Obesity and its effects on the esophageal mucosal barrier

2021 ◽  
Vol 321 (3) ◽  
pp. G335-G343
Author(s):  
Shere Paris ◽  
Rebecca Ekeanyanwu ◽  
Yuwei Jiang ◽  
Daniel Davis ◽  
Stuart Jon Spechler ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Gastroesophageal Reflux ◽  
Visceral Adipose Tissue ◽  
Esophagogastric Junction ◽  
Mechanical Effect ◽  
Mucosal Barrier ◽  
Abdominal Pressure ◽  
Esophageal Mucosa ◽  
Barrier Integrity ◽  
Visceral Adipose

Obesity is associated with gastroesophageal reflux disease (GERD) and its complications including reflux esophagitis, Barrett’s esophagus, and esophageal adenocarcinoma. Traditionally, these associations have been attributed to the mechanical effect of abdominal fat in increasing intra-abdominal pressure, thereby promoting gastroesophageal reflux and causing disruption of antireflux mechanisms at the esophagogastric junction. However, recent studies suggest that visceral adipose tissue (VAT) produces numerous cytokines that can cause esophageal inflammation and impair esophageal mucosal barrier integrity through reflux-independent mechanisms that render the esophageal mucosa especially susceptible to GERD-induced injury. In this report, we review mechanisms of esophageal mucosal defense, the genesis and remodeling of visceral adipose tissue during obesity, and the potential role of substances produced by VAT, especially the VAT that encircles the esophagogastric junction, in the impairment of esophageal mucosal barrier integrity that leads to the development of GERD complications.

The crosstalk between gut microbiota, intestinal immunological niche and visceral adipose tissue as a new model for the pathogenesis of metabolic and inflammatory diseases: the paradigm of type 2 diabetes mellitus

2022 ◽  
Vol 29 ◽  
Author(s):  
Cianci Rossella ◽  
Franza Laura ◽  
Massaro Maria Grazia ◽  
Borriello Raffaele ◽  
Tota Antonio ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Visceral Adipose Tissue ◽  
Bacterial Species ◽  
Hormone Secretion ◽  
Mucosal Barrier ◽  
Sexual Hormones ◽  
Gut Dysbiosis ◽  
Visceral Adipose

Abstract: Gut microbiota (GM) comprises more than one thousand microorganisms between bacterial species, viruses, fungi, and protozoa, and represents the main actor of a wide net of molecular interactions, involving, among others, the endocrine system, immune responses, and metabolism. GM influences many endocrine functions such as adrenal steroidogenesis, thyroid function, sexual hormones, IGF-1 pathway and peptides produced in gastrointestinal system. It is fundamental in glycaemic control and obesity, while also exerting an important function in modulating the immune system and associated inflammatory disease. The result of this crosstalk in gut mucosa is the formation of the intestinal immunological niche. Visceral adipose tissue (VAT) produces about 600 different peptides, it is involved in lipid and glucose metabolism and in some immune reactions through several adipokines. GM and VAT interact in a bidirectional fashion: while gut dysbiosis can modify VAT adipokines and hormone secretion, VAT hyperplasia modifies GM composition. Acquired or genetic factors leading to gut dysbiosis or increasing VAT (i.e., Western diet) induce a proinflammatory condition, which plays a pivotal role in the development of dysmetabolic and immunologic conditions, such as diabetes mellitus. Diabetes is clearly associated with specific patterns of GM alterations, with an abundance or reduction of GM species involved in controlling mucosal barrier status, glycaemic levels and exerting a pro- or anti-inflammatory activity. All these factors could explain the higher incidence of several inflammatory conditions in Western countries; furthermore, besides the specific alterations observed in diabetes, this paradigm could represent a common pathway acting in many metabolic conditions and could pave the way to a new, interesting therapeutic approach.

