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Journal articles on the topic 'Metaflammation'

Author: Grafiati

Published: 13 April 2024

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1

Wei, Lisha, Yan-Yan Zheng, Jie Sun, Pei Wang, Tao Tao, Yeqiong Li, Xin Chen, et al. "GGPP depletion initiates metaflammation through disequilibrating CYB5R3-dependent eicosanoid metabolism." Journal of Biological Chemistry 295, no. 47 (September 10, 2020): 15988–6001. http://dx.doi.org/10.1074/jbc.ra120.015020.

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Metaflammation is a primary inflammatory complication of metabolic disorders characterized by altered production of many inflammatory cytokines, adipokines, and lipid mediators. Whereas multiple inflammation networks have been identified, the mechanisms by which metaflammation is initiated have long been controversial. As the mevalonate pathway (MVA) produces abundant bioactive isoprenoids and abnormal MVA has a phenotypic association with inflammation/immunity, we speculate that isoprenoids from the MVA may provide a causal link between metaflammation and metabolic disorders. Using a line with the MVA isoprenoid producer geranylgeranyl diphosphate synthase (GGPPS) deleted, we find that geranylgeranyl pyrophosphate (GGPP) depletion causes an apparent metaflammation as evidenced by abnormal accumulation of fatty acids, eicosanoid intermediates, and proinflammatory cytokines. We also find that GGPP prenylate cytochrome b5 reductase 3 (CYB5R3) and the prenylated CYB5R3 then translocate from the mitochondrial to the endoplasmic reticulum (ER) pool. As CYB5R3 is a critical NADH-dependent reductase necessary for eicosanoid metabolism in ER, we thus suggest that GGPP-mediated CYB5R3 prenylation is necessary for metabolism. In addition, we observe that pharmacological inhibition of the MVA pathway by simvastatin is sufficient to inhibit CYB5R3 translocation and induces smooth muscle death. Therefore, we conclude that the dysregulation of MVA intermediates is an essential mechanism for metaflammation initiation, in which the imbalanced production of eicosanoid intermediates in the ER serve as an important pathogenic factor. Moreover, the interplay of MVA and eicosanoid metabolism as we reported here illustrates a model for the coordinating regulation among metabolite pathways.

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2

Embgenbroich, Maria, Hendrik J. P. van der Zande, Leonie Hussaarts, Jonas Schulte-Schrepping, Leonard R. Pelgrom, Noemí García-Tardón, Laura Schlautmann, et al. "Soluble mannose receptor induces proinflammatory macrophage activation and metaflammation." Proceedings of the National Academy of Sciences 118, no. 31 (July 29, 2021): e2103304118. http://dx.doi.org/10.1073/pnas.2103304118.

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Proinflammatory activation of macrophages in metabolic tissues is critically important in the induction of obesity-induced metaflammation. Here, we demonstrate that the soluble mannose receptor (sMR) plays a direct functional role in both macrophage activation and metaflammation. We show that sMR binds CD45 on macrophages and inhibits its phosphatase activity, leading to an Src/Akt/NF-κB–mediated cellular reprogramming toward an inflammatory phenotype both in vitro and in vivo. Remarkably, increased serum sMR levels were observed in obese mice and humans and directly correlated with body weight. Importantly, enhanced sMR levels increase serum proinflammatory cytokines, activate tissue macrophages, and promote insulin resistance. Altogether, our results reveal sMR as regulator of proinflammatory macrophage activation, which could constitute a therapeutic target for metaflammation and other hyperinflammatory diseases.

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3

Hotamisligil, Gökhan S. "Inflammation, metaflammation and immunometabolic disorders." Nature 542, no. 7640 (February 2017): 177–85. http://dx.doi.org/10.1038/nature21363.

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Furuhashi, Masato, Shutaro Ishimura, Hideki Ota, and Tetsuji Miura. "Lipid Chaperones and Metabolic Inflammation." International Journal of Inflammation 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/642612.

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Over the past decade, a large body of evidence has emerged demonstrating an integration of metabolic and immune response pathways. It is now clear that obesity and associated disorders such as insulin resistance and type 2 diabetes are associated with a metabolically driven, low-grade, chronic inflammatory state, referred to as “metaflammation.” Several inflammatory cytokines as well as lipids and metabolic stress pathways can activate metaflammation, which targets metabolically critical organs and tissues including adipocytes and macrophages to adversely affect systemic homeostasis. On the other hand, inside the cell, fatty acid-binding proteins (FABPs), a family of lipid chaperones, as well as endoplasmic reticulum (ER) stress, and reactive oxygen species derived from mitochondria play significant roles in promotion of metabolically triggered inflammation. Here, we discuss the molecular and cellular basis of the roles of FABPs, especially FABP4 and FABP5, in metaflammation and related diseases including obesity, diabetes, and atherosclerosis.

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Muskiet, Frits A. J., Pedro Carrera-Bastos, Leo Pruimboom, Alejandro Lucia, and David Furman. "Obesity and Leptin Resistance in the Regulation of the Type I Interferon Early Response and the Increased Risk for Severe COVID-19." Nutrients 14, no. 7 (March 26, 2022): 1388. http://dx.doi.org/10.3390/nu14071388.

