Cardiovascular Research Group, University of Manchester, Manchester, United Kingdom; Manchester Wellcome Trust Clinical Research Facility, Manchester, United Kingdom.
Cardiovascular Research Group, University of Manchester, Manchester, United Kingdom; Manchester Wellcome Trust Clinical Research Facility, Manchester, United Kingdom.
J Am Coll Cardiol. 2013 Jul 9;62(2):128-135. doi: 10.1016/j.jacc.2013.04.027. Epub 2013 May 9.
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.
本研究旨在探讨减重手术对小动脉功能的影响及其机制。
在瘦健康人群中,血管周围脂肪组织(PVAT)对邻近小动脉具有抗收缩作用,但在肥胖相关疾病如代谢综合征和 2 型糖尿病中,这种作用会丧失,这些疾病存在脂肪细胞炎症和氧化应激增加的证据。
从小面积肥胖个体(术前 n = 20,术后 n = 15)中采集小动脉段和血管周围脂肪组织。采用血管张力测定法体外检测小动脉收缩功能,采用免疫组织化学法评估血管周围脂肪组织(PVAT)形态。
与健康志愿者相比,肥胖患者术前 PVAT 的抗收缩活性丧失,减重手术后 6 个月恢复。体外超氧化物歧化酶和过氧化氢酶实验方案恢复了肥胖个体术前 PVAT 的抗收缩功能。手术后抗收缩功能的改善伴随着胰岛素敏感性、血糖指数、炎症细胞因子、脂肪因子谱和收缩压的改善,同时伴随着 PVAT 脂联素和一氧化氮生物利用度的增加以及巨噬细胞浸润和炎症的减少。尽管患者仍处于严重肥胖状态,但仍观察到这些变化。
减重手术及其伴随的体重、血压、炎症和代谢改善共同逆转了肥胖引起的 PVAT 抗收缩功能改变。这种逆转归因于局部脂肪炎症和氧化应激的减少,以及脂联素和一氧化氮生物利用度的提高。