Lack of association between colorectal adenoma recurrence and visceral adipose tissue

2001 ◽  
Vol 120 (5) ◽  
pp. A254-A254
Author(s):  
D SASS ◽  
R SCHOEN ◽  
J WEISSFELD ◽  
L KULLER ◽  
F THAETE ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Colorectal Adenoma ◽  
Visceral Adipose Tissue ◽  
Adenoma Recurrence ◽  
Colorectal Adenoma Recurrence ◽  
Visceral Adipose

Correction of morphofunctional disorders with grapes polyphenols in rats with experimental metabolic syndrome

2018 ◽  
pp. 43-48
Author(s):  
Ю.И. Шрамко ◽  
А.В. Кубышкин ◽  
А.А. Давыдова ◽  
И.И. Фомочкина ◽  
Л.Л. Алиев ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Normal Structure ◽  
Hepatic Tissue ◽  
Standard Diet ◽  
Grape Polyphenols ◽  
Morphological Studies ◽  
Visceral Adipose ◽  
Experimental Group

Цель работы состояла в изучении влияния полифенолов винограда на органы-мишени при экспериментальном метаболическом синдроме у крыс. Методы. В течение 12 недель полифенолы винограда применялись у крыс линии Вистар. Все крысы находились на стандартном рационе. Животные были разделены на 6 групп: 1-я контрольная получала питьевую воду; 2-я контрольная и все 4 экспериментальные - 2,5% раствор фруктозы в качестве питья. 1-я экспериментальная группа дополнительно получала препарат «Фэнокор» с суммарным содержанием полифенолов 181,53 г/дм, 2-я экспериментальная - виноматериал с суммарным содержанием полифенолов 1,73 г/дм; 3-я экспериментальная - виноматериал с суммарным содержанием полифенолов 4,33 г/дм и 4-я экспериментальная - виноматериал с суммарным содержанием полифенолов 8,58 г/дм. После окончания опыта у крыс проводили морфологические исследования висцеральной жировой ткани, тканей миокарда и печени. Результаты. Анализ результатов показал, что применение полифенольных продуктов переработки винограда в концентрациях 181,53 г/дм при моделировании метаболического синдрома приводило к минимизации морфофункциональных нарушений в висцеральной жировой ткани (уменьшение интенсивности лимфоплазмоцитарной инфильтрации), миокарде (мышечные волокна имели типичное строение и адипоциты между ними встречались лишь очагово) и печени (имелись лишь слабые очаговые дистрофические изменения гепатоцитов). Заключение. Результаты работы свидетельствуют о возможности применения виноматериалов с наибольшей концентрацией полифенолов и препарата «Фэнокор» в коррекции и профилактике поражений при метаболическом синдроме. The aim of this work was to study the effect of grape polyphenols on target organs in rats with experimental metabolic syndrome. Methods. Grape polyphenols were used in Wistar rats for 12 weeks. All rats received a standard diet. The animals were divided into 6 groups: group 1, control, received drinking water; group 2, the second control, and four experimental groups received a 2.5% fructose solution for drinking. The first experimental group additionally received a drug, Fenocor, containing polyphenols at 181.53 g/dm; the second experimental group - wine material containing polyphenols at 1,73 g/dm; the third experimental group - wine material containing polyphenols at 4,33 g/dm; and the fourth experimental group - wine material containing polyphenols at 8,58 g/dm. At the end of experiment, morphological studies of visceral adipose tissue, myocardial tissue, and hepatic tissue were performed. Results. The treatment of rats with experimental metabolic syndrome with grape polyphenolic products at a concentration of 181.53 g/dm minimized morphological and functional disorders in visceral adipose tissue (intensity of lymphoplasmocytic infiltration was decreased), myocardium (muscle fibers had normal structure with only occasional adipocytes between them), and liver (only slight focal degenerative changes were observed in hepatocytes). Conclusion. The study indicated a possibility of using wine materials with the highest concentration of polyphenols and the drug Fenocor for correction and prevention of damages in metabolic syndrome.

scholarly journals Cross calibration of two dual-energy X-ray densitometers and comparison of visceral adipose tissue measurements by iDXA and MRI

