scholarly journals Changes in Visceral Fat and Its Correlation With Changes in Metabolic Variables After Bariatric Surgery

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A6-A7
Author(s):  
Eduardo Doval ◽  
Susana Reyes Lopez ◽  
Alejandra Albarran ◽  
Ernesto Sosa ◽  
Claudia Ramirez ◽  
...  

Abstract Obesity is a health problem. There is a relationship between visceral adipose tissue (VAT) and various metabolic components. So far the most effective treatment for weight reduction and control of comorbidities is bariatric surgery. After bariatric surgery there is a reduction in VAT and a correlation with better control of metabolic variables would be expected. Objective: To determine the decrease in VAT, calculated by bioimpedance at 3 and 6 months after bariatric surgery and its correlation with changes in metabolic parameters (fasting glucose, HOMA, HbA1c, lipid profile). MATERIAL AND Methods: Patients belonging to the HECMNSXXI Obesity Clinic undergoing bariatric surgery during 2020 who agreed to participate in the study were included. VAT volume was determined before surgery and at 3 and 6 months after the procedure by bioimpedance using the SECA mBCA525 body analyzer. At the same time, biochemical metabolic markers were determined (fasting glucose, HOMA, HbA1c, CT, HDL, LDL, and triglycerides). The results were reported using descriptive statistics. A Pearson or Spearman correlation was carried out according to the distribution of the variables. P <0.05 was taken as significant. Results: Eleven patients with a mean age of 49 ± 7 years were included, 73% of them were women. Their average initial BMI was 42 ± 4 kg/m2. VAT prior to surgery had a mean of 10.6 ± 2.5L for men and 6.4 ± 2.4L for women. Eighty-two percent of the patients fulfilled harmonized criteria for metabolic syndrome. There was a statistically significant decrease in VAT at 3 and 6 months after surgery in both men and women (Baseline 7.5 ± 3L, 3 months 3.8 ± 2.8 L (p <0.001), 6 months 2.5 ± 2 L (p = 0.001). An average decrease in visceral adipose tissue of 57 ± 24% in women and 34 ± 18% in men (p = 0.18) was found 3 months after surgery and 70 ± 22% in women and 60 ± 21% in men (p = 0.53) 6 months after surgery. Laparoscopic one-anastomosis gastric bypass (OAGB) was the type of surgery with the highest percentage of VAT loss at 3 and 6 months, however, this was not statistically significant when compared with Y-Roux Gastric bypass (YRGB). A statistically significant decrease in HbA1c, HOMA, total cholesterol, LDL, and triglycerides levels were found at 3 and 6 months after surgery. However, when correlating the proportion of VAT lost with the metabolic variables, only a significant correlation was found with the HbA1c levels. The higher the proportion of VAT lost, the lower the HbA1c levels (R2 -0.72 p = 0.01). Conclusions: Bariatric surgery produces a statistically significant reduction in visceral adipose tissue from 3 months after surgery. In this study, an inversely proportional correlation was found between the proportion of VAT lost and HbA1c levels.

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 245-247
Author(s):  
S Keshavjee ◽  
J Yadav ◽  
K Schwenger ◽  
S Fischer ◽  
T D Jackson ◽  
...  

