Effects of a lifestyle program on vascular reactivity in macro- and microcirculation in severely obese adolescents.

CONTEXT AND OBJECTIVE: This study aimed to comprehensively assess the macro- and microcirculation of severely obese adolescents (SOA) and normal-weight counterparts and to determine the longitudinal effects of weight loss on vascular function in SOA. DESIGN, SETTING, PARTICIPANTS, AND OUTCOME MEASURES: Seventeen SOA (body mass index z-score = 4.22 ± 0.73) and 19 puberty-matched normal-weight counterparts (body mass index z-score = -0.02 ± 1.04) were included. The SOA participated in a 4 month weight loss program. Brachial artery flow-mediated dilation and response to sublingual nitrate (nitrate-mediated dilation [NMD]) were assessed by high-resolution ultrasound. Microvascular reactivity was evaluated by laser Doppler flowmetry in response to NMD, iontophoresis of acetylcholine and sodium nitroprusside, and local hyperthermia. Plasma insulin, leptin, resistin, C-reactive protein, myeloperoxidase, and tissue plasminogen activator were measured.

RESULTS: At baseline, SOA had similar flow-mediated dilation and impaired NMD in the brachial artery compared to normal-weight adolescents. Similarly, peak responses to acetylcholine and sodium nitroprusside iontophoresis and to local hyperthermia were unaltered, whereas cutaneous blood flow after NMD was lower in the forearm microcirculation of SOA. All plasma measurements were significantly higher in SOA. After the 4-month program, SOA presented a weight reduction of 7.4 ± 3.1%, but neither brachial artery nor microvascular reactivity variables were improved. Significant decreases were detected in plasma leptin, myeloperoxidase, and tissue plasminogen activator.

CONCLUSIONS: Macro- and microvascular endothelial function are preserved in adolescents with severe obesity. Conversely, weight loss does not improve their impaired smooth muscle response to exogenous organic nitrate in both vascular beds, despite reducing plasma markers adversely related to vascular homeostasis.