vascular endothelial function in obese men.

METHODS AND RESULTS

Thirty-eight obese men (body mass index (BMI) > or = 26.0), aged 19-64 y (mean age 37.6 +/- 1.8 y) and 23 age-matched non-obese subjects were examined. According to the ratio of the maximum thickness of preperitoneal fat to the minimum thickness of subcutaneous fat (Pmax/Smin) obtained by longitudinal ultrasound scanning in the subxiphoid region in obese men, we divided obese subjects into two categories; visceral (Pmax/Smin > or = 1; n=23) and subcutaneous type (Pmax/Smin < 1; n=15). To investigate endothelial function, we performed ultrasound measurement of the brachial artery diameter non-invasively both at rest and during reactive hyperaemia in the muscle distal to the brachial artery which causes endothelium-dependent vasodilatation. The brachial diameter change was also measured after sublingual administration of nitroglycerin, which causes endothelium-independent vasodilatation. Flow-mediated diameter (D) increase (%FMD; deltaD/D x 100), in the subjects with visceral type obesity (3.09 +/- 0.43%) was significantly lower than those of the subjects with subcutaneous type obesity and non-obese subjects (7.90 +/- 0.51%, 8.91 +/- 0.44%, respectively, P < 0.01). The magnitude of endothelium-independent vasodilatation by nitroglycerin was similar in all groups. On multiple regression analysis, the Pmax/Smin showed a significant inverse correlation with %FMD.

CONCLUSIONS

The subjects with visceral type obesity, rather than those with the subcutaneous type, are associated with impaired flow-mediated endothelium-dependent vasodilatation of the brachial artery.