Abstract 040: Comparison of Effects of Reux en Y Gastric Bypass and Intra-abdominal Lipectomy on Cardiovascular Function in the Metabolic Syndrome

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Amanda Soler ◽  
Brenda Hutcheson ◽  
Jenny Yang ◽  
Chastity Bradford ◽  
Frank Zhang ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Gastric Bypass ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Carotid Artery ◽  
Abdominal Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Artery Stiffness ◽  
Abdominal Lipectomy

Central (visceral) obesity is a key feature of the metabolic syndrome and an independent predictor of cardiovascular disease. Reux en Y gastric bypass (RnY) has been shown to offer protection against cardiovascular disease, but residual risk remains. It is also unknown whether the cardiovascular benefit is a consequence of a decrease in visceral (intra-abdominal) adipose tissue or of other factors. In this study, we compared the effects of RnY vs. removal of 90% of visceral adipose tissue (=5% body weight) by intra-abdominal lipectomy on cardiac function (echocardiography), macrovascular function (carotid artery stiffness) and microvascular function (coronary artery endothelium-dependent vasorelaxation) in a metabolic syndrome rat model (JCR:LA-cp, JCR). Cardiac output (CO) and ejection fraction (EF) were significantly decreased in JCR vs. normal (Sprague-Dawley, SD) rats (CO=50±5%, EF=45±2% of normal), and were significantly improved by both RnY and intra-abdominal lipectomy (CO=75±6%, EF=82±2% and CO=80±3%, EF=90±2% of normal, respectively). Likewise, acetylcholine-dependent coronary artery vasorelaxation was impaired in JCR rats (50±1% of normal), and was significantly improved by both RnY and intra-abdominal lipectomy (98±2% and 98±3% of normal, respectively). Carotid artery stiffness was significantly increased in JCR rats (~2 fold vs. SD), and was normalized by intra-abdominal lipectomy (to equal SD), but not by RnY (~2 fold vs. SD). Intra-abdominal lipectomy but not RnY also decreased cardiac and vascular elastin degradation in JCR rats (Lipectomy: ~50% (heart), ~75% (carotid); RnY: ~15% (heart), ~5% (carotid) vs. untreated JCR, respectively), concomitant with a decrease in matrix metalloproteinase 12 (MMP12), a major elastase, activation (~50% (heart), ~75% (carotid), ~87% (visceral fat), ~75% (circulating) vs. untreated JCR) and in 20-hydroxyeicosatetraeonic acid (20-HETE) levels (~4 (heart), ~7 (carotid), ~4 (visceral fat), ~4 (circulating) fold vs. untreated JCR). Thus, our data indicate that intra-abdominal adipose tissue itself is a source of factors that may be important negative regulators of micro- and macrovascular and cardiac function, but are not eliminated by RnY.

Abstract P211: Intra-abdominal Lipectomy Normalizes Arterial Stiffness and Blood Pressure via Reduction in 20-HETE

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Amanda A Soler ◽  
Brenda Hutcheson ◽  
Jenny Yang ◽  
Chastity Bradford ◽  
Frank F Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Large Artery ◽  
The Metabolic Syndrome ◽  
Elastin Degradation ◽  
Artery Stiffness ◽  
Abdominal Lipectomy ◽  
Visceral Adipose

