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Microvascular reactivity in subcutaneous and visceral fat tissue in human obesity

Microvascular dysfunction contributes to cardiovascular disease risk during obesity. Prior data suggest that visceral adipose tissue (VAT) is associated to cardiometabolic risk factors and endothelial dysfunction compared subcutaneous adipose tissue (SAT). The aim of this study was to determine flow induced dilation (FID) in human VAT and SAT resistance arteries. We hypothesized that microvascular FID is impaired in VAT compared to SAT during obesity. Microvessels were obtained from VAT and SAT biopsies in lean (LN ; BMI<27) and during bariatric surgery (OB ; BMI>48). Isolated vessels were cannulated for vascular reactivity to flow (pressure gradient cmH2O, 20, 40, 60, 100) in the absence and presence of the NOS inhibitor L- NAME (10–4 M). Dilations to papaverine (10–4M) were determined in each vessel. FID was reduced in VAT (at 60, 59±7%, p<0.05) compared to SAT (at 60, 100±10%). Interestingly, FID was increased in SAT but not VAT from OB compared to LN subjects. There was no change in maximal dilation to papaverine between groups. In addition, there was no effect of L-NAME on FID in SAT of OB and LN. However, L- NAME reduced FID in VAT of OB (at 60, 36±8% ; p<0.05) vs. baseline. These data suggest that 1) FID is reduced in visceral compared to subcutaneous fat of obese patients and 2) NO mediates FID in microvessels from visceral but not subcutaneous adipose during obesity. NIH (K23HL085614, R01HL095701), UKF (87/11, 88/11).

microvascular reactivity; obesity

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