Obesity ◽  
2016 ◽  
Vol 25 (2) ◽  
pp. 332-337 ◽  
Author(s):  
Martin Reinhardt ◽  
Paolo Piaggi ◽  
Barbara DeMers ◽  
Cathy Trinidad ◽  
Jonathan Krakoff
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Dual Energy ◽  
X Ray ◽  
Cross Calibration ◽  
Visceral Adipose

scholarly journals LMO3 reprograms visceral adipocyte metabolism during obesity

2021 ◽  
Author(s):  
Gabriel Wagner ◽  
Anna Fenzl ◽  
Josefine Lindroos-Christensen ◽  
Elisa Einwallner ◽  
Julia Husa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Visceral Adipose Tissue ◽  
Tissue Expansion ◽  
Oxidative Capacity ◽  
Glut4 Translocation ◽  
Mitochondrial Oxidative Capacity ◽  
Visceral Adipose

Abstract Obesity and body fat distribution are important risk factors for the development of type 2 diabetes and metabolic syndrome. Evidence has accumulated that this risk is related to intrinsic differences in behavior of adipocytes in different fat depots. We recently identified LIM domain only 3 (LMO3) in human mature visceral adipocytes; however, its function in these cells is currently unknown. The aim of this study was to determine the potential involvement of LMO3-dependent pathways in the modulation of key functions of mature adipocytes during obesity. Based on a recently engineered hybrid rAAV serotype Rec2 shown to efficiently transduce both brown adipose tissue (BAT) and white adipose tissue (WAT), we delivered YFP or Lmo3 to epididymal WAT (eWAT) of C57Bl6/J mice on a high-fat diet (HFD). The effects of eWAT transduction on metabolic parameters were evaluated 10 weeks later. To further define the role of LMO3 in insulin-stimulated glucose uptake, insulin signaling, adipocyte bioenergetics, as well as endocrine function, experiments were conducted in 3T3-L1 adipocytes and newly differentiated human primary mature adipocytes, engineered for transient gain or loss of LMO3 expression, respectively. AAV transduction of eWAT results in strong and stable Lmo3 expression specifically in the adipocyte fraction over a course of 10 weeks with HFD feeding. LMO3 expression in eWAT significantly improved insulin sensitivity and healthy visceral adipose tissue expansion in diet-induced obesity, paralleled by increased serum adiponectin. In vitro, LMO3 expression in 3T3-L1 adipocytes increased PPARγ transcriptional activity, insulin-stimulated GLUT4 translocation and glucose uptake, as well as mitochondrial oxidative capacity in addition to fatty acid oxidation. Mechanistically, LMO3 induced the PPARγ coregulator Ncoa1, which was required for LMO3 to enhance glucose uptake and mitochondrial oxidative gene expression. In human mature adipocytes, LMO3 overexpression promoted, while silencing of LMO3 suppressed mitochondrial oxidative capacity. LMO3 expression in visceral adipose tissue regulates multiple genes that preserve adipose tissue functionality during obesity, such as glucose metabolism, insulin sensitivity, mitochondrial function, and adiponectin secretion. Together with increased PPARγ activity and Ncoa1 expression, these gene expression changes promote insulin-induced GLUT4 translocation, glucose uptake in addition to increased mitochondrial oxidative capacity, limiting HFD-induced adipose dysfunction. These data add LMO3 as a novel regulator improving visceral adipose tissue function during obesity. Key messages LMO3 increases beneficial visceral adipose tissue expansion and insulin sensitivity in vivo. LMO3 increases glucose uptake and oxidative mitochondrial activity in adipocytes. LMO3 increases nuclear coactivator 1 (Ncoa1). LMO3-enhanced glucose uptake and mitochondrial gene expression requires Ncoa1.

scholarly journals Catch-up growth in juvenile rats, fat expansion, and dysregulation of visceral adipose tissue

2021 ◽  
Author(s):  
Esther Lizarraga-Mollinedo ◽  
Gemma Carreras-Badosa ◽  
Silvia Xargay-Torrent ◽  
Xavier Remesar ◽  
Berta Mas-Pares ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Juvenile Rats ◽  
Catch Up ◽  
Visceral Adipose
Sign in / Sign up

Export Citation Format

Share Document