Effects of Bariatric Surgery on Human Small Artery Function

医学 脂联素 脂肪组织 脂肪因子 电阻抗肌描记术 内科学 瘦素 内分泌学 炎症 氧化应激 糖尿病 外科 病理 肥胖 胰岛素抵抗 血管舒张
作者
Reza Aghamohammadzadeh,Adam Greenstein,Rahul Yadav,Maria Jeziorska,Salam Hama,Fardad Soltani,P. Pemberton,Basil Ammori,Rayaz A. Malik,Handrean Soran,Anthony M. Heagerty
出处
期刊:Journal of the American College of Cardiology [Elsevier]
卷期号:62 (2): 128-135 被引量:158
标识
DOI:10.1016/j.jacc.2013.04.027
摘要

The aim of this study was to investigate the effects of bariatric surgery on small artery function and the mechanisms underlying this.In lean healthy humans, perivascular adipose tissue (PVAT) exerts an anticontractile effect on adjacent small arteries, but this is lost in obesity-associated conditions such as the metabolic syndrome and type II diabetes where there is evidence of adipocyte inflammation and increased oxidative stress.Segments of small subcutaneous artery and perivascular fat were harvested from severely obese individuals before (n = 20) and 6 months after bariatric surgery (n = 15). Small artery contractile function was examined in vitro with wire myography, and perivascular adipose tissue (PVAT) morphology was assessed with immunohistochemistry.The anticontractile activity of PVAT was lost in obese patients before surgery when compared with healthy volunteers and was restored 6 months after bariatric surgery. In vitro protocols with superoxide dismutase and catalase rescued PVAT anticontractile function in tissue from obese individuals before surgery. The improvement in anticontractile function after surgery was accompanied by improvements in insulin sensitivity, serum glycemic indexes, inflammatory cytokines, adipokine profile, and systolic blood pressure together with increased PVAT adiponectin and nitric oxide bioavailability and reduced macrophage infiltration and inflammation. These changes were observed despite the patients remaining severely obese.Bariatric surgery and its attendant improvements in weight, blood pressure, inflammation, and metabolism collectively reverse the obesity-induced alteration to PVAT anticontractile function. This reversal is attributable to reductions in local adipose inflammation and oxidative stress with improved adiponectin and nitric oxide bioavailability.
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