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Obesity, and obesity-associated conditions such as hypertension, chronic kidney disease, type 2 diabetes, and cardiovascular disease, are important risk factors for severe Coronavirus disease-2019 (COVID-19). The common denominator is metaflammation, a portmanteau of metabolism and inflammation, which is characterized by chronically elevated levels of leptin and pro-inflammatory cytokines. These induce the “Suppressor Of Cytokine Signaling 1 and 3” (SOCS1/3), which deactivates the leptin receptor and also other SOCS1/3 sensitive cytokine receptors in immune cells, impairing the type I and III interferon early responses. By also upregulating SOCS1/3, Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 adds a significant boost to this. The ensuing consequence is a delayed but over-reactive immune response, characterized by high-grade inflammation (e.g., cytokine storm), endothelial damage, and hypercoagulation, thus leading to severe COVID-19. Superimposing an acute disturbance, such as a SARS-CoV-2 infection, on metaflammation severely tests resilience. In the long run, metaflammation causes the “typical western” conditions associated with metabolic syndrome. Severe COVID-19 and other serious infectious diseases can be added to the list of its short-term consequences. Therefore, preventive measures should include not only vaccination and the well-established actions intended to avoid infection, but also dietary and lifestyle interventions aimed at improving body composition and preventing or reversing metaflammation.

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Egger, Garry, and John Dixon. "Obesity and chronic disease: always offender or often just accomplice?" British Journal of Nutrition 102, no. 8 (May 18, 2009): 1238–42. http://dx.doi.org/10.1017/s0007114509371676.

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Over a decade ago, the finding of a form of low-grade systemic inflammation (‘metaflammation’) associated with obesity, insulin resistance and chronic disease proffered a causal explanation for the latter. However, recent work has shown that metaflammation is also associated with several modern lifestyle-related and environmental inducers, with or without obesity. Here, we present accumulating data to show a link between metaflammation and a number of non-microbial environmental and lifestyle stimulants, both with and without obesity. This implies that obesity may often be an accomplice to, as much as an offender in, major metabolic disease. The real (albeit distal) cause of such a disease appears to lie in aspects of the modern techno-industrial environment driving unhealthy lifestyle behaviours. If true, this suggests that while individual weight loss may be a component of chronic disease management, it may be neither ‘necessary’ nor ‘sufficient’ to reduce the problem at a population level. Greater multidisciplinary and policy input is needed to modify the economic and political drivers of the modern, obesogenic environment.

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7

Tufanli, Ozlem, Pelin Telkoparan Akillilar, Diego Acosta-Alvear, Begum Kocaturk, Umut Inci Onat, Syed Muhammad Hamid, Ismail Çimen, Peter Walter, Christian Weber, and Ebru Erbay. "Targeting IRE1 with small molecules counteracts progression of atherosclerosis." Proceedings of the National Academy of Sciences 114, no. 8 (January 30, 2017): E1395—E1404. http://dx.doi.org/10.1073/pnas.1621188114.

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Metaflammation, an atypical, metabolically induced, chronic low-grade inflammation, plays an important role in the development of obesity, diabetes, and atherosclerosis. An important primer for metaflammation is the persistent metabolic overloading of the endoplasmic reticulum (ER), leading to its functional impairment. Activation of the unfolded protein response (UPR), a homeostatic regulatory network that responds to ER stress, is a hallmark of all stages of atherosclerotic plaque formation. The most conserved ER-resident UPR regulator, the kinase/endoribonuclease inositol-requiring enzyme 1 (IRE1), is activated in lipid-laden macrophages that infiltrate the atherosclerotic lesions. Using RNA sequencing in macrophages, we discovered that IRE1 regulates the expression of many proatherogenic genes, including several important cytokines and chemokines. We show that IRE1 inhibitors uncouple lipid-induced ER stress from inflammasome activation in both mouse and human macrophages. In vivo, these IRE1 inhibitors led to a significant decrease in hyperlipidemia-induced IL-1β and IL-18 production, lowered T-helper type-1 immune responses, and reduced atherosclerotic plaque size without altering the plasma lipid profiles in apolipoprotein E-deficient mice. These results show that pharmacologic modulation of IRE1 counteracts metaflammation and alleviates atherosclerosis.

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8

Napitupulu, Rosalia E., Anna Meiliana, and Andi Wijaya. "Correlation of Progranulin, Granulin, Adiponectin and Vaspin with Metaflammation (hs-CRP) in Indonesian Obese Men." Indonesian Biomedical Journal 5, no. 2 (August 1, 2013): 107. http://dx.doi.org/10.18585/inabj.v5i2.59.

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BACKGROUND: Obesity is closely related to chronic, low grade systemic inflammation (metaflammation) and it leads to further metabolic complications such as hypertension, atherosclerosis, and type 2 diabetes due to the adipocytokine imbalance. This study was carried out to assess the correlation between progranulin, granulin, adiponectin and visceral adipose tissue-derived serine protease inhibitor (Vaspin) with metaflammation (high sensitivity C-reactive protein (hs-CRP)) in centrally obese men.METHODS: This study was observational with a cross sectional design involving 60 men aged 30-60 years, consisted of 43 obese men (waist circumference (WC) ≥90 cm) and 13 non obese men (WC <90 cm), with no hypertension, and no renal dysfunction. Anthropometric parameters, creatinine, serum glutamic oxaloacetic transferase (SGOT), serum glutamic piruvic transferase (SGPT) and hs-CRP levels were measured. Serum concentrations of progranulin, granulin, adiponectin and Vaspin were measured by ELISA.RESULTS: This study showed in obese men a significant correlation between hs-CRP and Vaspin (r=0.305; p=0.046), non-significant correlation between hs-CRP and progranulin (r=0.048; p=0.758), between hs-CRP and granulin (r=-0.223; p=0.150), also between hs-CRP and adiponectin (r=-0.121; p=0.439). Similar patterns were observed between adipokines level and WC. There were 3 patterns showing increase or decrease of adipokines value with WC between 80-86 cm; subsequently the pattern tended to become flat with WC between 86-105 cm, then showing increase or decrease of adipokines value with WC >105 cm.CONCLUSION: We found metaflammation (hs-CRP) was significantly correlated with Vaspin, but not with progranulin, granulin and adiponectin, in obese men. We suggest the possibility of a dynamic expression of adipokines related to WC that are subjected to adipocytes hypertrophy-hyperplasia phenomenon.KEYWORDS: progranulin, granulin, adiponectin, Vaspin, hs-CRP, metaflammation, central obesity

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9

Paccoud, Romain, Céline Saint-Laurent, Enzo Piccolo, Mylène Tajan, Alizée Dortignac, Ophélie Pereira, Sophie Le Gonidec, et al. "SHP2 drives inflammation-triggered insulin resistance by reshaping tissue macrophage populations." Science Translational Medicine 13, no. 591 (April 28, 2021): eabe2587. http://dx.doi.org/10.1126/scitranslmed.abe2587.

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Insulin resistance is a key event in type 2 diabetes onset and a major comorbidity of obesity. It results from a combination of fat excess–triggered defects, including lipotoxicity and metaflammation, but the causal mechanisms remain difficult to identify. Here, we report that hyperactivation of the tyrosine phosphatase SHP2 found in Noonan syndrome (NS) led to an unsuspected insulin resistance profile uncoupled from altered lipid management (for example, obesity or ectopic lipid deposits) in both patients and mice. Functional exploration of an NS mouse model revealed this insulin resistance phenotype correlated with constitutive inflammation of tissues involved in the regulation of glucose metabolism. Bone marrow transplantation and macrophage depletion improved glucose homeostasis and decreased metaflammation in the mice, highlighting a key role of macrophages. In-depth analysis of bone marrow–derived macrophages in vitro and liver macrophages showed that hyperactive SHP2 promoted a proinflammatory phenotype, modified resident macrophage homeostasis, and triggered monocyte infiltration. Consistent with a role of SHP2 in promoting inflammation-driven insulin resistance, pharmaceutical SHP2 inhibition in obese diabetic mice improved insulin sensitivity even better than conventional antidiabetic molecules by specifically reducing metaflammation and alleviating macrophage activation. Together, these results reveal that SHP2 hyperactivation leads to inflammation-triggered metabolic impairments and highlight the therapeutical potential of SHP2 inhibition to ameliorate insulin resistance.

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Kanbay, Mehmet, Aslihan Yerlikaya, Alan A. Sag, Alberto Ortiz, Masanari Kuwabara, Adrian Covic, Andrzej Wiecek, Peter Stenvinkel, and Baris Afsar. "A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease." Clinical Kidney Journal 12, no. 6 (September 18, 2019): 861–70. http://dx.doi.org/10.1093/ckj/sfz106.

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Abstract Chronic non-communicable diseases have become a pandemic public problem in the 21st century, causing enormous burden on the economy, health and quality of life of societies. The role of a chronic inflammatory state in the pathogenesis of chronic disease has been more comprehensively recognized by recent findings. The new paradigm ‘metaflammation’ focuses on metabolism-induced (high fat or fructose-based diet or excessive calorie intake) chronic inflammation. There is a close correlation between the increased incidence of chronic kidney disease (CKD) and chronic heart failure with both increased inflammatory marker levels and western-type diet. In this review we describe the concept of metaflammation, its role in the development of CKD and chronic heart disease, the molecular and signalling pathways involved and the therapeutic consequences.

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11

Meiliana, Anna, and Andi Wijaya. "Metaflammation, NLRP3 Inflammasome Obesity and Metabolic Disease." Indonesian Biomedical Journal 3, no. 3 (December 1, 2011): 168. http://dx.doi.org/10.18585/inabj.v3i3.148.

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BACKGROUND: Increasing prevalence of obesity gives rise to many problems associated with multiple morbidities, such as diabetes, hypertension, heart disease, sleep apnea and cancer. The mechanism of obesity is very complex, thus its link to various disease is poorly understood. This review highlights important concepts in our understanding of the pathogenesis of obesity and related complications.CONTENT: Many studies have tried to explore the exciting and puzzling links between metabolic homeostasis and inflammatory responses. A form of subclinical, low-grade systemic inflammation is known to be associated with both obesity and chronic disease. This, later called as "metaflammation", refers to metabolically triggered inflammation. The nutrient-sensing pathway and the immune response coordination are facilitated by these molecular sites in order to maintain homeostasis under diverse metabolic and immune conditions. Recent studies have found that the NLRP3 inflammasome during metabolic stress forms a tie linking TXNIP, oxidative stress, and IL-1β production. This provides new opportunities for research and therapy for the disease often described as the next global pandemic: type 2 diabetes mellitus (T2DM).SUMMARY: The crucial role of metaflammation in many complications of obesity shown by the unexpected overlap between inflammatory and metabolic sensors and their downstream tissue responses. Then great interest arose to explore the pathways that integrate nutrient and pathogen sensing, give more understanding in the mechanisms of insulin resistance type 2 diabetes, and other chronic metabolic pathologies. A family of intracellular sensors called NLR family is a critical component of the innate immune system. They can form multiprotein complexes, called inflammasome which is capable of responding to a wide range of stimuli including both microbial and self molecules by activating the cysteine protease caspase-1, leading to processing and secretion of the proinflammatory cytokines IL-1β and IL-18, which play crucial roles in host defense. Inflammasome dysregulation has been linked to some autoinflammatory and metabolic diseases. These provide opportunities to continue to improve our understanding of the nature of metaflammation in the hope of modifying it to prevent and treat diseasese.KEYWORDS: Inflammation, metaflammation, inflammasome, metabolic disease, obesity

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12

Khilazheva, Elena D., Angelina I. Mosiagina, Yulia A. Panina, Olga S. Belozor, and Yulia K. Komleva. "Impact of NLRP3 Depletion on Aging-Related Metaflammation, Cognitive Function, and Social Behavior in Mice." International Journal of Molecular Sciences 24, no. 23 (November 21, 2023): 16580. http://dx.doi.org/10.3390/ijms242316580.

