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Journal articles on the topic 'Adipose tissue inflammation'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Gómez-Ambrosi, Javier. "Adipose Tissue Inflammation." Cells 12, no. 11 (2023): 1484. http://dx.doi.org/10.3390/cells12111484.

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Ramos-Ramírez, Patricia, Carina Malmhäll, Kristina Johansson, Mikael Adner, Jan Lötvall, and Apostolos Bossios. "Lung Regulatory T Cells Express Adiponectin Receptor 1: Modulation by Obesity and Airway Allergic Inflammation." International Journal of Molecular Sciences 21, no. 23 (2020): 8990. http://dx.doi.org/10.3390/ijms21238990.

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Regulatory T cells (Tregs) decrease in the adipose tissue upon weight gain, contributing to persistent low-grade inflammation in obesity. We previously showed that adipose tissue Tregs express the adiponectin receptor 1 (AdipoR1); however, the expression in lung Tregs is still unknown. Here, we aimed to determine whether Helios+ and Helios− Treg subsets expressed AdipoR1 in the lungs of obese mice and whether different obesity grades affected the expression upon allergic lung inflammation. For diet-induced obesity (DIO), mice were fed a high-fat diet (HFD) for up to 15 weeks (overweight), 21 w

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3

Mulder, P., A.M. van den Hoek, and R. Kleenann. "The CCR2 Inhibitor Propagermanium Attenuates Diet-Induced Insulin Resistance, Adipose Tissue Inflammation and Non-Alcoholic Steatohepatitis." Plos One 12, no. 1 (2017): e016974. https://doi.org/10.1371/journal.pone.0169740.

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Background and aim. Obese patients with chronic inflammation in white adipose tissue (WAT) have an increased risk of developing non-alcoholic steatohepatitis (NASH). The C-C chemokine receptor-2 (CCR2) has a crucial role in the recruitment of immune cells to WAT and liver, thereby promoting the inflammatory component of the disease. Herein, we examined whether intervention with propagermanium, an inhibitor of CCR2, would attenuate tissue inflammation and NASH development. Methods. Male C57BL/6J mice received a high-fat diet (HFD) for 0, 6, 12 and 24 weeks to characterize the development of ear

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4

McGinty, A., and I. S. Young. "Adipose tissue and inflammation." International Journal of Clinical Practice 65, no. 9 (2011): 913–17. http://dx.doi.org/10.1111/j.1742-1241.2011.02757.x.

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5

Stienstra, Rinke, Caroline Duval, Michael Müller, and Sander Kersten. "PPARs, Obesity, and Inflammation." PPAR Research 2007 (2007): 1–10. http://dx.doi.org/10.1155/2007/95974.

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The worldwide prevalence of obesity and related metabolic disorders is rising rapidly, increasing the burden on our healthcare system. Obesity is often accompanied by excess fat storage in tissues other than adipose tissue, including liver and skeletal muscle, which may lead to local insulin resistance and may stimulate inflammation, as in steatohepatitis. In addition, obesity changes the morphology and composition of adipose tissue, leading to changes in protein production and secretion. Some of these secreted proteins, including several proinflammatory mediators, may be produced by macrophag

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Szczepankiewicz, Dawid, Wojciech Langwiński, Paweł Kołodziejski, et al. "Allergic Inflammation Alters microRNA Expression Profile in Adipose Tissue in the Rat." Genes 11, no. 9 (2020): 1034. http://dx.doi.org/10.3390/genes11091034.

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Adipose tissue is a major source of circulating exosomal microRNAs (miRNAs) that are modulators of the immune response in various types of tissues and organs, including airways. Still, no evidence exists if allergic airway inflammation may affect fat tissue inflammation via alterations in the miRNA expression profile. Therefore, we investigated the miRNA expression profile in the adipose tissue upon induced allergic inflammation in the airways in the rat. Brown Norway rats were chronically sensitized to house dust mite extract for seven weeks. Body composition was performed using MiniSpec Plus

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7

Burhans, Maggie S., Derek K. Hagman, Jessica N. Kuzma, Kelsey A. Schmidt, and Mario Kratz. "Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus." Comprehensive Physiology 9, no. 1 (2019): 1–58. https://doi.org/10.1002/j.2040-4603.2019.tb00055.x.

