Early postprandial low-grade inflammation after high-fat meal in healthy rats: possible involvement of visceral adipose tissue

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

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Multinucleated giant cells in adipose tissue are specialized in adipocyte degradation

10.2337/figshare.13168862 ◽

2020 ◽

Author(s):

Ada Admin ◽

Julia Braune ◽

Andreas Lindhorst ◽

Janine Fröba ◽

Constance Hobusch ◽

...

Keyword(s):

Adipose Tissue ◽

High Fat Diet ◽

Ex Vivo ◽

Giant Cells ◽

Low Grade ◽

Adipose Tissue Macrophages ◽

Visceral Adipose ◽

Low Grade Inflammation

Obesity is associated with a chronic low-grade inflammation in visceral adipose tissue (AT) characterized by an increasing number of adipose tissue macrophages (ATMs) and linked to type 2 diabetes. AT inflammation is histologically indicated by the formation of so-called crown-like structures (CLS), as accumulation of ATMs around dying adipocytes, and the occurrence of multi-nucleated giant cells (MGCs). However to date, the function of MGCs in obesity is unknown. Hence, the aim of this study was to characterize MGCs in AT and unravel the function of these cells. We demonstrate that MGCs occur in obese patients and after 24 weeks of high fat diet (HFD) in mice, accompanying signs of AT inflammation and then represent ~3% of ATMs in mice. Mechanistically, we found evidence that adipocyte death triggers MGC formation. Most importantly, MGCs in obese AT have a higher capacity to phagocytose oversized particles, such as adipocytes, as shown by live-imaging of AT, 45 µm bead uptake ex vivo and a higher lipid content in vivo. Finally, we show that IL-4 treatment is sufficient to increase the number of MGCs in AT, whereas other factors maybe more important for endogenous MGC formation in vivo.

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Enhanced Inflammation without Impairment of Insulin Signaling in the Visceral Adipose Tissue of 5α-Dihydrotestosterone-Induced Animal Model of Polycystic Ovary Syndrome

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-0043-104531 ◽

2017 ◽

Vol 125 (08) ◽

pp. 522-529 ◽

Cited By ~ 2

Author(s):

Danijela Milutinović ◽

Marina Nikolić ◽

Nataša Veličković ◽

Ana Djordjevic ◽

Biljana Bursać ◽

...

Keyword(s):

Animal Model ◽

Adipose Tissue ◽

Insulin Sensitivity ◽

Polycystic Ovary Syndrome ◽

Abdominal Obesity ◽

Visceral Adipose Tissue ◽

Polycystic Ovary ◽

Low Grade ◽

Ovary Syndrome ◽

Visceral Adipose

AbstractPolycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder associated with abdominal obesity, dyslipidemia and insulin resistance. Since abdominal obesity is characterized by low-grade inflammation, the aim of the study was to investigate whether visceral adipose tissue inflammation linked to abdominal obesity and dyslipidemia could lead to impaired insulin sensitivity in the animal model of polycystic ovary syndrome.Female Wistar rats were treated with nonaromatizable 5α-dihydrotestosterone pellets in order to induce reproductive and metabolic characteristics of polycystic ovary syndrome. Glucose, triglycerides, non-esterified fatty acids and insulin were determined in blood plasma. Visceral adipose tissue inflammation was evaluated by the nuclear factor kappa B intracellular distribution, macrophage migration inhibitory factor protein level, as well as TNFα, IL6 and IL1β mRNA levels. Insulin sensitivity was assessed by intraperitoneal glucose tolerance test and homeostasis model assessment index, and through analysis of insulin signaling pathway in the visceral adipose tissue.Dihydrotestosterone treatment led to increased body weight, abdominal obesity and elevated triglycerides and non-esterified fatty acids, which were accompanied by the activation of nuclear factor kappa B and increase in macrophage migration inhibitory factor, IL6 and IL1β levels in the visceral adipose tissue. In parallel, insulin sensitivity was affected in 5α-dihydrotestosterone-treated animals only at the systemic and not at the level of visceral adipose tissue.The results showed that abdominal obesity and dyslipidemia in the animal model of polycystic ovary syndrome were accompanied with low-grade inflammation in the visceral adipose tissue. However, these metabolic disturbances did not result in decreased tissue insulin sensitivity.

