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Vascular responses of subcutaneous and visceral adipose tissue microvessels to flow and acetylcholine in human obesity (CROSBI ID 636049)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija

Jukić, Ivana ; Stupin, Ana ; Drenjančević, Ines ; Phillips, Shane A. Vascular responses of subcutaneous and visceral adipose tissue microvessels to flow and acetylcholine in human obesity // Book of Abstracts FAME 2016. 2016

Podaci o odgovornosti

Jukić, Ivana ; Stupin, Ana ; Drenjančević, Ines ; Phillips, Shane A.

engleski

Vascular responses of subcutaneous and visceral adipose tissue microvessels to flow and acetylcholine in human obesity

Objective: The primary goals of the present study were to 1) test the hypothesis that microvascular flow-induced dilation (FID) and acetylcholine-induced dilation (AChID) are reduced in visceral (VAT) compared to subcutaneous adipose tissue (SAT) in obese patients and 2) determine the mechanisms contributing to reduced vasodilator sensitivity to flow in human visceral and subcutaneous adipose tissue arterioles in human obesity. Methods: Vessels from 53 morbidly obese women (BMI>40 kg/m2) were collected from subcutaneous and visceral 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), cyclooxygenase inhibitor indomethacin (INDO ; 10-5M), the H2O2 scavenger poly ethyleneglycol catalase (PEG- CAT ; 500 U/ml), and non-selective cytochrome P450 pathway inhibitor 17-octadecynoic acid (17-ODYA ; 10- 5 M). Also, nitric oxide (NO) and hydrogen peroxide (H2O2) generation in arterioles was detected with fluorescence microscopy, in the presence and absence of flow. Results: 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. INDO reduced FID in SAT microvessels too, but had no additional effect in the presence of L-NAME. There was no effect of L-NAME or INDO alone on FID of VAT microvessels, but addition of L-NAME to INDO reduced FID at higher flow rates. The presence of 17-ODYA partially reduced FID of microvessels from both SAT and VAT, compared to baseline. PEG-CAT reduced FID of SAT microvessels, but had no effect on resistance arteries from VAT. There was a significant reduction in AChID in arterioles from SAT in the presence of L- NAME, INDO and PEG-CAT , but had no effect in microvessels from VAT. In the assence of intraluminal flow, NO production was increased in vessels from SAT compared to VAT, and presence of L-NAME reduced NO production in vessels from SAT, but not in vessels from VAT. In the presence of intraluminal flow, NO production was increased in both SAT and VAT microvessels, and was reduced in SAT by NOS inhibition with L-NAME. During flow PEG-CAT significantly reduced DCF fluorescence in SAT but not in VAT. Conclusion: During obesity, arterioles of visceral fat are less sensitive to flow-induced dilation and flow-induced NO generation compared to arterioles of subcutaneous adipose tissue. Microvascular reactivity to flow is mediated by different regulatory mechanisms in visceral and subcutaneous fat.

obesity; vascular function; microcirculation; subcutaneous adipose tissue; visceral adipose tissue

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

nije evidentirano

Podaci o prilogu

2016.

objavljeno

Podaci o matičnoj publikaciji

Book of Abstracts FAME 2016

Podaci o skupu

Joint Conference of the Hungarian Pharmacology, Anatomy, Microcirculation and Physiological Societies (FAME 2016)

predavanje

01.06.2016-04.06.2016

Pečuh, Mađarska

Povezanost rada

Temeljne medicinske znanosti