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ABSTRACTThe objective of this comprehensive review is to summarize and discuss the available evidence of how adipose tissue inflammation affects insulin sensitivity and glucose tolerance. Low‐grade, chronic adipose tissue inflammation is characterized by infiltration of macrophages and other immune cell populations into adipose tissue, and a shift toward more proinflammatory subtypes of leukocytes. The infiltration of proinflammatory cells in adipose tissue is associated with an increased production of key chemokines such as C‐C motif chemokine ligand 2, proinflammatory cytokines including tum

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Hui, Xiaoyan Hannah, and Tianshi Feng. "Adipocyte-Derived Lactate Potentiates Obesity-Evoked Adipose Macrophage Inflammation." Journal of the Endocrine Society 5, Supplement_1 (2021): A40—A41. http://dx.doi.org/10.1210/jendso/bvab048.079.

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Abstract Introduction: Obesity is characterized by mobilization of macrophage inflammation, which represents the major events of obesity-associated adipose tissue inflammation. . On the other hand, lactate accumulation in adipose tissue long been observed. However, whether elevation of lactate plays an essential role in adipose inflammation is not known. In this study, we sought to examine the intermediary role of lactate in macrophage polarization and adipose inflammation upon obesity. Method: Lactate level and activity of lactate dehydrogense (LDH), the key enzyme of lactate production, were

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9

Gustafson, Birgit. "Adipose Tissue, Inflammation and Atherosclerosis." Journal of Atherosclerosis and Thrombosis 17, no. 4 (2010): 332–41. http://dx.doi.org/10.5551/jat.3939.

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10

Gillum, M. P., M. E. Kotas, D. M. Erion, et al. "SirT1 Regulates Adipose Tissue Inflammation." Diabetes 60, no. 12 (2011): 3235–45. http://dx.doi.org/10.2337/db11-0616.

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11

Rohla, Miklos, and Thomas W. Weiss. "Adipose tissue, inflammation and atherosclerosis." Clinical Lipidology 9, no. 1 (2014): 71–81. http://dx.doi.org/10.2217/clp.13.80.

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12

Mau, Theresa, and Raymond Yung. "Adipose tissue inflammation in aging." Experimental Gerontology 105 (May 2018): 27–31. http://dx.doi.org/10.1016/j.exger.2017.10.014.

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13

González-Périz, Ana, and Joan Clària. "Resolution of Adipose Tissue Inflammation." Scientific World JOURNAL 10 (2010): 832–56. http://dx.doi.org/10.1100/tsw.2010.77.

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The presence of the so-called “low-grade” inflammatory state is recognized as a critical event in adipose tissue dysfunction in obesity. This chronic “low-grade” inflammation in white adipose tissue is powerfully augmented through the infiltration of macrophages, which, together with adipocytes, perpetuate a vicious cycle of macrophage recruitment and secretion of free fatty acids and deleterious adipokines that predispose the development of obesity-related comorbidities, such as insulin resistance and nonalcoholic fatty liver disease. In the last decade, many factors have been identified that

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14

FANTUZZI, G. "Adipose tissue, adipokines, and inflammation." Journal of Allergy and Clinical Immunology 115, no. 5 (2005): 911–19. http://dx.doi.org/10.1016/j.jaci.2005.02.023.

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15

Goodwill, Adam G. "Perivascular adipose tissue and inflammation." Obesity 24, no. 3 (2016): 547. http://dx.doi.org/10.1002/oby.21426.

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16

Huang, Ji, Chang Liu, Xiu-Fen Ming, and Zhihong Yang. "Inhibition of p38mapk Reduces Adipose Tissue Inflammation in Aging Mediated by Arginase-II." Pharmacology 105, no. 9-10 (2020): 491–504. http://dx.doi.org/10.1159/000507635.

