engleski

REDUCED ENDOTHELIUM-DEPENDENT DILATION IN VISCERAL COMPARED TOSUBCUTANEOUS ADIPOSE ARTERIOLES IN HUMAN OBESITY

Objective The main objective of this study is to determine the influence of adipose tissue on vascular reactivity and endothelial function of human resistance blood vessels, and seek to explain at least part of the mechanisms by which adipose tissue acts on vascular function in obese humans. Design and Methods Vessels from 53 morbidly obese women (BMI>40 kg/m2) were collected from subcutaneous (SAT) and visceral (VAT) adipose biopsies and were cannulated for vascular reactivity measurements in response to flow (pressure gradients of 10- 100 cmH2O) and in response to acetylcholine (ACh, 10-9-10-4 M). Flow- and acetylcholine- mediated vasodilation was observed in the presence and absence of nitric oxide synthase (NOS) inhibitor, Nω- nitro-L-arginine methyl ester (L-NAME, 10–4 M), and non selective cytochrome P450 pathway inhibitor, 17- octadecynoic acid (17-ODYA ; 10-5 M). Results The mean value of three blood pressure measurements showed that the participants were normotensive (125±16/73±11mmHg), which confirmed that all results we get are independent of blood pressure. Dilator responses of VAT resistance arteries were less sensitive to increase flow, but also to ACh compared to SAT vessels. L-NAME significantly reduced FID in SAT microvessels, while has no effect in VAT microvessels. 17-ODYA reduced FID of microvessels from both SAT and VAT, compared to baseline. There was a significant reduction in AChID in arterioles from SAT in the presence of L-NAME, but had no effect in microvessels from VAT. Conclusion In human obesity, vasodilator sensitivity to flow and acetylcholine in VAT resistance arteries are reduced compared to SAT. Nitric oxide is largely responsible for the flow- and acetylcholine- induced dilation of SAT arteries but not VAT. Metabolites of cytochrome P450 enzyme contribute to the mechanisms of flow- induced dilation of both microvessels from SAT and VAT, which indicates the essential role of CYP 450 metabolites in visceral fat arteries.

endothelium; flow induced dialtion; acetylcholin induced dilation; subcutaneous fat; visceral fat

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