engleski

Microvascular reactivity in subcutaneous and visceral adipose tissue in human obesity

Introduction: Clinical studies have shown that individuals with increased visceral adipose tissue are at higher risk of developing fatal diseases than those with similar amounts of subcutaneous adipose tissue. The purpose of this study was to test the hypothesis that microvascular flow induced dilation (FID) and acetylcholine induced dilation (AChID) are impaired in visceral compared to subcutaneous adipose tissue in obese subjects, and that mechanisms of FID and AChID in human obesity are different in the visceral than in the subcutaneous resistance arteries. Materials and methods: Resistance arteries from subcutanous and visceral adipose tissue biopsies were cannulated for vascular reactivity measurements in response to stepwise increasing pressure (Δ10-Δ100) and in response to acetylcholine (Ach, 10-9-10-4 M) with and without presence of Nω-nitro-L-arginine methyl ester (L-NAME), indomethacin (INDO), PEG-catalase (PEG-CAT) and 17-octadecynoic acid (17-ODYA). Nitric oxide (NO) generation in microvessels was detected with the NO Detection Kit. Results: FID and AChID in VIS OB were significantly reduced compared to the SubQ OB at each pressure gradient and Ach level. The presence of L-NAME, indomethacin or PEG-catalase significantlly reduced FID and AchID in the SubQ, while such reduction was not significant in the VIS compared to the baseline. The presence of 17-octadecynoic acid reduced FID and AchID in both SubQ and VIS compared to the baseline. Respectively, FID was significantly more reduced in the VIS than in the SubQ group. Conclusion: In conclusion, FID and AChID are reduced in VIS compared to the SubQ resistance arteries and mediated by different regulatory mechanisms with the emphasis on the role of the cytochrome P450 metabolites in VIS arterioles vasodilation.

blood flow; acetycholine; blood vessels; endothelium; vasodilation; obesity

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