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      Effects of Bariatric Surgery on Human Small Artery Function : Evidence for Reduction in Perivascular Adipocyte Inflammation, and the Restoration of Normal Anticontractile Activity Despite Persistent Obesity

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          Abstract

          Objectives

          The aim of this study was to investigate the effects of bariatric surgery on small artery function and the mechanisms underlying this.

          Background

          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.

          Methods

          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.

          Results

          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.

          Conclusions

          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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          Hypoxia-inducible factor 1alpha induces fibrosis and insulin resistance in white adipose tissue.

          Nils Halberg, Tayeba Khan, Maria Trujillo … (2009)
          Adipose tissue can undergo rapid expansion during times of excess caloric intake. Like a rapidly expanding tumor mass, obese adipose tissue becomes hypoxic due to the inability of the vasculature to keep pace with tissue growth. Consequently, during the early stages of obesity, hypoxic conditions cause an increase in the level of hypoxia-inducible factor 1alpha (HIF1alpha) expression. Using a transgenic model of overexpression of a constitutively active form of HIF1alpha, we determined that HIF1alpha fails to induce the expected proangiogenic response. In contrast, we observed that HIF1alpha initiates adipose tissue fibrosis, with an associated increase in local inflammation. "Trichrome- and picrosirius red-positive streaks," enriched in fibrillar collagens, are a hallmark of adipose tissue suffering from the early stages of hypoxia-induced fibrosis. Lysyl oxidase (LOX) is a transcriptional target of HIF1alpha and acts by cross-linking collagen I and III to form the fibrillar collagen fibers. Inhibition of LOX activity by beta-aminoproprionitrile treatment results in a significant improvement in several metabolic parameters and further reduces local adipose tissue inflammation. Collectively, our observations are consistent with a model in which adipose tissue hypoxia serves as an early upstream initiator for adipose tissue dysfunction by inducing a local state of fibrosis.
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            Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss.

            Raffaella Cancello, Corneliu Henegar, Nathalie Viguerie … (2005)
            In human obesity, the stroma vascular fraction (SVF) of white adipose tissue (WAT) is enriched in macrophages. These cells may contribute to low-grade inflammation and to its metabolic complications. Little is known about the effect of weight loss on macrophages and genes involved in macrophage attraction. We examined subcutaneous WAT (scWAT) of 7 lean and 17 morbidly obese subjects before and 3 months after bypass surgery. Immunomorphological changes of the number of scWAT-infiltrating macrophages were evaluated, along with concomitant changes in expression of SVF-overexpressed genes. The number of scWAT-infiltrating macrophages before surgery was higher in obese than in lean subjects (HAM56+/CD68+; 22.6 +/- 4.3 vs. 1.4 +/- 0.6%, P < 0.001). Typical "crowns" of macrophages were observed around adipocytes. Drastic weight loss resulted in a significant decrease in macrophage number (-11.63 +/- 2.3%, P < 0.001), and remaining macrophages stained positive for the anti-inflammatory protein interleukin 10. Genes involved in macrophage attraction (monocyte chemotactic protein [MCP]-1, plasminogen activator urokinase receptor [PLAUR], and colony-stimulating factor [CSF]-3) and hypoxia (hypoxia-inducible factor-1alpha [HIF-1alpha]), expression of which increases in obesity and decreases after surgery, were predominantly expressed in the SVF. We show that improvement of the inflammatory profile after weight loss is related to a reduced number of macrophages in scWAT. MCP-1, PLAUR, CSF-3, and HIF-1alpha may play roles in the attraction of macrophages in scWAT.
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              Reduced Adipose Tissue Oxygenation in Human Obesity

              Magdalena Pasarica, Olga Sereda, Leanne Redman … (2009)
              OBJECTIVE— Based on rodent studies, we examined the hypothesis that increased adipose tissue (AT) mass in obesity without an adequate support of vascularization might lead to hypoxia, macrophage infiltration, and inflammation. RESEARCH DESIGN AND METHODS— Oxygen partial pressure (AT pO2) and AT temperature in abdominal AT (9 lean and 12 overweight/obese men and women) was measured by direct insertion of a polarographic Clark electrode. Body composition was measured by dual-energy X-ray absorptiometry, and insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp. Abdominal subcutaneous tissue was used for staining, quantitative RT-PCR, and chemokine secretion assay. RESULTS— AT pO2 was lower in overweight/obese subjects than lean subjects (47 ± 10.6 vs. 55 ± 9.1 mmHg); however, this level of pO2 did not activate the classic hypoxia targets (pyruvate dehydrogenase kinase and vascular endothelial growth factor [VEGF]). AT pO2 was negatively correlated with percent body fat (R = −0.50, P < 0.05). Compared with lean subjects, overweight/obese subjects had 44% lower capillary density and 58% lower VEGF, suggesting AT rarefaction (capillary drop out). This might be due to lower peroxisome proliferator–activated receptor γ1 and higher collagen VI mRNA expression, which correlated with AT pO2 (P < 0.05). Of clinical importance, AT pO2 negatively correlated with CD68 mRNA and macrophage inflammatory protein 1α secretion (R = −0.58, R = −0.79, P < 0.05), suggesting that lower AT pO2 could drive AT inflammation in obesity. CONCLUSIONS— Adipose tissue rarefaction might lie upstream of both low AT pO2 and inflammation in obesity. These results suggest novel approaches to treat the dysfunctional AT found in obesity.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Am Coll Cardiol
                Journal ID (iso-abbrev): J. Am. Coll. Cardiol
                Title: Journal of the American College of Cardiology
                Publisher: Elsevier Biomedical
                ISSN (Print): 0735-1097
                ISSN (Electronic): 1558-3597
                Publication date PMC-release: 09 July 2013
                Publication date (Print): 09 July 2013
                Volume: 62
                Issue: 2
                Pages: 128-135
                Affiliations
                [∗ ]Cardiovascular Research Group, University of Manchester, Manchester, United Kingdom
                [† ]Manchester Wellcome Trust Clinical Research Facility, Manchester, United Kingdom
                [‡ ]Department of Clinical Biochemistry, Manchester Royal Infirmary, Manchester, United Kingdom
                [§ ]Salford Royal NHS Foundation Trust, Manchester, United Kingdom
                Author notes
                [∗ ] Reprint requests and correspondence: Dr. Reza Aghamohammadzadeh, Cardiovascular Research Group, Core Technology Facility (3rd floor), 46 Grafton Street, Manchester M13 9NT, United Kingdom. reza.zadeh@ 123456manchester.ac.uk
                Article
                Publisher ID: S0735-1097(13)01788-9
                DOI: 10.1016/j.jacc.2013.04.027
                PMC ID: 3791397
                PubMed ID: 23665100
                SO-VID: e064c907-c285-4679-99d9-e0fccd965402
                Copyright © © 2013 Elsevier Inc.
                License:

                This document may be redistributed and reused, subject to certain conditions.

                History
                Date received : 13 December 2012
                Date revision received : 11 April 2013
                Date accepted : 16 April 2013
                Categories
                Subject: Clinical Research
                Subject: Cardiometabolic Risk

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: bariatric,cardiovascular,obesity,adipor1, adiponectin receptor 1,bmi, body mass index,hscrp, high-sensitivity c-reactive protein,no, nitric oxide,pvat, perivascular adipose tissue,tnf, tumor necrosis factor
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: bariatric, cardiovascular, obesity, adipor1, adiponectin receptor 1, bmi, body mass index, hscrp, high-sensitivity c-reactive protein, no, nitric oxide, pvat, perivascular adipose tissue, tnf, tumor necrosis factor

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