Increased intra-abdominal (visceral) adipose tissue is a key feature of the metabolic syndrome affecting over 30% of the U.S. population. Expansion of visceral adipose tissue is linked to the development of hypertension and is a risk factor for cardiovascular disease that can ultimately lead to end-organ damage. While reduction in visceral adipose tissue volume offers cardioprotective effects, the cardiovascular mechanisms behind these beneficial effects remain unclear. In this study, we removed ~90% of visceral adipose tissue (=~5% body weight) by intra-abdominal lipectomy and assessed large arterial stiffness, large artery structural matrix components, and blood pressure in a metabolic syndrome rat model (JCR:LA-cp, JCR). Large artery stiffness was significantly elevated in JCR vs. normal (Sprague Dawley, SD) rats (75±2% JCR vs. SD (carotid)) with a concomitant significant increase in MMP12-dependent elastin degradation (3-6 fold vs. SD). Intra-abdominal lipectomy normalized large artery stiffness, blocked MMP12 activation and reduced elastin degradation in JCR animals (~75% (carotid) vs. untreated JCR). Likewise, hypertension in JCR animals was significantly attenuated by intra-abdominal lipectomy (MABP=156±3 mmHg JCR vs. 90±6 mmHg SD vs. 132±4 mmHg JCR+lipectomy). 20-hydroxyeicosatetraeonic acid (20-HETE), an arachidonic acid metabolite known to be a potent vasoconstrictor in resistance arteries, was significantly elevated in the visceral adipose tissue of JCR rats (~6 fold vs. SD). Intra-abdominal lipectomy normalized 20-HETE levels in JCR rats. Like intra-abdominal lipectomy, 20-HETE antagonists restored large artery elasticity, blocked MMP12 activation and elastin degradation, and significantly decreased blood pressure (125±3 mmHg JCR+20-HETE antagonists) in JCR rats. Thus, 20-HETE may be an important adipokine that mediates the adverse effects of expanded visceral fat volume in the metabolic syndrome and its inhibition may provide a pharmacological approach for the management of central obesity-driven large artery stiffness and hypertension.

Metabolic Syndrome, a Cardiovascular Disease Risk Factor: Role of Adipocytokines and Impact of Diet and Physical Activity

2004 ◽  
Vol 29 (6) ◽  
pp. 808-829 ◽  
Author(s):  
Lindsay E. Robinson ◽  
Terry E. Graham
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Key Words Insulin ◽  
Diet And Physical Activity ◽  
The Impact

The metabolic syndrome comprises an array of cardiovascular disease (CVD) risk factors such as abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Insulin resistance and/or increased abdominal (visceral) obesity have been suggested as potential etiological factors. More recently, increasing evidence has associated insulin resistance and subclinical inflammation involving cytokines derived from adipose tissue, or adipocytokines. Despite the fact that precise mechanisms have yet to be established, there is a significant role for both diet and physical activity to improve the many factors associated with the metabolic syndrome, including modulation of various adipocytokines. Although both diet and physical activity have been studied for their ability to modify cytokines in more traditional inflammatory conditions, such as rheumatoid arthritis, they have been less studied in relation to inflammation as an underlying cause of the metabolic syndrome and/or CVD. A more thorough understanding of the clustering of metabolic abnormalities and their underlying etiology will help to define diet and physical activity guidelines for preventing and treating the metabolic syndrome, an important aspect of CVD prevention. This paper will address potential underlying causes of the metabolic syndrome, with a focus on the putative mechanistic role of adipocytokines, and will discuss the impact of diet and physical activity on the metabolic syndrome. Key words: insulin resistance syndrome, obesity, adipose tissue, skeletal muscle, cytokines, TNF-α, IL-6, PAI-1, inflammation, nutrition, exercise

Metabolic syndrome, inflammation and atherothrombosis

2013 ◽  
Vol 33 (04) ◽  
pp. 283-294 ◽  
Author(s):  
T. W. Weiss ◽  
M. Rohla
Keyword(s):  
Physical Activity ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Atherosclerotic Plaques ◽  
Traditional Concept ◽  
The Past ◽  
The Metabolic Syndrome ◽  
Inflammatory Pattern

SummaryExtensive research of the past decades altered our traditional concept about the genesis of atherosclerosis fundamentally. Today, the crucial role of inflammation in the formation and progression of atherosclerotic plaques is indisputable. Patients at high risk for developing cardiovascular disease, owing to poor diet, obesity and low physical activity have been shown to exhibit a particular inflammatory pattern.Therefore, the present review highlights the crosslink between the metabolic syndrome (MetS), adipose tissue, adipokines and selected inflammatory cytokines in the context of atherothrombosis and cardiovascular disease.

scholarly journals From NAFLD to cardiovascular disease. Is it (still) the metabolic syndrome?

