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Adipose Tissue Inflammation 2022

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 46759

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Dr. Javier Gómez-Ambrosi

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Metabolic Research Lab, Clínica Universidad de Navarra, Irunlarrea 1, 31008 Pamplona, Spain
Interests: obesity; dietary treatment; lifestyle intervention; pharmacological treatment; metabolic surgery; intermittent fasting; cardiometabolic risk improvement; body composition changes
Special Issues, Collections and Topics in MDPI journals

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Dear Colleagues,

Over the last decades, obesity has become one of the most prevalent metabolic disorders. Excess adiposity favors the development of cardiometabolic alterations, such as type 2 diabetes (T2D), cardiovascular disease, dyslipidemia, steatohepatitis, and cancer. In the last years, adipose tissue inflammation has been shown to be one of the major mechanisms underlying adipose tissue dysfunction, contributing to the development of metabolic derangements in other organs. The contribution of the different adipose tissue depots, the discovery of the function of molecules such as MCP-1, the involvement of the inflammasome, or the dual effect of macrophage polarization have greatly contributed to the improved understating produced in the last years, of the role played by adipose tissue inflammation in the development of metabolic alterations.

In this Special Issue, we welcome contributions related to any aspect of adipose tissue inflammation, from mechanistic issues related to the different types of cells involved; the role of proinflammatory molecules; the effect of adipokines; the connection with other processes implicated such as fibrosis, hypoxia, angiogenesis, or extracellular matrix remodeling; to its metabolic consequences. We aim to provide readers with a clear view of the pathophysiological relevance of adipose tissue inflammation and the cross-talk with other organs such as the liver, the skeletal muscle, the pancreas, or the brain, not only in the development of obesity-associated comorbidities, such as T2D or cardiovascular problems, but also in the link with other metabolic alterations, such as non-alcoholic fatty liver disease or dyslipidemia, or in the development of cancer. Studies analyzing the role of adipose tissue inflammation in obesity subphenotyping in relation to the presence of metabolically healthy or unhealthy obesity will be also welcome.

Dr. Javier Gómez-Ambrosi
Guest Editor

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Keywords

adipose tissue
inflammation
obesity
adipokines
fibrosis
ECM remodeling
macrophage polarization
type 2 diabetes
NAFLD
oxidative stress
metabolically healthy obesity
cancer

Published Papers (11 papers)

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Editorial

Jump to: Research, Review

3 pages, 216 KiB

Open AccessEditorial

Adipose Tissue Inflammation

by Javier Gómez-Ambrosi

Cells 2023, 12(11), 1484; https://doi.org/10.3390/cells12111484 - 26 May 2023

Viewed by 818

Abstract

In recent decades, obesity has become one of the most common metabolic diseases [...] Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

Research

Jump to: Editorial, Review

18 pages, 3143 KiB

Open AccessArticle

Expression of Steroid Receptor RNA Activator 1 (SRA1) in the Adipose Tissue Is Associated with TLRs and IRFs in Diabesity

by Shihab Kochumon, Hossein Arefanian, Sardar Sindhu, Reeby Thomas, Texy Jacob, Amnah Al-Sayyar, Steve Shenouda, Fatema Al-Rashed, Heikki A. Koistinen, Fahd Al-Mulla, Jaakko Tuomilehto and Rasheed Ahmad