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<b><i>Background:</i></b> Adipose tissue inflammation occurs not only in obesity but also in aging and is mechanistically linked with age-associated diseases. Studies show that ablation of the l-arginine-metabolizing enzyme arginase-II (Arg-II) reduces adipose tissue inflammation and improves glucose tolerance in obesity. However, the role of Arg-II in aging adipose tissue inflammation is not clear. <b><i>Objective:</i></b> This study investigated the role of Arg-II in age-associated adipose tissue inflammation. <b><i>Methods:</i&g

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Barra, Nicole G., Brandyn D. Henriksbo, Fernando F. Anhê, and Jonathan D. Schertzer. "The NLRP3 inflammasome regulates adipose tissue metabolism." Biochemical Journal 477, no. 6 (2020): 1089–107. http://dx.doi.org/10.1042/bcj20190472.

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Adipose tissue regulates metabolic homeostasis by participating in endocrine and immune responses in addition to storing and releasing lipids from adipocytes. Obesity skews adipose tissue adipokine responses and degrades the coordination of adipocyte lipogenesis and lipolysis. These defects in adipose tissue metabolism can promote ectopic lipid deposition and inflammation in insulin-sensitive tissues such as skeletal muscle and liver. Sustained caloric excess can expand white adipose tissue to a point of maladaptation exacerbating both local and systemic inflammation. Multiple sources, instiga

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Srikakulapu, Prasad, and Coleen A. McNamara. "B Lymphocytes and Adipose Tissue Inflammation." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (2020): 1110–22. http://dx.doi.org/10.1161/atvbaha.119.312467.

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The immune system plays an important role in obesity-induced adipose tissue inflammation and the resultant metabolic dysfunction, which can lead to hypertension, dyslipidemia, and insulin resistance and their downstream sequelae of type 2 diabetes mellitus and cardiovascular disease. While macrophages are the most abundant immune cell type in adipose tissue, other immune cells are also present, such as B cells, which play important roles in regulating adipose tissue inflammation. This brief review will overview B-cell subsets, describe their localization in various adipose depots and summarize

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Lopez, CM, Sciullo MP Di, Casas FN Claveles, et al. "Therapeutic targets to reduce the contribution of pulmonary neutrophilic inflammation towards obesity-associated co-morbidities: a mini-review." Open Journal of Pharmaceutical Science and Research 1, no. 1 (2019): 123–33. https://doi.org/10.36811/ojpsr.2019.110006.

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Epidemiology and experimental models have shown a close link between adipose tissue inflammation, systemic inflammation and pulmonary neutrophilic inflammation, which predispose obese patients to pulmonary diseases, obesity-associated co-morbidities and cancer. Increased content and activation of neutrophils in the lung microvasculature, resulting from peripheral activation of neutrophils, and increased adhesion of neutrophils to the lung microvasculature are important factors explaining the increased susceptibility of obese patients towards respiratory diseases and loss of insulin sensitivity

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20

Itoh, Michiko, Takayoshi Suganami, Rumi Hachiya, and Yoshihiro Ogawa. "Adipose Tissue Remodeling as Homeostatic Inflammation." International Journal of Inflammation 2011 (2011): 1–8. http://dx.doi.org/10.4061/2011/720926.

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Evidence has accumulated indicating that obesity is associated with a state of chronic, low-grade inflammation. Obese adipose tissue is characterized by dynamic changes in cellular composition and function, which may be referred to as “adipose tissue remodeling”. Among stromal cells in the adipose tissue, infiltrated macrophages play an important role in adipose tissue inflammation and systemic insulin resistance. We have demonstrated that a paracrine loop involving saturated fatty acids and tumor necrosis factor-α derived from adipocytes and macrophages, respectively, aggravates obesity-induc

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Li, Run-Mei, Sui-Qing Chen, Ning-Xi Zeng, et al. "Browning of Abdominal Aorta Perivascular Adipose Tissue Inhibits Adipose Tissue Inflammation." Metabolic Syndrome and Related Disorders 15, no. 9 (2017): 450–57. http://dx.doi.org/10.1089/met.2017.0074.