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Immunosenescence and chronic inflammation associated with old age accompany brain aging and the loss of complex behaviors. Neuroinflammation in the hippocampus plays a pivotal role in the development of cognitive impairment and anxiety. However, the underlying mechanisms have not been fully explained. In this study, we aimed to investigate the disruption of insulin signaling and the mechanisms underlying metabolic inflammation (“metaflammation”) in the brains of wild-type (WT) and NLRP3 knockout (KO) mice of different ages. We found a significant upregulation of the NLRP3 inflammasome in the hippocampus during aging, leading to an increase in the expression of phosphorylated metaflammation proteinases and inflammatory markers, along with an increase in the number of senescent cells. Additionally, metaflammation causes anxiety and impairs social preference behavior in aged mice. On the other hand, deletion of NLRP3 improves some behavioral and biochemical characteristics associated with aging, such as signal memory, neuroinflammation, and metabolic inflammation, but not anxious behavior. These results are associated with reduced IL-18 signaling and the PKR/IKKβ/IRS1 pathway as well as the SASP phenotype. In NLRP3 gene deletion conditions, PKR is down-regulated. Therefore, it is likely that slowing aging through various NLRP3 inhibition mechanisms will lessen the corresponding cognitive decline with aging. Thus, the genetic knockout of the NLRP3 inflammasome can be seen as a new therapeutic strategy for slowing down central nervous system (CNS) aging.

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13

Christ, Anette, and Eicke Latz. "The Western lifestyle has lasting effects on metaflammation." Nature Reviews Immunology 19, no. 5 (March 25, 2019): 267–68. http://dx.doi.org/10.1038/s41577-019-0156-1.

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14

Naylor, Richard, Chris Hayes, and Garry Egger. "The Relationship Between Lifestyle, Metaflammation, and Chronic Pain." American Journal of Lifestyle Medicine 7, no. 2 (July 11, 2012): 130–37. http://dx.doi.org/10.1177/1559827612451710.

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15

Mitrofanova, Alla, Antonio M. Fontanella, Sandra Merscher, and Alessia Fornoni. "Lipid deposition and metaflammation in diabetic kidney disease." Current Opinion in Pharmacology 55 (December 2020): 60–72. http://dx.doi.org/10.1016/j.coph.2020.09.004.

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16

Xiong, Pingjie, Fan Zhang, Fang Liu, Jiayu Zhao, Xiaoqiang Huang, Duosheng Luo, and Jiao Guo. "Metaflammation in glucolipid metabolic disorders: Pathogenesis and treatment." Biomedicine & Pharmacotherapy 161 (May 2023): 114545. http://dx.doi.org/10.1016/j.biopha.2023.114545.

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Furuhashi, Masato, Shigeyuki Saitoh, Kazuaki Shimamoto, and Tetsuji Miura. "Fatty Acid-Binding Protein 4 (FABP4): Pathophysiological Insights and Potent Clinical Biomarker of Metabolic and Cardiovascular Diseases." Clinical Medicine Insights: Cardiology 8s3 (January 2014): CMC.S17067. http://dx.doi.org/10.4137/cmc.s17067.

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Over the past decade, evidences of an integration of metabolic and inflammatory pathways, referred to as metaflammation in several aspects of metabolic syndrome, have been accumulating. Fatty acid-binding protein 4 (FABP4), also known as adipocyte FABP (A-FABP) or aP2, is mainly expressed in adipocytes and macrophages and plays an important role in the development of insulin resistance and atherosclerosis in relation to metaflammation. Despite lack of a typical secretory signal peptide, FABP4 has been shown to be released from adipocytes in a non-classical pathway associated with lipolysis, possibly acting as an adipokine. Elevation of circulating FABP4 levels is associated with obesity, insulin resistance, diabetes mellitus, hypertension, cardiac dysfunction, atherosclerosis, and cardiovascular events. Furthermore, ectopic expression and function of FABP4 in several types of cells and tissues have been recently demonstrated. Here, we discuss both the significant role of FABP4 in pathophysiological insights and its usefulness as a biomarker of metabolic and cardiovascular diseases.

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Kuryłowicz, Alina, and Krzysztof Koźniewski. "Anti-Inflammatory Strategies Targeting Metaflammation in Type 2 Diabetes." Molecules 25, no. 9 (May 9, 2020): 2224. http://dx.doi.org/10.3390/molecules25092224.