Cells 2022, 11(24), 4007; https://doi.org/10.3390/cells11244007 - 11 Dec 2022

Cited by 3 | Viewed by 1393

Abstract

Steroid receptor RNA activator gene (SRA1) emerges as a player in pathophysiological responses of adipose tissue (AT) in metabolic disorders such as obesity and type 2 diabetes (T2D). We previously showed association of the AT SRA1 expression with inflammatory cytokines/chemokines involved in metabolic derangement. However, the relationship between altered adipose expression of SRA1 and the innate immune Toll-like receptors (TLRs) as players in nutrient sensing and metabolic inflammation as well as their downstream signaling partners, including interferon regulatory factors (IRFs), remains elusive. Herein, we investigated the association of AT SRA1 expression with TLRs, IRFs, and other TLR-downstream signaling mediators in a cohort of 108 individuals, classified based on their body mass index (BMI) as persons with normal-weight (N = 12), overweight (N = 32), and obesity (N = 64), including 55 with and 53 without T2D. The gene expression of SRA1, TLRs-2,3,4,7,8,9,10 and their downstream signaling mediators including IRFs-3,4,5, myeloid differentiation factor 88 (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK1), and nuclear factor-κB (NF-κB) were determined using qRT-PCR and SRA1 protein expression was determined by immunohistochemistry. AT SRA1 transcripts’ expression was significantly correlated with TLRs-3,4,7, MyD88, NF-κB, and IRF5 expression in individuals with T2D, while it associated with TLR9 and TRAF6 expression in all individuals, with/without T2D. SRA1 expression associated with TLR2, IRAK1, and IRF3 expression only in individuals with obesity, regardless of diabetes status. Furthermore, TLR3/TLR7/IRAK1 and TLR3/TLR9 were identified as independent predictors of AT SRA1 expression in individuals with obesity and T2D, respectively. Overall, our data demonstrate a direct association between the AT SRA1 expression and the TLRs together with their downstream signaling partners and IRFs in individuals with obesity and/or T2D. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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8 pages, 841 KiB

Open AccessArticle

Physiological Oxygen Levels Differentially Regulate Adipokine Production in Abdominal and Femoral Adipocytes from Individuals with Obesity Versus Normal Weight

by Ioannis G. Lempesis, Nicole Hoebers, Yvonne Essers, Johan W. E. Jocken, Kasper M. A. Rouschop, Ellen E. Blaak, Konstantinos N. Manolopoulos and Gijs H. Goossens

Cells 2022, 11(22), 3532; https://doi.org/10.3390/cells11223532 - 08 Nov 2022

Cited by 7 | Viewed by 1300

Abstract

Adipose tissue (AT) inflammation may increase obesity-related cardiometabolic complications. Altered AT oxygen partial pressure (pO₂) may impact the adipocyte inflammatory phenotype. Here, we investigated the effects of physiological pO₂ levels on the inflammatory phenotype of abdominal (ABD) and femoral (FEM) adipocytes derived from postmenopausal women with normal weight (NW) or obesity (OB). Biopsies were collected from ABD and FEM subcutaneous AT in eighteen postmenopausal women (aged 50–65 years) with NW (BMI 18–25 kg/m², n = 9) or OB (BMI 30–40 kg/m², n = 9). We compared the effects of prolonged exposure to different physiological pO₂ levels on adipokine expression and secretion in differentiated human multipotent adipose-derived stem cells. Low physiological pO₂ (5% O₂) significantly increased leptin gene expression/secretion in ABD and FEM adipocytes derived from individuals with NW and OB compared with high physiological pO₂ (10% O₂) and standard laboratory conditions (21% O₂). Gene expression/secretion of IL-6, DPP-4, and MCP-1 was reduced in differentiated ABD and FEM adipocytes from individuals with OB but not NW following exposure to low compared with high physiological pO₂ levels. Low physiological pO₂ decreases gene expression and secretion of several proinflammatory factors in ABD and FEM adipocytes derived from individuals with OB but not NW. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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18 pages, 2631 KiB

Open AccessFeature PaperArticle

Higher Mast Cell Accumulation in Human Adipose Tissues Defines Clinically Favorable Obesity Sub-Phenotypes

by Nir Goldstein, Yarden Kezerle, Yftach Gepner, Yulia Haim, Tal Pecht, Roi Gazit, Vera Polischuk, Idit F. Liberty, Boris Kirshtein, Ruthy Shaco-Levy, Matthias Blüher and Assaf Rudich