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22

Anthony, Sarah R., Adrienne R. Guarnieri, Anamarie Gozdiff, Robert N. Helsley, Albert Phillip Owens, and Michael Tranter. "Mechanisms linking adipose tissue inflammation to cardiac hypertrophy and fibrosis." Clinical Science 133, no. 22 (2019): 2329–44. http://dx.doi.org/10.1042/cs20190578.

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Abstract Adipose tissue is classically recognized as the primary site of lipid storage, but in recent years has garnered appreciation for its broad role as an endocrine organ comprising multiple cell types whose collective secretome, termed as adipokines, is highly interdependent on metabolic homeostasis and inflammatory state. Anatomical location (e.g. visceral, subcutaneous, epicardial etc) and cellular composition of adipose tissue (e.g. white, beige, and brown adipocytes, macrophages etc.) also plays a critical role in determining its response to metabolic state, the resulting secretome, a

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23

Rajala, Michael W., and Philipp E. Scherer. "Minireview: The Adipocyte—At the Crossroads of Energy Homeostasis, Inflammation, and Atherosclerosis." Endocrinology 144, no. 9 (2003): 3765–73. http://dx.doi.org/10.1210/en.2003-0580.

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Abstract Adipose tissue evolved to efficiently store energy for times of caloric restriction. The large caloric excess common in many Western diets has negated the need for this thrifty function, leaving adipose tissue ill-equipped to handle this increased load. An excess of adipose tissue increases risk for a number of conditions including coronary artery disease, hypertension, dyslipidemias, type 2 diabetes, and even cancer. Indeed, the ability of the adipocyte to function properly when engorged with lipid can lead to lipid accumulation in other tissues, reducing their ability to function an

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24

Sebastian, Becky M., Sanjoy Roychowdhury, Hui Tang, et al. "Identification of a Cytochrome P4502E1/Bid/C1q-dependent Axis Mediating Inflammation in Adipose Tissue after Chronic Ethanol Feeding to Mice." Journal of Biological Chemistry 286, no. 41 (2011): 35989–97. http://dx.doi.org/10.1074/jbc.m111.254201.

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Chronic, heavy alcohol exposure results in inflammation in adipose tissue, insulin resistance, and liver injury. Here we have identified a CYP2E1/Bid/C1q-dependent pathway that is activated in response to chronic ethanol and is required for the development of inflammation in adipose tissue. Ethanol feeding for 25 days to wild-type (C57BL/6J) mice increased expression of multiple markers of adipose tissue inflammation relative to pair-fed controls independent of increased body weight or adipocyte size. Ethanol feeding increased the expression of CYP2E1 in adipocytes, but not stromal vascular ce

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25

Meiliana, Anna, Nurrani Mustika Dewi, and Andi Wijaya. "Adipose Tissue, Inflammation (Meta-inflammation) and Obesity Management." Indonesian Biomedical Journal 7, no. 3 (2015): 129. http://dx.doi.org/10.18585/inabj.v7i3.185.

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BACKGROUND: Obesity-induced inflammation contributes to the development of type 2 diabetes, metabolic syndrome, and cardiovascular disease.CONTENT:The last decade has seen a sharp increase in our appreciation for the macrophage as a critical regulator of metabolic status in obesity. Activation of adipose tissue (AT) macrophages within fat depots is coupled with the development of obesity-induced proinflammatory state and insulin resistance (IR). The activation of classically activated M1 macrophages at the expense of anti-inflammatory M2 macrophages has been causally linked to the development

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Veličković, Nataša, Ana Djordjevic, Ana Vasiljević, Biljana Bursać, Danijela Vojnović Milutinović, and Gordana Matić. "Tissue-specific regulation of inflammation by macrophage migration inhibitory factor and glucocorticoids in fructose-fed Wistar rats." British Journal of Nutrition 110, no. 3 (2013): 456–65. http://dx.doi.org/10.1017/s0007114512005193.