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A Mouse Model of Metabolic Syndrome; Increase in Visceral Adipose Tissue Precedes the Development of Fatty Liver and Insulin Resistance in High-Fat Diet-Fed Male KK/Ta Mice

Journal of Clinical Biochemistry and Nutrition ◽

10.3164/jcbn.2008022 ◽

2008 ◽

Vol 42 (2) ◽

pp. 150-157 ◽

Cited By ~ 64

Author(s):

Satomi Akagiri ◽

Yuji Naito ◽

Hiroshi Ichikawa ◽

Katsura Mizushima ◽

Tomohisa Takagi ◽

...

Keyword(s):

Insulin Resistance ◽

Metabolic Syndrome ◽

Adipose Tissue ◽

Mouse Model ◽

Fatty Liver ◽

Visceral Adipose Tissue ◽

High Fat Diet ◽

High Fat ◽

Visceral Adipose

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Green Tea Extract Supplementation Induces the Lipolytic Pathway, Attenuates Obesity, and Reduces Low-Grade Inflammation in Mice Fed a High-Fat Diet

Mediators of Inflammation ◽

10.1155/2013/635470 ◽

2013 ◽

Vol 2013 ◽

pp. 1-8 ◽

Cited By ~ 48

Author(s):

Cláudio A. Cunha ◽

Fábio S. Lira ◽

José C. Rosa Neto ◽

Gustavo D. Pimentel ◽

Gabriel I. H. Souza ◽

...

Keyword(s):

Adipose Tissue ◽

Green Tea ◽

High Fat Diet ◽

Green Tea Extract ◽

Chow Diet ◽

Low Grade ◽

Obese Mice ◽

High Fat ◽

Tea Extract ◽

Low Grade Inflammation

The aim of this study was to evaluate the effects of green teaCamellia sinensisextract on proinflammatory molecules and lipolytic protein levels in adipose tissue of diet-induced obese mice. Animals were randomized into four groups: CW (chow diet and water); CG (chow diet and water + green tea extract); HW (high-fat diet and water); HG (high-fat diet and water + green tea extract). The mice were fedad libitumwith chow or high-fat diet and concomitantly supplemented (oral gavage) with 400 mg/kg body weight/day of green tea extract (CG and HG, resp.). The treatments were performed for eight weeks. UPLC showed that in 10 mg/mL green tea extract, there were 15 μg/mg epigallocatechin, 95 μg/mg epigallocatechin gallate, 20.8 μg/mg epicatechin gallate, and 4.9 μg/mg gallocatechin gallate. Green tea administered concomitantly with a high-fat diet increased HSL, ABHD5, and perilipin in mesenteric adipose tissue, and this was associated with reduced body weight and adipose tissue gain. Further, we observed that green tea supplementation reduced inflammatory cytokine TNFαlevels, as well as TLR4, MYD88, and TRAF6 proinflammatory signalling. Our results show that green tea increases the lipolytic pathway and reduces adipose tissue, and this may explain the attenuation of low-grade inflammation in obese mice.

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The Angiogenesis Inhibitor ALS-L1023 from Lemon-Balm Leaves Attenuates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease through Regulating the Visceral Adipose-Tissue Function

International Journal of Molecular Sciences ◽

10.3390/ijms18040846 ◽

2017 ◽

Vol 18 (4) ◽

pp. 846 ◽

Cited By ~ 19

Author(s):

Jeongjun Kim ◽

Haerim Lee ◽

Jonghoon Lim ◽

Jaeho Oh ◽

Soon Shin ◽

...

Keyword(s):

Adipose Tissue ◽

Liver Disease ◽

Visceral Adipose Tissue ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Angiogenesis Inhibitor ◽

High Fat ◽

Lemon Balm ◽

Nonalcoholic Fatty Liver ◽

Visceral Adipose

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COVID-19 and Obesity: Role of Ectopic Visceral and Epicardial Adipose Tissues in Myocardial Injury

Frontiers in Endocrinology ◽

10.3389/fendo.2021.726967 ◽

2021 ◽

Vol 12 ◽

Author(s):

Adèle Lasbleiz ◽

Bénédicte Gaborit ◽

Astrid Soghomonian ◽

Axel Bartoli ◽

Patricia Ancel ◽

...

Keyword(s):

Adipose Tissue ◽

Intensive Care ◽

Inflammatory Cytokines ◽

Visceral Adipose Tissue ◽

Cardiovascular Events ◽

Low Grade ◽

Viral Spread ◽

Visceral Adipose ◽

Pro Inflammatory Cytokines

In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 via angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the “cytokine storm” and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.

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