Cells 2020, 9(6), 1508; https://doi.org/10.3390/cells9061508 - 20 Jun 2020

Cited by 13 | Viewed by 3686

Abstract

The identification of human obesity sub-types may improve the clinical management of patients with obesity and uncover previously unrecognized obesity mechanisms. Here, we hypothesized that adipose tissue (AT) mast cells (MC) estimation could be a mark for human obesity sub-phenotyping beyond current clinical-based stratifications, both cross-sectionally and prospectively. We estimated MC accumulation using immunohistochemistry and gene expression in abdominal visceral AT (VAT) and subcutaneous (SAT) in a human cohort of 65 persons with obesity who underwent elective abdominal (mainly bariatric) surgery, and we validated key results in two clinically similar, independent cohorts (n = 33, n = 56). AT-MC were readily detectable by immunostaining for either c-kit or tryptase and by assessing the gene expression of KIT (KIT Proto-Oncogene, Receptor Tyrosine Kinase), TPSB2 (tryptase beta 2), and CMA1 (chymase 1). Participants were characterized as VAT-MC^low if the expression of both CMA1 and TPSB2 was below the median. Higher expressers of MC genes (MC^high) were metabolically healthier (lower fasting glucose and glycated hemoglobin, with higher pancreatic beta cell reserve (HOMA-β), and lower triglycerides and alkaline-phosphatase) than people with low expression (MC^low). Prospectively, higher MC accumulation in VAT or SAT obtained during surgery predicted greater postoperative weight-loss response to bariatric surgery. Jointly, high AT-MC accumulation may be used to clinically define obesity sub-phenotypes, which are associated with a “healthier” cardiometabolic risk profile and a better weight-loss response to bariatric surgery. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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13 pages, 1390 KiB

Open AccessArticle

Melatonin Supplementation Attenuates the Pro-Inflammatory Adipokines Expression in Visceral Fat from Obese Mice Induced by A High-Fat Diet

by Talita da Silva Mendes de Farias, Regislane Ino da Paixao, Maysa Mariana Cruz, Roberta Dourado Cavalcante da Cunha de Sa, Jussara de Jesus Simão, Vitor Jaco Antraco and Maria Isabel Cardoso Alonso-Vale

Cells 2019, 8(9), 1041; https://doi.org/10.3390/cells8091041 - 06 Sep 2019

Cited by 34 | Viewed by 5059

Abstract

Obesity is defined as a condition of abnormal or excessive fat accumulation in white adipose tissue that results from the exacerbated consumption of calories associated with low energy expenditure. Fat accumulation in both adipose tissue and other organs contributes to a systemic inflammation leading to the development of metabolic disorders such as type 2 diabetes, hypertension, and dyslipidemia. Melatonin is a potent antioxidant and improves inflammatory processes and energy metabolism. Using male mice fed a high-fat diet (HFD—59% fat from lard and soybean oil; 9:1) as an obesity model, we investigated the effects of melatonin supplementation on the prevention of obesity-associated complications through an analysis of plasma biochemical profile, body and fat depots mass, adipocytes size and inflammatory cytokines expression in epididymal (EPI) adipose depot. Melatonin prevented a gain of body weight and fat depot mass as well as adipocyte hypertrophy. Melatonin also reversed the increase of total cholesterol, triglycerides and LDL-cholesterol. In addition, this neurohormone was effective in completely decreasing the inflammatory cytokines leptin and resistin in plasma. In the EPI depot, melatonin reversed the increase of leptin, Il-6, Mcp-1 and Tnf-α triggered by obesity. These data allow us to infer that melatonin presents an anti-obesity effect since it acts to prevent the progression of pro-inflammatory markers in the epididymal adipose tissue together with a reduction in adiposity. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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18 pages, 2541 KiB

Open AccessArticle

Physical Exercise Affects Adipose Tissue Profile and Prevents Arterial Thrombosis in BDNF Val66Met Mice

by Leonardo Sandrini, Alessandro Ieraci, Patrizia Amadio, Marta Zarà, Nico Mitro, Francis S. Lee, Elena Tremoli and Silvia Stella Barbieri