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High fructose consumption is commonly associated with insulin resistance, disturbed glucose homeostasis and low-grade inflammation. Increased glucocorticoid production within adipose tissue has been implicated in the pathogenesis of fructose-induced metabolic syndrome. Immunosuppressive actions of glucocorticoids can be counter-regulated by macrophage migration inhibitory factor (MIF), which is recognised as a key molecule in metabolic inflammation. In the present study, we hypothesised that coordinated action of glucocorticoids and MIF can mediate the effects of a high-fructose diet on adipos

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27

Röszer, Tamás. "Adipose Tissue Immunometabolism and Apoptotic Cell Clearance." Cells 10, no. 9 (2021): 2288. http://dx.doi.org/10.3390/cells10092288.

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The safe removal of apoptotic debris by macrophages—often referred to as efferocytosis—is crucial for maintaining tissue integrity and preventing self-immunity or tissue damaging inflammation. Macrophages clear tissues of hazardous materials from dying cells and ultimately adopt a pro-resolving activation state. However, adipocyte apoptosis is an inflammation-generating process, and the removal of apoptotic adipocytes by so-called adipose tissue macrophages triggers a sequence of events that lead to meta-inflammation and obesity-associated metabolic diseases. Signals that allow apoptotic cells

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Mehta, Pooja, та C. Wayne Smith. "γδ T Cells and diet-induced inflammation in adipose tissue (173.2)". Journal of Immunology 188, № 1_Supplement (2012): 173.2. http://dx.doi.org/10.4049/jimmunol.188.supp.173.2.

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Abstract Adipose tissues contain several subsets of immune cells. Relatively little is known about their contributions to adipose tissue inflammation induced by feeding mice a diet rich in saturated fats. Using a model of diet-induced obesity in male C57BL/6J mice, we investigated the possible contributions of γδ T cells to this inflammation. γδ T cells make up about one-third of the total T cell population in the epididymal adipose tissue. The γδ T cell receptor was blocked in wild-type mice using an anti-TCRδ antibody. A decrease in macrophage marker F4/80 was observed in these mice as compa

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Gerner, Romana R., Verena Wieser, Alexander R. Moschen, and Herbert Tilg. "Metabolic inflammation: role of cytokines in the crosstalk between adipose tissue and liver." Canadian Journal of Physiology and Pharmacology 91, no. 11 (2013): 867–72. http://dx.doi.org/10.1139/cjpp-2013-0050.

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The innate immune system and its major mediators, i.e., cytokines, are increasingly recognized as being of crucial importance in metabolic inflammation as observed in morbid obesity and type 2 diabetes (T2D). Morbid obesity is commonly associated with adipose tissue inflammation. Adipose tissue inflammation is characterized by an increased expression of various pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1 and -6, and by a rather heterogenous cellular infiltrate including monocytes/macrophages, neutrophils, B lymphocytes, T lymphocytes, and others. It has been d

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de Castro, J., J. Sevillano, J. Marciniak, et al. "Implication of Low Level Inflammation in the Insulin Resistance of Adipose Tissue at Late Pregnancy." Endocrinology 152, no. 11 (2011): 4094–105. http://dx.doi.org/10.1210/en.2011-0068.

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Insulin resistance is a characteristic of late pregnancy, and adipose tissue is one of the tissues that most actively contributes to the reduced maternal insulin sensitivity. There is evidence that pregnancy is a condition of moderate inflammation, although the physiological role of this low-grade inflammation remains unclear. The present study was designed to validate whether low-grade inflammation plays a role in the development of insulin resistance in adipose tissue during late pregnancy. To this end, we analyzed proinflammatory adipokines and kinases in lumbar adipose tissue of nonpregnan

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31

Blüher, Matthias. "Adipose tissue inflammation: a cause or consequence of obesity-related insulin resistance?" Clinical Science 130, no. 18 (2016): 1603–14. http://dx.doi.org/10.1042/cs20160005.

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The worldwide obesity epidemic has become a major health concern, because it contributes to higher mortality due to an increased risk for noncommunicable diseases including cardiovascular diseases, type 2 diabetes, musculoskeletal disorders and some cancers. Insulin resistance may link accumulation of adipose tissue in obesity to metabolic diseases, although the underlying mechanisms are not completely understood. In the past decades, data from human studies and transgenic animal models strongly suggested correlative, but also causative associations between activation of proinflammatory pathwa

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Yang, X. F., Z. Y. Jiang, Z. M. Tian, et al. "Inflammation-related oxidative stress in white adipose tissues of an inbred obese pig." Annals of Animal Science 17, no. 2 (2017): 433–46. http://dx.doi.org/10.1515/aoas-2016-0054.