Abstract Background Non-alcoholic fatty liver disease (NAFLD) includes simple steatosis (SS) and nonalcoholic steatohepatitis (NASH). It affects 74–98% of individuals with morbid obesity undergoing bariatric surgery (BSX). Among several factors contributing to NAFLD pathogenesis, adipokines secreted by visceral adipose tissue (VAT) can play a role by regulating glucose/lipid metabolism and inflammation. Aims This study aims to determine if visceral adipose tissue adipokine and cytokine gene expression are associated with NAFLD (SS and NASH) at the time of BSX. Methods Patients were recruited from the Toronto Western Hospital Bariatric Clinic. Demographic data was recorded. The VAT and liver biopsies were collected at the time of bariatric surgery. VAT adipokines and other mediators were assessed by RT-PCR and included markers of thermogenic capacity, inflammation, fibrosis, adipokines, and others. Liver histology was assessed by a pathologist using the Brunt system and individuals were diagnosed as either SS, NASH, or having a healthy liver (HL). Blood samples were collected pre-BSX to measure liver and metabolic syndrome related parameters, including HOMA-IR, HbA1c, liver enzymes, and lipid profile. Anthropometry was also assessed. Groups were compared using Kruskal-Wallis test followed by Wilcoxon ranked sum, or chi-square and Fisher’s exact test as necessary. Data was considered to be statistically significant with a p-value less than 0.05. Results We are presenting data on 126 patients, 80.2% females with a median age of 49 and a body mass index (BMI) of 46.9. Fifty-seven patients had SS, 34 had NASH and 35 had a healthy liver (HL). BMI, age, and sex did not differ between the three groups. First, we found that those with NASH had significantly higher VAT expression of fibrosis (Loxl2), inflammation (CCL4 and TGFb1) and proliferation markers (E2F1) and significantly lower expression of adipokines (TNFa and resistin) compared to HL. Also, we found that SS had significantly higher fibrosis (Col3a1, Col6a1, Loxl2, CD9 and Acta2), inflammation (Nox2, TGFb1, IFNg and Clec10a), browning (PPARa, PPARg and Glut1) and proliferation (E2F1) marker expression compared to HL. Conclusions Results show that there is a significant difference in the expression pattern of VAT fibrotic and inflammatory markers between HL, SS and NASH patients. The observed increase of inflammatory markers in NAFLD is in line with prior research outlining the ability of inflammatory mediators from VAT to contribute to liver pathology via portal circulation. The relationship between VAT characteristics and NAFLD are important in understanding the widespread metabolic effects of obesity. Funding Agencies CIHRCanadian Liver foundation


2021 ◽  
Author(s):  
Luise Müller ◽  
Lena Gras ◽  
Anne Hoffmann ◽  
Tobias Hagemann ◽  
Stephan H. Bernhart ◽  
...  

2019 ◽  
Vol 18 (3) ◽  
pp. 430-435 ◽  
Author(s):  
Moriah P. Bellissimo ◽  
Ivana Zhang ◽  
Elizabeth A. Ivie ◽  
Phong H. Tran ◽  
Vin Tangpricha ◽  
...  

2019 ◽  
Vol 91 (3) ◽  
pp. 400-410 ◽  
Author(s):  
Judith Brock ◽  
Andreas Schmid ◽  
Thomas Karrasch ◽  
Petra Pfefferle ◽  
Jutta Schlegel ◽  
...  

2014 ◽  
Vol 99 (1) ◽  
pp. E53-E61 ◽  
Author(s):  
Julie Lasselin ◽  
Eric Magne ◽  
Cédric Beau ◽  
Patrick Ledaguenel ◽  
Sandra Dexpert ◽  
...  

Context: The inflammatory state of the adipose tissue is believed to contribute to systemic low-grade inflammation in obesity. Objective: This study assessed the relationship between adipose and circulating inflammatory markers as well as the influence of adipose inflammation on bariatric surgery-induced weight reduction. Design: This was a cross-sectional and longitudinal study (up to 14 mo). Setting: The study was conducted in the digestive/bariatric surgery department of the Tivoli and Jean Villar clinics, Bordeaux, France. Patients: Thirty-seven obese patients [body mass index (BMI) > 35–40 kg/m2)] seeking bariatric surgery were included. Twenty-eight of them were successively followed up at 1–3 months after surgery and 25 between 6 and 14 months after surgery. Main Outcome Measures: Fasting serum samples were collected before surgery to assess concentrations of inflammatory markers. Samples of visceral adipose tissue were extracted during surgery and gene expression of cytokines and immune cell markers were evaluated using quantitative RT-PCR. Pre- and postsurgery weight and BMI were collected. Results: Gene expression of several cytokines were strongly intercorrelated in the visceral adipose tissue. Adipose expression of macrophage and T cell markers were related to adipose expression of TNF-α and IL-1 receptor antagonist (P < .01) and to systemic levels of TNF-α (P < .01) and IL-6 (P < .05). A higher inflammatory state of the adipose tissue predicted a lower BMI reduction after surgery (P < .05), notably at early stages after surgery. Conclusions: These findings support the involvement of macrophages and T cells in adipose inflammation and provide new information regarding the role of the visceral adipose tissue in the inflammatory state of obesity and its impact on obesity treatment outcomes, such as surgery-induced weight loss.


