scholarly journals Right Heart Morphology and Its Association With Excessive and Deficient Cardiac Visceral Adipose Tissue

2021 ◽  
Vol 15 ◽  
pp. 117954682110413
Author(s):  
Domagoj Vučić ◽  
Nikola Bijelić ◽  
Edi Rođak ◽  
Jasmina Rajc ◽  
Boris Dumenčić ◽  
...  

Visceral adipose tissue is an independent risk factor for the development of atherosclerotic coronary disease, arterial hypertension, diabetes and metabolic syndrome. Right heart morphology often involves the presence of adipose tissue, which can be quantified by non-invasive imaging methods. The last decade brought a wealth of new insights into the function and morphology of adipose tissue, with great emphasis on its role in the pathogenesis of heart disease. Cardiac adipose tissue is involved in thermogenesis, mechanical protection of the heart and energy storage. However, it can also be an endocrine organ that synthesises numerous pro-inflammatory and anti-inflammatory cytokines, the effect of which is accomplished by paracrine and vasocrine mechanisms. Visceral adipose tissue has several compartments that differ in their embryological origin and vascularisation. Deficiency of cardiac adipose tissue, often due to chronic pathological conditions such as oncological diseases or chronic infectious diseases, predicts increased mortality and morbidity. To date, knowledge about the influence of visceral adipose tissue on cardiac morphology is limited, especially the effect on the morphology of the right heart in a state of excess or deficient visceral adipose tissue.

2007 ◽  
Vol 1 (1) ◽  
pp. 7-13 ◽  
Author(s):  
Kaisa E. Liukko ◽  
Vesa J. Oikonen ◽  
Tuula K. Tolvanen ◽  
Kirsi A. Virtanen ◽  
Antti P. Viljanen ◽  
...  

Author(s):  
G.D. Fadieienko ◽  
Ya.V. Nikiforova

A review of the literature on the metabolic role of visceral adipose tissue and the main methods for its diagnosis is presented. Visceral adipose tissue is an active endocrine organ what secretes a number of biologically active substances. With an increase in the proportion of visceral adipose tissue, moderate inflammation is observed with a chronic systemic increase in the activity of adipokines. Adipokines carry out several immune or metabolic functions associated with inflammatory infiltration. Active substances such as leptin, adiponectin, resistin, etc., the source of which is visceral adipose tissue, have peripheral, central and local effects on the metabolism of glucose and lipids, glycolysis processes in the liver, etc. It is the activity of visceral adipose tissue that should be considered among the main pathophysiological development factors obesity and its potential metabolic cardiovascular and/or liver complications.


2001 ◽  
Vol 120 (5) ◽  
pp. A254-A254
Author(s):  
D SASS ◽  
R SCHOEN ◽  
J WEISSFELD ◽  
L KULLER ◽  
F THAETE ◽  
...  

Author(s):  
Ю.И. Шрамко ◽  
А.В. Кубышкин ◽  
А.А. Давыдова ◽  
И.И. Фомочкина ◽  
Л.Л. Алиев ◽  
...  

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.


Obesity ◽  
2016 ◽  
Vol 25 (2) ◽  
pp. 332-337 ◽  
Author(s):  
Martin Reinhardt ◽  
Paolo Piaggi ◽  
Barbara DeMers ◽  
Cathy Trinidad ◽  
Jonathan Krakoff

Author(s):  
Gabriel Wagner ◽  
Anna Fenzl ◽  
Josefine Lindroos-Christensen ◽  
Elisa Einwallner ◽  
Julia Husa ◽  
...  

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.


Author(s):  
Esther Lizarraga-Mollinedo ◽  
Gemma Carreras-Badosa ◽  
Silvia Xargay-Torrent ◽  
Xavier Remesar ◽  
Berta Mas-Pares ◽  
...  

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