Pregled bibliografske jedinice broj: 626610
Mitochondrial reactive oxygen species contribute to impaired flow-induced dilation in visceral but not subcutaneous adipose tissue resistance arteries in human obesity
Mitochondrial reactive oxygen species contribute to impaired flow-induced dilation in visceral but not subcutaneous adipose tissue resistance arteries in human obesity // The FASEB Journal 2013 ; 27 (Meeting Abstract Supplement) / Weissmann, Gerald (ur.).
Bethesda (MD): Federation of American Societies for Experimental Biology (FASEB), 2013. (poster, međunarodna recenzija, sažetak, znanstveni)
CROSBI ID: 626610 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Mitochondrial reactive oxygen species contribute to impaired flow-induced dilation in visceral but not subcutaneous adipose tissue resistance arteries in human obesity
Autori
Robinson, Austin T ; Szczurek, Mary ; Bian, Jing-Tan ; Čavka, Ana ; Grizelj, Ivana ; Phillips, Shane A
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
The FASEB Journal 2013 ; 27 (Meeting Abstract Supplement)
/ Weissmann, Gerald - Bethesda (MD) : Federation of American Societies for Experimental Biology (FASEB), 2013
Skup
Experimental Biology 2013
Mjesto i datum
Boston (MA), Sjedinjene Američke Države, 20.04.2013. - 24.04.2013
Vrsta sudjelovanja
Poster
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
microcirculation; obesity; reactive oxygen species
Sažetak
Microvascular dysfunction contributes to cardiovascular disease risk. Previous studies indicate that flow-induced dilation (FID) is impaired in resistance arteries from visceral adipose tissue (VAT) compared to subcutaneous adipose tissue (SAT), in obese subjects. We hypothesized that mitochondrial reactive oxygen species contribute to altered mechanisms of FID in VAT. Resistance arteries (RAs) were dissected from VAT and SAT biopsies obtained from obese subjects during bariatric surgery (n=17 BMI: 48±2). Intraluminal diameters were measured via videomicroscopy before and during flow (pressure gradient 10 to 100 cmH2O) in the presence and absence of Tempol (100μM), PEG- catalase (PEG-CAT ; 500 U/ml), L-NAME 100 μM), and Rotenone (50 μM). Fluorescent quantification of flow-induced H2O2 and nitric oxide (NO) production was also determined. Rotenone improved FID (77±8% vs. 39±4% P<.001) and increased generation of H2O2 and NO in RAs of VAT. There was no effect of Rotenone on FID or H2O2 production in SAT. The addition of PEG- CAT or L-NAME to rotenone eliminated the improved FID in VAT. Tempol improved FID in RAs of both VAT and SAT, but was abolished by PEG- CAT. Taken together these data suggest that 1) mitochondrial ROS contribute to impaired FID in VAT and 2) H2O2 and NO contribute to the restored dilation induced by rotenone and Tempol in visceral adipose during obesity.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Ustanove:
Medicinski fakultet, Osijek
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE