scholarly journals Inflammatory Role of Toll-Like Receptors in Human and Murine Adipose Tissue

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Odile Poulain-Godefroy ◽  
Olivier Le Bacquer ◽  
Pauline Plancq ◽  
Cécile Lecœur ◽  
François Pattou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Dietary Lipids ◽  
Toll Like Receptors ◽  
Fat Tissue ◽  
Omental Adipose Tissue ◽  
Adipocyte Cell ◽  
Inflammatory Processes ◽  
Insulin Responsiveness ◽  
Tlr4 Activation

It was recently demonstrated that TLR4 activation via dietary lipids triggers inflammatory pathway and alters insulin responsiveness in the fat tissue during obesity. Here, we question whether other TLR family members could participate in the TLR-mediated inflammatory processes occurring in the obese adipose tissue. We thus studied the expression of TLR1, TLR2, TLR4, and TLR6 in adipose tissue. These receptors are expressed in omental and subcutaneous human fat tissue, the expression being higher in the omental tissue, independently of the metabolic status of the subject. We demonstrated a correlation of TLRs expression within and between each depot suggesting a coregulation. Murine 3T3-L1 preadipocyte cells stimulated with Pam3CSK4 induced the expression of some proinflammatory markers. Therefore, beside TLR4, other toll-like receptors are differentially expressed in human fat tissue, and functional in an adipocyte cell line, suggesting that they might participate omental adipose tissue-related inflammation that occurs in obesity.

Chronic binge alcohol and ovariectomy dysregulate omental adipose tissue metaboproteome in simian immunodeficiency virus-infected female macaques

2021 ◽  
Author(s):  
Jonquil Marie Poret ◽  
Jessie J Guidry ◽  
Liz Simon ◽  
Patricia E. Molina
Keyword(s):  
Metabolic Disease ◽  
Adipose Tissue ◽  
Simian Immunodeficiency Virus ◽  
People Living With Hiv ◽  
Infected Female ◽  
Omental Adipose Tissue ◽  
Immunodeficiency Virus ◽  
Z Scores ◽  
Functional Pathways

Effective antiretroviral therapy (ART) has significantly reduced mortality of people living with HIV (PLWH), and the prevalence of at-risk alcohol use is higher among PLWH. Increased survival and aging of PLWH is associated with increased prevalence of metabolic comorbidities especially among menopausal women, and adipose tissue metabolic dysregulation may be a significant contributing factor. We examined the differential effects of chronic binge alcohol (CBA) administration and ovariectomy (OVX) on the omental adipose tissue (OmAT) proteome in a subset of simian immunodeficiency virus (SIV)-infected macaques of a longitudinal parent study. Quantitative discovery-based proteomics identified 1429 differentially expressed proteins. Ingenuity Pathway Analysis (IPA) was used to calculate z-scores, or activation predictions, for functional pathways and diseases. Results revealed protein changes associated with functional pathways centered around the "OmAT metaboproteome profile". Based on z-scores, CBA did not affect functional pathways of metabolic disease but dysregulated proteins involved in AMPK signaling and lipid metabolism. OVX-mediated proteome changes were predicted to promote pathways involved in glucose- and lipid-associated metabolic disease. Proteins involved in apoptosis, necrosis, and reactive oxygen species (ROS) pathways were also predicted to be activated by OVX, and these were predicted to be inhibited by CBA. These results provide evidence for the role of ovarian hormone loss in mediating OmAT metaboproteome dysregulation in SIV and suggest that CBA modifies OVX-associated changes. In the context of OVX, CBA administration produced larger metabolic and cellular effects, which we speculate may reflect a protective role of estrogen against CBA-mediated adipose tissue injury in female SIV-infected macaques.

scholarly journals Release of Inflammatory Mediators by Human Adipose Tissue Is Enhanced in Obesity and Primarily by the Nonfat Cells: A Review

2010 ◽  
Vol 2010 ◽  
pp. 1-20 ◽  
Author(s):  
John N. Fain
Keyword(s):  
Adipose Tissue ◽  
In Vitro Release ◽  
Human Adipose Tissue ◽  
Fat Cells ◽  
Omental Adipose Tissue ◽  
Subcutaneous Adipose ◽  
Circulating Levels ◽  
Pai 1

This paper considers the role of putative adipokines that might be involved in the enhanced inflammatory response of human adipose tissue seen in obesity. Inflammatory adipokines [IL-6, IL-10, ACE, TGFβ1, TNFα, IL-1β, PAI-1, and IL-8] plus one anti-inflammatory [IL-10] adipokine were identified whose circulating levels as well as in vitro release by fat are enhanced in obesity and are primarily released by the nonfat cells of human adipose tissue. In contrast, the circulating levels of leptin and FABP-4 are also enhanced in obesity and they are primarily released by fat cells of human adipose tissue. The relative expression of adipokines and other proteins in human omental as compared to subcutaneous adipose tissue as well as their expression in the nonfat as compared to the fat cells of human omental adipose tissue is also reviewed. The conclusion is that the release of many inflammatory adipokines by adipose tissue is enhanced in obese humans.

scholarly journals Cellular adaptations in fat tissue of exercise-trained miniature swine: role of excess energy intake

2000 ◽  
Vol 88 (3) ◽  
pp. 881-887 ◽  
Author(s):  
Gale B. Carey
Keyword(s):  
Adipose Tissue ◽  
Energy Intake ◽  
Excess Energy ◽  
Fat Tissue ◽  
Cellular Mechanisms ◽  
Miniature Swine ◽  
Extracellular Adenosine

This study examined the influence of energy expenditure and energy intake on cellular mechanisms regulating adipose tissue metabolism. 1 Twenty-four swine were assigned to restricted-fed sedentary, restricted-fed exercise-trained, full-fed sedentary, or full-fed exercise-trained groups. After 3 mo of treatment, adipocytes were isolated and adipocyte size, adenosine A1 receptor characteristics, and lipolytic sensitivity were measured. Swine were infused with epinephrine during which adipose tissue extracellular adenosine, plasma fatty acids, and plasma glycerol were measured. Results revealed that adipocytes isolated from restricted-fed exercised swine had a smaller diameter, a lower number of A1 receptors, and a greater sensitivity to lipolytic stimulation, compared with adipocytes from full-fed exercised swine. Extracellular adenosine levels were transiently increased on infusion of epinephrine in adipose tissue of restricted-fed exercised but not full-fed exercised swine. These results suggest a role for adenosine in explaining the discrepancy between in vitro and in vivo lipolysis findings and underscore the notion that excess energy intake dampens the lipolytic sensitivity of adipocytes to β-agonists and adenosine, even if accompanied by exercise training.

scholarly journals Osteopontin Expression in Human and Murine Obesity: Extensive Local Up-Regulation in Adipose Tissue but Minimal Systemic Alterations

Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1350-1357 ◽  
Author(s):  
Florian W. Kiefer ◽  
Maximilian Zeyda ◽  
Jelena Todoric ◽  
Joakim Huber ◽  
René Geyeregger ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Plasma Concentrations ◽  
Morbidly Obese ◽  
Low Grade ◽  
Obese Patients ◽  
Multifunctional Protein ◽  
Inflammatory Processes ◽  
Low Grade Inflammation

Obesity is associated with a chronic low-grade inflammation characterized by macrophage infiltration of adipose tissue (AT) that may underlie the development of insulin resistance and type 2 diabetes. Osteopontin (OPN) is a multifunctional protein involved in various inflammatory processes, cell migration, and tissue remodeling. Because these processes occur in the AT of obese patients, we studied in detail the regulation of OPN expression in human and murine obesity. The study included 20 morbidly obese patients and 20 age- and sex-matched control subjects, as well as two models (diet-induced and genetic) of murine obesity. In high-fat diet-induced and genetically obese mice, OPN expression was drastically up-regulated in AT (40 and 80-fold, respectively) but remained largely unaltered in liver (<2-fold). Moreover, OPN plasma concentrations remained unchanged in both murine models of obesity, suggesting a particular local but not systemic importance for OPN. OPN expression was strongly elevated also in the AT of obese patients compared with lean subjects in both omental and sc AT. In addition, we detected three OPN isoforms to be expressed in human AT and, strikingly, an obesity induced alteration of the OPN isoform expression pattern. Analysis of AT cellular fractions revealed that OPN is exceptionally highly expressed in AT macrophages in humans and mice. Moreover, OPN expression in AT macrophages was strongly up-regulated by obesity. In conclusion, our data point toward a specific local role of OPN in obese AT. Therefore, OPN could be a critical regulator in obesity induced AT inflammation and insulin resistance.

Cytoplasmic p16 Is Expressed in Normal Brown Fat and Hibernomas

2020 ◽  
Vol 28 (5) ◽  
pp. 496-501
Author(s):  
Georgia Karpathiou ◽  
Jean Marc Dumollard ◽  
Zoe Evangelou ◽  
Anna Batistatou ◽  
Michel Peoc’h ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Brown Fat ◽  
Fat Tissue ◽  
P16 Expression ◽  
Tissue Browning

White adipose tissue browning has emerged as a putative therapy of obesity, and studies in mice have shown that Cdkn2a is implicated in white-to-brown transition. However, the role of Cdkn2a product p16 has been never studied in human brown fat tissue. The aim of the study is to investigate the expression of p16 in normal brown fat and in hibernoma, a lipoma containing brown fat-like adipocytes. Ten normal brown fat tissues and 5 hibernomas were immunohistochemically studied for p16 expression. Nearby white adipose tissue was used for comparison. All brown fat and hibernomas specimens express p16 in a cytoplasmic manner. Neighboring white adipose tissue is negative for p16 expression. Thus, cytoplasmic p16 may be associated with fat tissue browning.

Transcriptome of the subcutaneous adipose tissue in response to oral supplementation of type 2 Leprdb obese diabetic mice with niacin-bound chromium

2006 ◽  
Vol 27 (3) ◽  
pp. 370-379 ◽  
Author(s):  
Cameron Rink ◽  
Sashwati Roy ◽  
Savita Khanna ◽  
Trenton Rink ◽  
Debasis Bagchi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Blood Glucose ◽  
Specific Gene ◽  
Oral Glucose ◽  
Diabetic Mice ◽  
Fat Tissue ◽  
Obesity And Diabetes ◽  
Brown Adipose

The effects of oral niacin-bound chromium (NBC) supplementation on the subcutaneous fat tissue of type 2 Lepr db obese diabetic mice were examined using high-density comprehensive mouse genome (45,101 probe sets) expression arrays. The influence of such supplementation on the plasma cardiovascular risk factors of these mice was also investigated. Supplementation of NBC had no significant effect on age-dependent weight gain in the Lepr db obese diabetic mice. However, NBC lowered total cholesterol (TC), TC-to-HDL ratio, LDL cholesterol, and triglyceride levels while increasing HDL cholesterol in the blood plasma. No effect of NBC supplementation was observed on fasting blood glucose levels. Oral glucose tolerance test revealed a significantly improved clearance of blood glucose between 1 and 2 h of glucose challenge in NBC-supplemented mice. Unbiased genome-wide interrogation demonstrated that NBC resulted in the upregulation of muscle-specific gene expression in the fat tissue. Genes encoding proteins involved in glycolysis, muscle contraction, muscle metabolism, and muscle development were specifically upregulated in response to NBC supplementation. Genes in the adipose tissue that were downregulated in response to NBC supplementation included cell death-inducing DNA fragmentation factor (CIDEA) and uncoupling protein-1, which represent key components involved in the thermogenic role of brown adipose tissue and tocopherol transfer protein, the primary carrier of α-tocopherol to adipose tissue. The observation that CIDEA-null mice are resistant to obesity and diabetes suggests that the inhibitory role of NBC on CIDEA expression was favorable. Further studies testing the molecular basis of NBC function and long-term outcomes are warranted.

scholarly journals Role of Cytokines and Toll-Like Receptors in the Immunopathogenesis of Guillain-Barré Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Kishan Kumar Nyati ◽  
Kashi Nath Prasad
Keyword(s):  
Immune Response ◽  
Single Agent ◽  
Host Factors ◽  
Guillain Barre Syndrome ◽  
Toll Like Receptors ◽  
Guillain Barré Syndrome ◽  
Microbial Infections ◽  
Inflammatory Processes ◽  
Guillain Barré