2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Daniel Harmon ◽  
Stephanie N Oldham ◽  
Chantel C McSkimming ◽  
Heather M Perry ◽  
Jennifer L Kirby ◽  
...  

Innate B-1 B cells can protect against inflammatory disease through production of natural IgM antibodies, but little is known regarding their role in obesity-induced metabolic dysfunction. In this study, we explore the role murine B-1 B cells play in regulating diet-induced glucose intolerance. In addition, we examine bariatric surgery samples for the presence of B cells in human adipose tissue and circulating natural IgM antibodies. We show that mice with increased visceral adipose tissue B-1b B cells due to B cell specific deletion of Id3 (Id3 BcellKO ) have attenuated high-fat diet-induced glucose intolerance compared to littermate controls. Omental visceral adipose tissue from Id3 BcellKO mice had enhanced local natural IgM antibody secretion (49.0 ± 5.9 vs. 17.5 ± 4.2 U/mg fat), and demonstrated attenuated HFD-induced secretion of TNFa (2.5 ± 0.3 vs. 6.7 ± 1.3 pg/mg fat) and IFNg (0.10 ± 0.02 vs. 0.48 ± 0.14 pg/mg fat). Adoptive transfer of B-1b B cells null for Id3 protected against diet-induced glucose intolerance in Rag1 -/- hosts, while B-1b B cells unable to secrete IgM had no effect. Additional studies in humans undergoing bariatric surgery showed CD20+CD27+CD43+ B cells, previously shown to have B-1-like characteristics, within omental adipose tissue. A correlation was found between their presence and serum natural IgM levels (r=0.52). In addition, natural IgM levels were inversely associated with the inflammatory chemokine, MCP-1 (r=-0.21). Finally, IgM, but not IgG, natural antibodies were inversely associated with insulin resistance (r=0.32). Together, our findings provide the first evidence that B-1b B cells protect against diet-induced glucose intolerance in an IgM-dependent manner in mice, and suggest that anti-inflammatory natural IgM antibodies may modulate the inflammatory and metabolic consequences of obesity in humans.


2018 ◽  
Vol 28 (12) ◽  
pp. 4006-4013 ◽  
Author(s):  
Lucie Favre ◽  
Laura Marino ◽  
Aline Roth ◽  
James Acierno ◽  
Didier Hans ◽  
...  

2019 ◽  
Vol 316 (2) ◽  
pp. E168-E177 ◽  
Author(s):  
Doan T. M. Ngo ◽  
Aaron L. Sverdlov ◽  
Shakun Karki ◽  
Donia Macartney-Coxson ◽  
Richard S. Stubbs ◽  
...  

Obesity, particularly visceral adiposity, has been linked to mitochondrial dysfunction and increased oxidative stress, which have been suggested as mechanisms of insulin resistance. The mechanism(s) behind this remains incompletely understood. In this study, we hypothesized that mitochondrial complex II dysfunction plays a role in impaired insulin sensitivity in visceral adipose tissue of subjects with obesity. We obtained subcutaneous and visceral adipose tissue biopsies from 43 subjects with obesity (body mass index ≥ 30 kg/m2) during planned bariatric surgery. Compared with subcutaneous adipose tissue, visceral adipose tissue exhibited decreased complex II activity, which was restored with the reducing agent dithiothreitol (5 mM) ( P < 0.01). A biotin switch assay identified that cysteine oxidative posttranslational modifications (OPTM) in complex II subunit A (succinate dehydrogenase A) were increased in visceral vs. subcutaneous fat ( P < 0.05). Insulin treatment (100 nM) stimulated complex II activity in subcutaneous fat ( P < 0.05). In contrast, insulin treatment of visceral fat led to a decrease in complex II activity ( P < 0.01), which was restored with addition of the mitochondria-specific oxidant scavenger mito-TEMPO (10 µM). In a cohort of 10 subjects with severe obesity, surgical weight loss decreased OPTM and restored complex II activity, exclusively in the visceral depot. Mitochondrial complex II may be an unrecognized and novel mediator of insulin resistance associated with visceral adiposity. The activity of complex II is improved by weight loss, which may contribute to metabolic improvements associated with bariatric surgery.


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