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One of the concepts explaining the coincidence of obesity and type 2 diabetes (T2D) is the metaflammation theory. This chronic, low-grade inflammatory state originating from metabolic cells in response to excess nutrients, contributes to the development of T2D by increasing insulin resistance in peripheral tissues (mainly in the liver, muscles, and adipose tissue) and by targeting pancreatic islets and in this way impairing insulin secretion. Given the role of this not related to infection inflammation in the development of both: insulin resistance and insulitis, anti-inflammatory strategies could be helpful not only to control T2D symptoms but also to treat its causes. This review presents current concepts regarding the role of metaflammation in the development of T2D in obese individuals as well as data concerning possible application of different anti-inflammatory strategies (including lifestyle interventions, the extra-glycemic potential of classical antidiabetic compounds, nonsteroidal anti-inflammatory drugs, immunomodulatory therapies, and bariatric surgery) in the management of T2D.

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Vrousgos, George. "Lifestyle Factors that can Induce an Independent and Persistent Low-Grade Systemic Inflammatory Response: A Wholistic Approach." Open Medicine Journal 3, no. 1 (June 18, 2016): 34–48. http://dx.doi.org/10.2174/1874220301603010034.

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Subclinical inflammation was first shown in numerous chronic medical illnesses and in the early 1900s, activation of immune-inflammatory pathways was initially observed in a lifestyle-related disorder such as depression. A chronic mild inflammatory state is also a key feature of obesity as well as insulin resistance and other metabolic diseases. This particular form of immune process has given rise to the concept of “metaflammation” (metabolically triggered inflammation) because it can target vital organs and tissues that are critical for the regulation of metabolism, and ultimately disrupt systemic homoeostasis with detrimental health effects. However, accumulating evidence demonstrates a link between metaflammation and a number of lifestyle factors. Lifestyle variables such as ultra-endurance exercise, physical inactivity, extremes of sleep duration, cigarette smoking, burnout, anxiety, and depression can activate multiple immune-inflammatory pathways. Therefore, this review of the literature that bears hallmarks of a systematic review investigates and presents published research data of these lifestyle factors that can induce an independent and persistent low-grade systemic inflammatory response, within the human body, evaluated through the measurement of various biomarkers.

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20

Yang, Soo Jin, and Yunsook Lim. "Resveratrol ameliorates hepatic metaflammation and inhibits NLRP3 inflammasome activation." Metabolism 63, no. 5 (May 2014): 693–701. http://dx.doi.org/10.1016/j.metabol.2014.02.003.

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21

Collotta, Debora, and Massimo Collino. "NLRP3 Inflammasome Signaling Platform as New Pharmacological Target for Metaflammation." Diabetes Research - Open Journal 3, no. 1 (April 28, 2017): e1-e3. http://dx.doi.org/10.17140/droj-3-e008.

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22

Ghosh, Amrit Raj, Roopkatha Bhattacharya, Shamik Bhattacharya, Titli Nargis, Oindrila Rahaman, Pritam Duttagupta, Deblina Raychaudhuri, et al. "Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation." Diabetes 65, no. 11 (August 25, 2016): 3440–52. http://dx.doi.org/10.2337/db16-0331.

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23

Patel, Meghana N., William G. Bernard, Nikolay B. Milev, William P. Cawthorn, Nichola Figg, Dan Hart, Xavier Prieur, et al. "Hematopoietic IKBKE limits the chronicity of inflammasome priming and metaflammation." Proceedings of the National Academy of Sciences 112, no. 2 (December 24, 2014): 506–11. http://dx.doi.org/10.1073/pnas.1414536112.

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Obesity increases the risk of developing life-threatening metabolic diseases including cardiovascular disease, fatty liver disease, diabetes, and cancer. Efforts to curb the global obesity epidemic and its impact have proven unsuccessful in part by a limited understanding of these chronic progressive diseases. It is clear that low-grade chronic inflammation, or metaflammation, underlies the pathogenesis of obesity-associated type 2 diabetes and atherosclerosis. However, the mechanisms that maintain chronicity and prevent inflammatory resolution are poorly understood. Here, we show that inhibitor of κB kinase epsilon (IKBKE) is a novel regulator that limits chronic inflammation during metabolic disease and atherosclerosis. The pathogenic relevance of IKBKE was indicated by the colocalization with macrophages in human and murine tissues and in atherosclerotic plaques. Genetic ablation of IKBKE resulted in enhanced and prolonged priming of the NLRP3 inflammasome in cultured macrophages, in hypertrophic adipose tissue, and in livers of hypercholesterolemic mice. This altered profile associated with enhanced acute phase response, deregulated cholesterol metabolism, and steatoheptatitis. Restoring IKBKE only in hematopoietic cells was sufficient to reverse elevated inflammasome priming and these metabolic features. In advanced atherosclerotic plaques, loss of IKBKE and hematopoietic cell restoration altered plaque composition. These studies reveal a new role for hematopoietic IKBKE: to limit inflammasome priming and metaflammation.

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Russo, Giorgio Ivan, Luca Vanella, Tommaso Castelli, Sebastiano Cimino, Giulio Reale, Daniele Urzì, Giovanni Li Volti, et al. "Heme oxygenase levels and metaflammation in benign prostatic hyperplasia patients." World Journal of Urology 34, no. 8 (November 30, 2015): 1183–92. http://dx.doi.org/10.1007/s00345-015-1736-8.

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Wang, Anlu, Baoyi Guan, He Zhang, and Hao Xu. "Danger-associated metabolites trigger metaflammation: A crowbar in cardiometabolic diseases." Pharmacological Research 198 (December 2023): 106983. http://dx.doi.org/10.1016/j.phrs.2023.106983.

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Fu, Wei, Yujin Ma, Liping Li, Jie Liu, Liujun Fu, Yu Guo, Zhiyin Zhang, Jiaxi Li, and Hongwei Jiang. "Artemether Regulates Metaflammation to Improve Glycolipid Metabolism in db/db Mice." Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy Volume 13 (May 2020): 1703–13. http://dx.doi.org/10.2147/dmso.s240786.