2014 ◽  
Vol 87 (2) ◽  
pp. 80-86 ◽  
Author(s):  
Mihai Alexandru Munteanu ◽  
Petru Adrian Mircea
Keyword(s):  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Liver Disease ◽  
Geographical Area ◽  
Developed Countries ◽  
Active Monitoring ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Visceral Adipose

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease in developed countries. The incidence of NAFLD in the general population is 30-38% deppending on the geographical area and the diagnostic method used. NAFLD is considered to be the liver manifestation of the metabolic syndrome. A better understanding of the natural evolution would have practical consequences related mainly to the need of early and aggressive diagnosis, active monitoring and therapeutic solutions. Cardiovascular disease appears to be the main cause of death in these patients. The mechanisms linking NAFLD with cardiovascular disease are not fully understood yet, but attention was focused primarily on insulin resistance. The visceral adipose tissue, the epicardial adipose tissue, the systemic inflammatory response syndrome, the lipid profile, the procoagulants factors, the oxidative stress, and type 2 diabetes mellitus, they all might play a role in the link between NAFLD and cardiovascular disease. Currently, there isn’t any medication specifically recommended for the treatment of NAFLD. Although the mechanisms underlying the association between NAFLD and cardiovascular disease are not fully known, attention must be paid to this association, given that these patients are more likely to die due to heart disease rather than liver disease.

Carotid Artery Stiffness in Obese Children With the Metabolic Syndrome

2006 ◽  
Vol 97 (4) ◽  
pp. 528-531 ◽  
Author(s):  
Arcangelo Iannuzzi ◽  
Maria Rosaria Licenziati ◽  
Ciro Acampora ◽  
Maurizio Renis ◽  
Mariano Agrusta ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Carotid Artery ◽  
Obese Children ◽  
The Metabolic Syndrome ◽  
Artery Stiffness

scholarly journals Altered subcutaneous abdominal adipose tissue lipid synthesis in obese, insulin-resistant humans

2013 ◽  
Vol 305 (8) ◽  
pp. E999-E1006 ◽  
Author(s):  
Demidmaa Tuvdendorj ◽  
Manisha Chandalia ◽  
Tumurbaatar Batbayar ◽  
Manish Saraf ◽  
Carine Beysen ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Nonesterified Fatty Acid ◽  
Oral Glucose ◽  
Large Variability ◽  
Abdominal Adipose Tissue ◽  
The Metabolic Syndrome ◽  
Wide Range ◽  
Obese Subjects ◽  
Subcutaneous Abdominal Adipose Tissue

The purpose of this study was to evaluate the variability of subcutaneous abdominal adipose tissue (AT) dynamics in obese subjects with a wide range of insulin sensitivity (IS) and the correlation between these two metabolic measures. Ten obese (BMI 30–40 kg/m2) nondiabetic subjects with ( n = 6) and without ( n = 4) the metabolic syndrome were studied following a 12-wk 2H2O labeling period. Subcutaneous abdominal AT biopsies were collected. Deuterium incorporation into triglyceride (TG)-glycerol and TG-palmitate were measured by gas chromatography-mass spectrometry for the calculation of fractional TG synthesis ( fTG) and fractional de novo lipogenesis ( fDNL). Muscle IS and insulin-mediated nonesterified fatty acid (NEFA) suppression (a measure for adipose IS) indexes were derived from the oral glucose tolerance test (OGTT). The ability of subcutaneous abdominal AT to synthesize lipids varied significantly in obese subjects ( fTG range 7–28%, fDNL range 1.1–4.6%) with significantly lower values (>35% reduction) for both parameters in obese with the metabolic syndrome. fTG correlated positively with muscle IS ( r = 0.64, P = 0.04) and inversely with NEFA suppression during the OGTT ( r = −0.69, P = 0.03). These results demonstrate a large variability in subcutaneous abdominal AT lipid turnover in obesity. Moreover, a reduced capacity for subcutaneous abdominal AT fat storage is associated with muscle and adipose tissue insulin resistance as well as with the metabolic syndrome, thus identifying a form of obesity at heightened risk for type 2 diabetes and cardiovascular disease.

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