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Abstract The uneven development of adipose tissues reflects a differential occurrence of biological events in vivo while the underlying molecular mechanism remains largely unknown. In the present study, the in vivo inflammatory status of an inbred obese porcine model, Lantang pig, was assessed, aiming to provide evidence for obesity biology. Compared with genetically lean pigs (crossbred, Duroc × Landrace × Large White), Lantang pigs exhibited a larger amount of ultra large adipocytes in subcutaneous adipose tissue accompanied with higher expression of macrophage/monocytes markers and pro-infl

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Mathur, Sandeep Kumar, Priyanka Jain, and Prashant Mathur. "Microarray Evidences the Role of Pathologic Adipose Tissue in Insulin Resistance and Their Clinical Implications." Journal of Obesity 2011 (2011): 1–16. http://dx.doi.org/10.1155/2011/587495.

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Clustering of insulin resistance and dysmetabolism with obesity is attributed to pathologic adipose tissue. The morphologic hallmarks of this pathology are adipocye hypertrophy and heightened inflammation. However, it's underlying molecular mechanisms remains unknown. Study of gene function in metabolically active tissues like adipose tissue, skeletal muscle and liver is a promising strategy. Microarray is a powerful technique of assessment of gene function by measuring transcription of large number of genes in an array. This technique has several potential applications in understanding pathol

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Ikeoka, Dimas, Julia K. Mader, and Thomas R. Pieber. "Adipose tissue, inflammation and cardiovascular disease." Revista da Associação Médica Brasileira 56, no. 1 (2010): 116–21. http://dx.doi.org/10.1590/s0104-42302010000100026.

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Barazzoni, Rocco, Gianni Biolo, Michela Zanetti, Annamaria Bernardi, and Gianfranco Guarnieri. "Inflammation and Adipose Tissue in Uremia." Journal of Renal Nutrition 16, no. 3 (2006): 204–7. http://dx.doi.org/10.1053/j.jrn.2006.04.005.

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36

Mosley, M., and A. Marette. "Inflammation, Adipose Tissue, and Cardiometabolic Risk." MD Conference Express 13, no. 16 (2013): 8–9. http://dx.doi.org/10.1177/155989771316005.

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37

Berg, Anders H., and Philipp E. Scherer. "Adipose Tissue, Inflammation, and Cardiovascular Disease." Circulation Research 96, no. 9 (2005): 939–49. http://dx.doi.org/10.1161/01.res.0000163635.62927.34.

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38

Scalia, Rosario. "The microcirculation in adipose tissue inflammation." Reviews in Endocrine and Metabolic Disorders 14, no. 1 (2013): 69–76. http://dx.doi.org/10.1007/s11154-013-9236-x.

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Kammoun, H. L., M. J. Kraakman, and M. A. Febbraio. "Adipose tissue inflammation in glucose metabolism." Reviews in Endocrine and Metabolic Disorders 15, no. 1 (2013): 31–44. http://dx.doi.org/10.1007/s11154-013-9274-4.

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Juge-Aubry, Cristiana E., Elvire Henrichot, and Christoph A. Meier. "Adipose tissue: a regulator of inflammation." Best Practice & Research Clinical Endocrinology & Metabolism 19, no. 4 (2005): 547–66. http://dx.doi.org/10.1016/j.beem.2005.07.009.

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Zhang, Ruoyi, Xin Ling, Xianwen Guo, and Zhen Ding. "CD36 Induces Inflammation by Promoting Ferroptosis in Pancreas, Epididymal Adipose Tissue, and Adipose Tissue Macrophages in Obesity-Related Severe Acute Pancreatitis." International Journal of Molecular Sciences 26, no. 8 (2025): 3482. https://doi.org/10.3390/ijms26083482.