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Sánchez-Sánchez, Marina A., Adelaida Sara Minia Zepeda-Morales, Lucrecia Carrera-Quintanar, Juan Manuel Viveros-Paredes, Noel Noé Franco-Arroyo, Marisol Godínez-Rubí, Daniel Ortuño-Sahagun, and Rocío Ivette López-Roa. "Alliin, An Allium sativum Nutraceutical, Reduces Metaflammation Markers in DIO Mice." Nutrients 12, no. 3 (February 27, 2020): 624. http://dx.doi.org/10.3390/nu12030624.

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Obesity generates a chronic low-grade inflammatory state which promotes oxidative stress and triggers comorbidities. Alliin is the main organosulfur compound in garlic and has been shown to induce a decrease in the expression of proinflammatory cytokines; its systemic effect on metabolic parameters and adipose tissue is not yet known, however. After nine weeks of HFD and with obesity established in C57BL/6 mice, we observed that a daily treatment with alliin for 3.5 weeks (15 mg/kg) did not affect body weight, but significantly improved insulin sensitivity and glucose tolerance, both evaluated through a blood glucose monitoring system. Once alliin treatment was completed, serum, adipose tissue, and organs of interest related to metabolism were removed for further analysis. We observed that alliin significantly decreased the size of adipocytes from epididymal adipose tissue, evaluated via microscopy. A decrease in gene expression and serum protein levels of the adipocytokines leptin and resistin, as well as decreased serum IL-6 concentration, were detected by qRT-PCR and ELISA, respectively. It did not, however, affect mRNA expression of antioxidant enzymes in the liver. Taken altogether, these results indicate that treatment with alliin reduces metaflammation markers in DIO mice and improves some metabolic parameters without affecting others.

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Prattichizzo, Francesco, Valeria De Nigris, Rosangela Spiga, Elettra Mancuso, Lucia La Sala, Roberto Antonicelli, Roberto Testa, Antonio Domenico Procopio, Fabiola Olivieri, and Antonio Ceriello. "Inflammageing and metaflammation: The yin and yang of type 2 diabetes." Ageing Research Reviews 41 (January 2018): 1–17. http://dx.doi.org/10.1016/j.arr.2017.10.003.

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Mastrocola, Raffaella, Manuela Aragno, Giuseppe Alloatti, Massimo Collino, Claudia Penna, and Pasquale Pagliaro. "Metaflammation: Tissue-Specific Alterations of the NLRP3 Inflammasome Platform in Metabolic Syndrome." Current Medicinal Chemistry 25, no. 11 (April 17, 2018): 1294–310. http://dx.doi.org/10.2174/0929867324666170407123522.

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In the last decades, the extension of life expectancy and the increased consumption of foods rich in saturated fats and added sugars have exposed the general population to emerging health problems. The prevalence of metabolic syndrome (MS), composed of a cluster of factors as obesity, dyslipidemia, hyperglycemia, and hypertension, is rapidly increasing in industrialized and developing countries leading to precocious onset of age-related diseases. Indeed, oxidative stress, accumulation of advanced glycation endproducts, and a chronic low-grade inflammation are common features of MS and physiological ageing. In particular, the entire set of MS factors contributes to the development of an inflammatory status named metaflammation, which has been associated with activation of early innate immune response through the assembling of the multiprotein complex inflammasome. The most investigated family of inflammasome platforms is the NOD-like receptor pyridine containing (NLRP) 3, which is activated by several exogenous and endogenous stimuli, leading to the sequential cleavage of caspase-1 and IL-1β, followed by secretion of active IL-1β. We here collect the most recent findings on NLRP3 activation in MS providing evidence of its central role in disease progression and organ dysfunction in target tissues of metaflammation, in particular in cardiovascular, hepatic and renal complications, with a focus on oxidative stress and advanced glycation endproducts. A wide overview of the most promising strategies for the modulation of NLRP3 activation and related metabolic repercussions is also provided, since the finding of specific pharmacological tools is an urgent requirement to reduce the social and economic burden of MS- and elderly-associated diseases.

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Collotta, Debora, William Hull, Raffaella Mastrocola, Fausto Chiazza, Alessia Sofia Cento, Catherine Murphy, Roberta Verta, et al. "Baricitinib counteracts metaflammation, thus protecting against diet-induced metabolic abnormalities in mice." Molecular Metabolism 39 (September 2020): 101009. http://dx.doi.org/10.1016/j.molmet.2020.101009.

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Luo, Yongde, Sheng Ye, Xiong Chen, Fanghua Gong, Weiqin Lu, and Xiaokun Li. "Rush to the fire: FGF21 extinguishes metabolic stress, metaflammation and tissue damage." Cytokine & Growth Factor Reviews 38 (December 2017): 59–65. http://dx.doi.org/10.1016/j.cytogfr.2017.08.001.

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Morales-Villegas, Enrique. "Dyslipidemia, Hypertension and Diabetes Metaflammation: A Unique Mechanism for 3 Risk Factors." Current Hypertension Reviews 9, no. 4 (July 1, 2014): 278–96. http://dx.doi.org/10.2174/1573402110666140702091315.

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Jais, Alexander, Elisa Einwallner, Omar Sharif, Klaus Gossens, Tess Tsai-Hsiu Lu, Selma M. Soyal, David Medgyesi, et al. "Heme Oxygenase-1 Drives Metaflammation and Insulin Resistance in Mouse and Man." Cell 158, no. 1 (July 2014): 25–40. http://dx.doi.org/10.1016/j.cell.2014.04.043.