Cells 2019, 8(8), 875; https://doi.org/10.3390/cells8080875 - 11 Aug 2019

Cited by 16 | Viewed by 4442

Abstract

Adipose tissue accumulation is an independent and modifiable risk factor for cardiovascular disease (CVD). The recent CVD European Guidelines strongly recommend regular physical exercise (PE) as a management strategy for prevention and treatment of CVD associated with metabolic disorders and obesity. Although mutations as well as common genetic variants, including the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism, are associated with increased body weight, eating and neuropsychiatric disorders, and myocardial infarction, the effect of this polymorphism on adipose tissue accumulation and regulation as well as its relation to obesity/thrombosis remains to be elucidated. Here, we showed that white adipose tissue (WAT) of humanized knock-in BDNFVal66Met (BDNF^Met/Met) mice is characterized by an altered morphology and an enhanced inflammatory profile compared to wild-type BDNF^Val/Val. Four weeks of voluntary PE restored the adipocyte size distribution, counteracted the inflammatory profile of adipose tissue, and prevented the prothrombotic phenotype displayed, per se, by BDNF^Met/Met mice. C3H10T1/2 cells treated with the Pro-BDNFMet peptide well recapitulated the gene alterations observed in BDNF^Met/Met WAT mice. In conclusion, these data indicate the strong impact of lifestyle, in particular of the beneficial effect of PE, on the management of arterial thrombosis and inflammation associated with obesity in relation to the specific BDNF Val66Met mutation. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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12 pages, 1470 KiB

Open AccessArticle

Obesity as an Inflammatory Agent Can Cause Cellular Changes in Human Milk due to the Actions of the Adipokines Leptin and Adiponectin

by Tassiane C. Morais, Luiz C. de Abreu, Ocilma B. de Quental, Rafael S. Pessoa, Mahmi Fujimori, Blanca E. G. Daboin, Eduardo L. França and Adenilda C. Honorio-França

Cells 2019, 8(6), 519; https://doi.org/10.3390/cells8060519 - 29 May 2019

Cited by 13 | Viewed by 3314

Abstract

Adiponectin and leptin play roles in the hunger response, and they can induce the inflammatory process as the initial mechanism of the innate immune response. It is possible for alterations in the levels of these adipokines to compromise the functional activity of human colostrum phagocytes. Therefore, the objective of this study is to analyze the effects of adiponectin and leptin on colostrum mononuclear (MN) cells. Colostrum was collected from 80 healthy donors, who were divided into two groups: the control group and the high body mass index (BMI) group. MN cells were used to analyze phagocytosis by flow cytometry, and reactive oxygen species (ROS), intracellular calcium, and apoptosis were assessed by fluorimetry using a microplate reader. Adipokines restored the levels of phagocytosis to the high BMI group (p < 0.05), with a mechanism that is action-dependent on the release of ROS and intracellular calcium. However, adiponectin and leptin simultaneously contributed to better microbicidal activity, thus reflecting an increase in the apoptosis level (p < 0.05) in the high BMI group. Probably, the maintenance of the balance between adiponectin and leptin levels enhances the protection and decreases the indices of neonatal infection in the breastfeeding infants of women with high BMI values. Therefore, policies that support pre-gestational weight control should be encouraged. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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Review

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19 pages, 819 KiB

Open AccessReview

Obesity as a Risk Factor for Severe COVID-19 and Complications: A Review

by Fien Demeulemeester, Karin de Punder, Marloes van Heijningen and Femke van Doesburg

Cells 2021, 10(4), 933; https://doi.org/10.3390/cells10040933 - 17 Apr 2021

Cited by 63 | Viewed by 11213

Abstract

Emerging data suggest that obesity is a major risk factor for the progression of major complications such as acute respiratory distress syndrome (ARDS), cytokine storm and coagulopathy in COVID-19. Understanding the mechanisms underlying the link between obesity and disease severity as a result of SARS-CoV-2 infection is crucial for the development of new therapeutic interventions and preventive measures in this high-risk group. We propose that multiple features of obesity contribute to the prevalence of severe COVID-19 and complications. First, viral entry can be facilitated by the upregulation of viral entry receptors, like angiotensin-converting enzyme 2 (ACE2), among others. Second, obesity-induced chronic inflammation and disruptions of insulin and leptin signaling can result in impaired viral clearance and a disproportionate or hyper-inflammatory response, which together with elevated ferritin levels can be a direct cause for ARDS and cytokine storm. Third, the negative consequences of obesity on blood coagulation can contribute to the progression of thrombus formation and hemorrhage. In this review we first summarize clinical findings on the relationship between obesity and COVID-19 disease severity and then further discuss potential mechanisms that could explain the risk for major complications in patients suffering from obesity. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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15 pages, 1545 KiB

Open AccessReview

New Insights into the Liver–Visceral Adipose Axis During Hepatic Resection and Liver Transplantation

by María Eugenia Cornide-Petronio, Mónica B. Jiménez-Castro, Jordi Gracia-Sancho and Carmen Peralta