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Severe acute pancreatitis (SAP) is mainly triggered by the abnormal activation of pancreatic enzymes. Obesity acts as an independent risk factor for SAP; however, the underlying mechanism has not been fully elucidated. In this study, SAP models were established in mice with normal and high-fat diets. Subsequently, this study examined ferroptosis and inflammatory markers in pancreas and epididymal adipose tissues. To mimic obesity-related SAP in adipose tissue macrophages (ATMs), lipopolysaccharide (LPS) and palmitic acid (PA) were introduced, and alterations in ferroptosis and inflammation wer

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Watanabe, Yasuharu, Yoshinori Nagai, Tomoya Nakamura, Shizuo Akira, Kensuke Miyake, and Kiyoshi Takatsu. "The Radioprotective 105/MD-1 Complex Contributes to Diet-induced Obesity and Adipose Tissue Inflammation (172.23)." Journal of Immunology 188, no. 1_Supplement (2012): 172.23. http://dx.doi.org/10.4049/jimmunol.188.supp.172.23.

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Abstract Accumulating evidence suggest that innate immunity is associated with obesity-induced chronic inflammation and metabolic disorders. For example, the TLR4/MD-2 complex recognizes free fatty acids (FAAs) derived from adipose tissue and promotes adipose tissue inflammation and insulin resistance. The RP105/MD-1 complex is a homolog of the TLR4/MD-2 complex. However, the roles of RP105/MD-1 complex in adipose tissue inflammation have remained elusive. We now report that the RP105/MD-1 complex contributes to high-fat diet (HFD)-induced obesity, adipose tissue inflammation, and insulin resi

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Hua, Lun, Yi Yang, Haoqi Zhang, et al. "Adipocyte FGF21 Signaling Defect Aggravated Adipose Tissue Inflammation in Gestational Diabetes Mellitus." Nutrients 16, no. 22 (2024): 3826. http://dx.doi.org/10.3390/nu16223826.

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Gestational diabetes mellitus (GDM) is associated with increased inflammation in adipose tissues. Fibroblast growth factor 21 (FGF21) is an endocrine hormone which signals to multiple tissues to regulate metabolism. However, its role in GDM remains largely unknown. In this study, we found that impaired FGF21 signaling in GDM correlates with worsened inflammation and insulin resistance in white adipose tissues in mice. Mechanistically, the pregnancy-related upregulation of FGF21 signaling in adipocytes promotes the differentiation of regulatory T cells (Tregs), which are critical for reducing p

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Lai, Kar Neng, and Joseph C. K. Leung. "Peritoneal Adipocytes and Their Role in Inflammation during Peritoneal Dialysis." Mediators of Inflammation 2010 (2010): 1–10. http://dx.doi.org/10.1155/2010/495416.

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Adipose tissue is a major site of chronic inflammation associated with peritoneal dialysis (PD) frequently complicating peritonitis. Adiposity-associated inflammation plays a significant contributory role in the development of chronic inflammation in patients undergoing maintenance PD. However, the molecular and cellular mechanisms of this link remain uncertain. Adipose tissue synthesizes different adipokines and cytokines that orchestrate and regulate inflammation, insulin action, and glucose metabolism locally and systemically. In return, inflammation retards adipocyte differentiation and fu

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Liska, Jan, Per Eriksson, Eva Sverremark-Ekström, Per Tornvall, and Mattias Ekström. "Stimulated in vivo synthesis of plasminogen activator inhibitor-1 in human adipose tissue." Thrombosis and Haemostasis 108, no. 09 (2012): 485–92. http://dx.doi.org/10.1160/th11-11-0822.

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SummaryPlasminogen activator inhibitor type-1 (PAI-1) is one of the most important inhibitors of endogenous fibrinolysis. Adipose tissue is a suggested source of the elevated plasma levels of PAI-1 in obesity. The relation between PAI-1 and inflammation is of particular interest, but current knowledge regarding regulation of PAI-1 in adipose tissue is mainly based on animal studies or ex vivo experiments on human cultured adipocytes. So far, no study has described stimulated gene expression and protein synthesis of PAI-1 in vivo in human adipose tissue. We used open heart surgery as a model of

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Gao, Feng, Benjamin Litchfield, and Huaizhu Wu. "Adipose tissue lymphocytes and obesity." Journal of Cardiovascular Aging 4, no. 1 (2024): 5. http://dx.doi.org/10.20517/jca.2023.38.