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Reginato, Andressa, Alana Carolina Costa Veras, Mayara da Nóbrega Baqueiro, Carolina Panzarin, Beatriz Piatezzi Siqueira, Marciane Milanski, Patrícia Cristina Lisboa, and Adriana Souza Torsoni. "The Role of Fatty Acids in Ceramide Pathways and Their Influence on Hypothalamic Regulation of Energy Balance: A Systematic Review." International Journal of Molecular Sciences 22, no. 10 (May 19, 2021): 5357. http://dx.doi.org/10.3390/ijms22105357.

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Obesity is a global health issue for which no major effective treatments have been well established. High-fat diet consumption is closely related to the development of obesity because it negatively modulates the hypothalamic control of food intake due to metaflammation and lipotoxicity. The use of animal models, such as rodents, in conjunction with in vitro models of hypothalamic cells, can enhance the understanding of hypothalamic functions related to the control of energy balance, thereby providing knowledge about the impact of diet on the hypothalamus, in addition to targets for the development of new drugs that can be used in humans to decrease body weight. Recently, sphingolipids were described as having a lipotoxic effect in peripheral tissues and the central nervous system. Specifically, lipid overload, mainly from long-chain saturated fatty acids, such as palmitate, leads to excessive ceramide levels that can be sensed by the hypothalamus, triggering the dysregulation of energy balance control. However, no systematic review has been undertaken regarding studies of sphingolipids, particularly ceramide and sphingosine-1-phosphate (S1P), the hypothalamus, and obesity. This review confirms that ceramides are associated with hypothalamic dysfunction in response to metaflammation, endoplasmic reticulum (ER) stress, and lipotoxicity, leading to insulin/leptin resistance. However, in contrast to ceramide, S1P appears to be a central satiety factor in the hypothalamus. Thus, our work describes current evidence related to sphingolipids and their role in hypothalamic energy balance control. Hypothetically, the manipulation of sphingolipid levels could be useful in enabling clinicians to treat obesity, particularly by decreasing ceramide levels and the inflammation/endoplasmic reticulum stress induced in response to overfeeding with saturated fatty acids.

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Wang, Xu, Mingyue Liu, Jifeng Zhang, Nicholas K. Brown, Peng Zhang, Yan Zhang, Heng Liu, et al. "CD24-Siglec axis is an innate immune checkpoint against metaflammation and metabolic disorder." Cell Metabolism 34, no. 8 (August 2022): 1088–103. http://dx.doi.org/10.1016/j.cmet.2022.07.005.

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Ertunc, Meric Erikci, and Gökhan S. Hotamisligil. "Lipid signaling and lipotoxicity in metaflammation: indications for metabolic disease pathogenesis and treatment." Journal of Lipid Research 57, no. 12 (June 21, 2016): 2099–114. http://dx.doi.org/10.1194/jlr.r066514.

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Potenza, Maria Assunta, Carmela Nacci, Maria Antonietta De Salvia, Luca Sgarra, Massimo Collino, and Monica Montagnani. "Targeting endothelial metaflammation to counteract diabesity cardiovascular risk: Current and perspective therapeutic options." Pharmacological Research 120 (June 2017): 226–41. http://dx.doi.org/10.1016/j.phrs.2017.04.009.

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Pejnovic, Nada N., Jelena M. Pantic, Ivan P. Jovanovic, Gordana D. Radosavljevic, Aleksandar Lj Djukic, Nebojsa N. Arsenijevic, and Miodrag L. Lukic. "Galectin-3 is a regulator of metaflammation in adipose tissue and pancreatic islets." Adipocyte 2, no. 4 (October 22, 2013): 266–71. http://dx.doi.org/10.4161/adip.24881.

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Caputo, Tiziana, Federica Gilardi, and Béatrice Desvergne. "From chronic overnutrition to metaflammation and insulin resistance: adipose tissue and liver contributions." FEBS Letters 591, no. 19 (July 25, 2017): 3061–88. http://dx.doi.org/10.1002/1873-3468.12742.

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Lischka:, Julia, Andrea Schanzer, Charlotte de Gier, Susanne Greber-Platzer, and Maximilian Zeyda. "Macrophage-associated markers of metaflammation are linked to metabolic dysfunction in pediatric obesity." Cytokine 171 (November 2023): 156372. http://dx.doi.org/10.1016/j.cyto.2023.156372.

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Sun, Xiaoxiao, Suyuan Liu, Jiangxue Cai, Miaoxin Yang, Chenxuan Li, Meiling Tan, and Bin He. "Mitochondrial Methionyl-tRNA Formyltransferase Deficiency Alleviates Metaflammation by Modulating Mitochondrial Activity in Mice." International Journal of Molecular Sciences 24, no. 6 (March 22, 2023): 5999. http://dx.doi.org/10.3390/ijms24065999.