Guillain-Barré syndrome (GBS) is an autoimmune disease of the peripheral nervous system, mostly triggered by an aberrant immune response to an infectious pathogen. Although several infections have been implicated in the pathogenesis of GBS, not all such infected individuals develop this disease. Moreover, infection with a single agent might also lead to different subtypes of GBS emphasizing the role of host factors in the development of GBS. The host factors regulate a broad range of inflammatory processes that are involved in the pathogenesis of autoimmune diseases including GBS. Evidences suggest that systemically and locally released cytokines and their involvement in immune-mediated demyelination and axonal damage of peripheral nerves are important in the pathogenesis of GBS. Toll-like receptors (TLRs) link innate and adaptive immunity through transcription of several proinflammatory cytokines. TLR genes may increase susceptibility to microbial infections; an attenuated immune response towards antigen and downregulation of cytokines occurs due to mutation in the gene. Herein, we discuss the crucial role of host factors such as cytokines and TLRs that activate the immune response and are involved in the pathogenesis of the disease.

scholarly journals Acinetobacter baumanniiLipopolysaccharide Influences Adipokine Expression in 3T3-L1 Adipocytes

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yuka Unno ◽  
Yoshinori Sato ◽  
Satoshi Nishida ◽  
Akiyo Nakano ◽  
Ryuichi Nakano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Potential Role ◽  
Molecular Level ◽  
Opportunistic Pathogen ◽  
Lipocalin 2 ◽  
Increased Risk ◽  
Adipocyte Cell

Acinetobacter baumanniiis one of the most important nosocomial opportunistic pathogen worldwide. In addition, obesity has been associated with an increased risk of nosocomial infection, suggesting that there may be an association betweenA. baumanniiand white adipose tissue. However, the effects ofA. baumanniion adipocytes have not been well studied at the molecular level. Here, we investigated the potential role ofA. baumannii-derived lipopolysaccharides (LPS) as signaling molecules that affect adipocyte functionality. We tested the effect of increasing concentrations ofA. baumannii-derived LPS (10, 100, or 1000 ng/mL) on the 3T3-L1 adipocyte cell line. Exposure to LPS was found to increase the expression of several adipokines (e.g., MIP-2, MCP-1, TNF-α, IL-6, lipocalin-2, and FABP4) in 3T3-L1 adipocytes and significantly reduced the expression of leptin and adiponectin. The effects ofA. baumannii-derived LPS on MIP-2 expression were similar in comparison with that of LPS prepared fromPseudomonas aeruginosaandEscherichia coliin our cell culture-based system. This study suggests thatA. baumannii-derived LPS functions as a signaling molecule that impacts the inflammatory function of white adipose tissue on the level of gene expression.

scholarly journals Role of Adipose Tissue in Inflammatory Bowel Disease

2021 ◽  
Vol 22 (8) ◽  
pp. 4226
Author(s):  
Eva Karaskova ◽  
Maria Velganova-Veghova ◽  
Milos Geryk ◽  
Hana Foltenova ◽  
Veronika Kucerova ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Potential Role ◽  
Endocrine Activity ◽  
Mesenteric Fat ◽  
Principal Source ◽  
Bowel Diseases ◽  
Inflammatory Processes ◽  
Inflammatory Bowel ◽  
Visceral Adipose

Inflammatory bowel diseases (IBDs), chronic inflammatory disorders affecting the gastrointestinal tract, include Crohn’s disease and ulcerative colitis. There are increasing clinical and experimental data showing that obesity, especially visceral adiposity, plays a substantial role in the pathogenesis of IBD. Obesity seems to be an important risk factor also for IBD disease severity and clinical outcomes. Visceral adipose tissue is an active multifunctional metabolic organ involved in lipid storage and immunological and endocrine activity. Bowel inflammation penetrates the surrounding adipose tissue along the mesentery. Mesenteric fat serves as a barrier to inflammation and controls immune responses to the translocation of gut bacteria. At the same time, mesenteric adipose tissue may be the principal source of cytokines and adipokines responsible for inflammatory processes associated with IBD. This review is particularly focusing on the potential role of adipokines in IBD pathogenesis and their possible use as promising therapeutic targets.

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