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Obesity is associated with chronic inflammation in adipose tissue (AT), mainly evidenced by infiltration and phenotypic changes of various types of immune cells. Macrophages are the major innate immune cells and represent the predominant immune cell population within AT. Lymphocytes, including T cells and B cells, are adaptive immune cells and constitute another important immune cell population in AT. In obesity, CD8+ effector memory T cells, CD4+ Th1 cells, and B2 cells are increased in AT and promote AT inflammation, while regulatory T cells and Th2 cells, which usually function as immune re

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Watanabe, Yasuharu, Yoshinori Nagai, and Kiyoshi Takatsu. "Bidirectional crosstalk between neutrophils and adipocytes promotes adipose tissue inflammation." Journal of Immunology 204, no. 1_Supplement (2020): 75.14. http://dx.doi.org/10.4049/jimmunol.204.supp.75.14.

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Abstract Obesity-associated adipose tissue inflammation contributes to the development of type 2 diabetes. Chronic activation of IL-1β system in adipose tissue on metabolic disorders is well demonstrated. However, a mechanism for its expression and activation in the tissue has remained unexplored. Here we demonstrate that IL-1β transcript was enriched in neutrophils of white adipose tissue (WAT), and the expression of IL-1β was up-regulated by a high-fat diet in the WAT but not in other tissues, including bone marrow, peripheral blood, and spleen. The co-culture of neutrophils with 3T3-L1 adip

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Pei, Ya, Honggui Li, Yuli Cai, et al. "Regulation of adipose tissue inflammation by adenosine 2A receptor in obese mice." Journal of Endocrinology 239, no. 3 (2018): 365–76. http://dx.doi.org/10.1530/joe-18-0169.

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Adenosine 2A receptor (A2AR) exerts anti-inflammatory effects. However, the role of A2AR in obesity-associated adipose tissue inflammation remains to be elucidated. The present study examined the expression of A2AR in adipose tissue of mice with diet-induced obesity and determined the effect of A2AR disruption on the status of obesity-associated adipose tissue inflammation. WT C57BL/6J mice and A2AR-disrupted mice were fed a high-fat diet (HFD) for 12 weeks to induce obesity and adipose tissue inflammation. In vitro, bone marrow-derived macrophages from A2AR-disrupted mice and WT control mice

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Taniguchi, Kaori, and Toru Miyazaki. "Putative roles of specific T cells in progression of obesity-associated inflammation in adipose tissue. (173.36)." Journal of Immunology 188, no. 1_Supplement (2012): 173.36. http://dx.doi.org/10.4049/jimmunol.188.supp.173.36.

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Abstract The metabolic syndrome is known as a chain of illness, triggered by obesity followed by diabetes, hepatic steatosis and atherosclerosis. It is well known that adipose tissues in obesity are in a state of chronic inflammation, and that such inflammatory state is tightly associated with multiple metabolic disorders. Accumulating evidence has shown that the inflammation is mainly lead by the recruitment of macrophages into adipose tissues. Although it has recently been suggested that T cells may also play a role in establishment of inflammation in adipose tissue during the early phase of

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Matz, Alyssa, Lili Qu, Keaton Karlinsey, and Beiyan Zhou. "Impact of microRNA Regulated Macrophage Actions on Adipose Tissue Function in Obesity." Cells 11, no. 8 (2022): 1336. http://dx.doi.org/10.3390/cells11081336.

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Obesity-induced adipose tissue dysfunction is bolstered by chronic, low-grade inflammation and impairs systemic metabolic health. Adipose tissue macrophages (ATMs) perpetuate local inflammation but are crucial to adipose tissue homeostasis, exerting heterogeneous, niche-specific functions. Diversified macrophage actions are shaped through finely regulated factors, including microRNAs, which post-transcriptionally alter macrophage activation. Numerous studies have highlighted microRNAs’ importance to immune function and potential as inflammation-modulatory. This review summarizes current knowle

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