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Atherosclerosis and Lipoproteins |
From the Departments of Clinical Physiology (J.H., O.T.R.), Clinical Chemistry (M.R., P.S.), PET-Centre (O.T.R.), Physiology (M.A.) (MCA Research Laboratory), University of Turku, Finland; Medical Centre Mehiläinen (T.I., P.S., J.H. O.T.R.), Turku, Finland; Leiras Finland, Inc. (J.E.), Turku, Finland; and Laboratory of Atherosclerosis Genetics, Department of Clinical Chemistry, Centre for Laboratory Medicine (T.L., A.H.), Tampere University Hospital and University of Tampere, Finland.
Correspondence to Olli T. Raitakari, Turku PET-Centre, Kiinamyllynkatu 48, FIN-20521 Turku, Finland. E-mail olli.raitakari{at}utu.fi
Objective Obesity is associated with endothelial dysfunction that may contribute to the development of atherosclerosis. We studied whether weight reduction improves endothelial function in overweight individuals.
Methods and Results Flow-mediated endothelium-dependent vasodilation of the brachial artery was measured in 67 adults (age: 46±7 years, body mass index: 35.2±5.4 kg/m2) before and after a 6-week weight reduction program induced by very-low-calorie diet (daily energy: 580 kcal/2.3 MJ). Caloric restriction reduced body weight from 101±18 to 90±17 kg. Flow-mediated vasodilation increased from 5.5%±3.7 to 8.8%±3.7% (P<0.0001). Nitrate-mediated vasodilation was not significantly affected. The improvement in flow-mediated dilation was associated with the reduction in plasma glucose concentration (P=0.0003). This relationship was independent of changes in weight, serum lipids, oxidized LDL, C-reactive protein, adiponectin, blood pressure, and insulin.
Conclusions Weight reduction with very-low-calorie diet improves flow-mediated vasodilation in obese individuals. This improvement is related to the reduction in plasma glucose concentration. These observations suggest that changes in glucose metabolism may determine endothelial vasodilatory function in obesity.
Key Words: endothelium obesity risk factors glucose weight reduction
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