Abstract

Objective: Abdominal obesity represents a systemic metabolic pathology, being related to the development of insulin resistance and cardiovascular diseases. Microvascular dysfunction is multifactorial and alters, among other things, insulin-mediated glucose disposal. We have previously shown that insulin-mediated microvascular recruitment in skeletal muscle is impaired in obese men and that weight loss can reverse this impairment. Our objective was to examine whether impairment of insulin-mediated microvascular function and subsequent reversal by weight loss can be detected in skin as well using flowmotion analyses. Design and method: Twenty-five lean and 53 abdominally obese men (waist circumference 102–110 cm; aged18–65 yrs.; no cardiovascular diseases or type 2 diabetes) were recruited. Following baseline measurements, the obese men were randomized to either an 8-week program of low calorie diet (LCD), or usual diet (control). Skin flowmotion was measured by laser-doppler flowmetry and Fourier analyses resulted in the contribution of five frequency domains: endothelial, 0.01–0.02 Hz; neurogenic, 0.02–0.06 Hz; myogenic, 0.06–0.15 Hz; respiratory, 0.15–0.40 Hz and cardiac, 0.40–1.60 Hz. Flowmotion was measured before and during a hyperinsulinaemic euglycaemic clamp. Results: Baseline flowmotion was not different between lean and obese men. In both lean and obese men, hyperinsulinaemia induced a similar increase in total flowmotion (lean: 6.5% (1.5, 11.5); obese: 3.6% (0.6, 6.6); p = 0.309 vs lean) and the endothelial domain (lean: 12.3% (1.7, 22.9); obese: 8.6% (2.5, 14.7); p = 0.538 vs lean), and a decrease in the neurogenic domain (lean: -14.2% (-24.8, -3.7); obese: -4.6% (-13, 3.8); p = 0.149 vs lean). The LCD intervention did not statistically significantly affect flowmotion. Conclusions: In contrast to insulin-mediated microvascular recruitment in skeletal muscle, skin microvascular flowmotion is unaltered in abdominally obese men versus lean. In addition, a weight loss intervention in the obese men did not affect skin microvascular flowmotion. These findings indicate that the sensitivity of the microvasculature to systemic mediators may differ between tissues.

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