Cells 2019, 8(9), 1100; https://doi.org/10.3390/cells8091100 - 18 Sep 2019

Cited by 7 | Viewed by 3604

Abstract

In the last decade, adipose tissue has emerged as an endocrine organ with a key role in energy homeostasis. In addition, there is close crosstalk between the adipose tissue and the liver, since pro- and anti-inflammatory substances produced at the visceral adipose tissue level directly target the liver through the portal vein. During surgical procedures, including hepatic resection and liver transplantation, ischemia–reperfusion injury induces damage and regenerative failure. It has been suggested that adipose tissue is associated with both pathological or, on the contrary, with protective effects on damage and regenerative response after liver surgery. The present review aims to summarize the current knowledge on the crosstalk between the adipose tissue and the liver during liver surgery. Therapeutic strategies as well as the clinical and scientific controversies in this field are discussed. The different experimental models, such as lipectomy, to evaluate the role of adipose tissue in both steatotic and nonsteatotic livers undergoing surgery, are described. Such information may be useful for the establishment of protective strategies aimed at regulating the liver–visceral adipose tissue axis and improving the postoperative outcomes in clinical liver surgery. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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16 pages, 542 KiB

Open AccessReview

Obesity-Induced Adipose Tissue Inflammation as a Strong Promotional Factor for Pancreatic Ductal Adenocarcinoma

by Hui-Hua Chang and Guido Eibl

Cells 2019, 8(7), 673; https://doi.org/10.3390/cells8070673 - 03 Jul 2019

Cited by 23 | Viewed by 3889

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is expected to soon become the second leading cause of cancer related deaths in the United States. This may be due to the rising obesity prevalence, which is a recognized risk factor for PDAC. There is great interest in deciphering the underlying driving mechanisms of the obesity–PDAC link. Visceral adiposity has a strong correlation to certain metabolic diseases and gastrointestinal cancers, including PDAC. In fact, our own data strongly suggest that visceral adipose tissue inflammation is a strong promoter for PDAC growth and progression in a genetically engineered mouse model of PDAC and diet-induced obesity. In this review, we will discuss the relationship between obesity-associated adipose tissue inflammation and PDAC development, with a focus on the key molecular and cellular components in the dysfunctional visceral adipose tissue, which provides a tumor permissive environment. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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15 pages, 1072 KiB

Open AccessReview

Associations between Fatty Acid-Binding Protein 4–A Proinflammatory Adipokine and Insulin Resistance, Gestational and Type 2 Diabetes Mellitus

by Marcin Trojnar, Jolanta Patro-Małysza, Żaneta Kimber-Trojnar, Bożena Leszczyńska-Gorzelak and Jerzy Mosiewicz

Cells 2019, 8(3), 227; https://doi.org/10.3390/cells8030227 - 08 Mar 2019

Cited by 67 | Viewed by 6911

Abstract

There is ample scientific evidence to suggest a link between the fatty acid-binding protein 4 (FABP4) and insulin resistance, gestational (GDM), and type 2 (T2DM) diabetes mellitus. This novel proinflammatory adipokine is engaged in the regulation of lipid metabolism at the cellular level. The molecule takes part in lipid oxidation, the regulation of transcription as well as the synthesis of membranes. An involvement of FABP4 in the pathogenesis of obesity and insulin resistance seems to be mediated via FABP4-dependent peroxisome proliferator-activated receptor γ (PPARγ) inhibition. A considerable number of studies have shown that plasma concentrations of FABP4 is increased in obesity and T2DM, and that circulating FABP4 levels are correlated with certain clinical parameters, such as body mass index, insulin resistance, and dyslipidemia. Since plasma-circulating FABP4 has the potential to modulate the function of several types of cells, it appears to be of extreme interest to try to develop potential therapeutic strategies targeting the pathogenesis of metabolic diseases in this respect. In this manuscript, representing a detailed review of the literature on FABP4 and the abovementioned metabolic disorders, various mechanisms of the interaction of FABP4 with insulin signaling pathways are thoroughly discussed. Clinical aspects of insulin resistance in diabetic patients, including women diagnosed with GDM, are analyzed as well. Full article

(This article belongs to the Special Issue Adipose Tissue Inflammation 2022)

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