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Various studies have revealed the association of metabolic diseases with inflammation. Mitochondria are key organelles involved in metabolic regulation and important drivers of inflammation. However, it is uncertain whether the inhibition of mitochondrial protein translation results in the development of metabolic diseases, such that the metabolic benefits related to the inhibition of mitochondrial activity remain unclear. Mitochondrial methionyl-tRNA formyltransferase (Mtfmt) functions in the early stages of mitochondrial translation. In this study, we reveal that feeding with a high-fat diet led to the upregulation of Mtfmt in the livers of mice and that a negative correlation existed between hepatic Mtfmt gene expression and fasting blood glucose levels. A knockout mouse model of Mtfmt was generated to explore its possible role in metabolic diseases and its underlying molecular mechanisms. Homozygous knockout mice experienced embryonic lethality, but heterozygous knockout mice showed a global reduction in Mtfmt expression and activity. Moreover, heterozygous mice showed increased glucose tolerance and reduced inflammation, which effects were induced by the high-fat diet. The cellular assays showed that Mtfmt deficiency reduced mitochondrial activity and the production of mitochondrial reactive oxygen species and blunted nuclear factor-κB activation, which, in turn, downregulated inflammation in macrophages. The results of this study indicate that targeting Mtfmt-mediated mitochondrial protein translation to regulate inflammation might provide a potential therapeutic strategy for metabolic diseases.

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Wang, Guisheng, Rongrong Hua, Xiaoxia Chen, Xucheng He, Yao Dingming, Hua Chen, Buhuan Zhang, et al. "MX1 and UBE2L6 are potential metaflammation gene targets in both diabetes and atherosclerosis." PeerJ 12 (February 21, 2024): e16975. http://dx.doi.org/10.7717/peerj.16975.

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Background The coexistence of diabetes mellitus (DM) and atherosclerosis (AS) is widespread, although the explicit metabolism and metabolism-associated molecular patterns (MAMPs) responsible for the correlation are still unclear. Methods Twenty-four genetically wild-type male Ba-Ma mini pigs were randomly divided into five groups distinguished by different combinations of 90 mg/kg streptozotocin (STZ) intravenous injection and high-cholesterol/lipid (HC) or high-lipid (HL) diet feeding for 9 months in total. Pigs in the STZ+HC and STZ+HL groups were injected with STZ first and then fed the HC or HL diet for 9 months. In contrast, pigs in the HC+STZ and HL+STZ groups were fed the HC or HL diet for 9 months and injected with STZ at 3 months. The controls were only fed a regular diet for 9 months. The blood glucose and abdominal aortic plaque observed through oil red O staining were used as evaluation indicators for successful modelling of DM and AS. A microarray gene expression analysis of all subjects was performed. Results Atherosclerotic lesions were observed only in the HC+STZ and STZ+HC groups. A total of 103 differentially expressed genes (DEGs) were identified as common between them. The most significantly enriched pathways of 103 common DEGs were influenza A, hepatitis C, and measles. The global and internal protein–protein interaction (PPI) networks of the 103 common DEGs consisted of 648 and 14 nodes, respectively. The top 10 hub proteins, namely, ISG15, IRG6, IRF7, IFIT3, MX1, UBE2L6, DDX58, IFIT2, USP18, and IFI44L, drive aspects of DM and AS. MX1 and UBE2L6 were the intersection of internal and global PPI networks. The expression of MX1 and UBE2L6 was 507.22 ± 342.56 and 96.99 ± 49.92 in the HC+STZ group, respectively, which was significantly higher than others and may be linked to the severity of hyperglycaemia-related atherosclerosis. Further PPI network analysis of calcium/micronutrients, including MX1 and UBE2L6, consisted of 58 and 18 nodes, respectively. The most significantly enriched KEGG pathways were glutathione metabolism, pyrimidine metabolism, purine metabolism, and metabolic pathways. Conclusions The global and internal PPI network of the 103 common DEGs consisted of 648 and 14 nodes, respectively. The intersection of the nodes of internal and global PPI networks was MX1 and UBE2L6, suggesting their key role in the comorbidity mechanism of DM and AS. This inference was partly verified by the overexpression of MX1 and UBE2L6 in the HC+STZ group but not others. Further calcium- and micronutrient-related enriched KEGG pathway analysis supported that MX1 and UBE2L6 may affect the inflammatory response through micronutrient metabolic pathways, conceptually named metaflammation. Collectively, MX1 and UBE2L6 may be potential common biomarkers for DM and AS that may reveal metaflammatory aspects of the pathological process, although proper validation is still needed to determine their contribution to the detailed mechanism.

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Liu, Lunhua, Karen Etsuko Inouye, Windy Rose Allman, Adam Steven Coleman, Shafiuddin Siddiqui, Gökhan Siddik Hotamisligil, and Mustafa Akkoyunlu. "TACI-Deficient Macrophages Protect Mice Against Metaflammation and Obesity-Induced Dysregulation of Glucose Homeostasis." Diabetes 67, no. 8 (June 5, 2018): 1589–603. http://dx.doi.org/10.2337/db17-1089.

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Höpfinger, Alexandra, Andreas Schmid, Leonie Schweitzer, Marissa Patz, Anja Weber, Andreas Schäffler, and Thomas Karrasch. "Regulation of Cathelicidin Antimicrobial Peptide (CAMP) Gene Expression by TNFα and cfDNA in Adipocytes." International Journal of Molecular Sciences 24, no. 21 (October 31, 2023): 15820. http://dx.doi.org/10.3390/ijms242115820.

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Understanding the complex interactions between metabolism and the immune system (“metaflammation”) is crucial for the identification of key immunomodulatory factors as potential therapeutic targets in obesity and in cardiovascular diseases. Cathelicidin antimicrobial peptide (CAMP) is an important factor of innate immunity and is expressed in adipocytes. CAMP, therefore, might play a role as an adipokine in metaflammation and adipose inflammation. TNFα, cell-free nucleic acids (cfDNA), and toll-like receptor (TLR) 9 are components of the innate immune system and are functionally active in adipose tissue. The aim of the present study was to investigate the impact of TNFα and cfDNA on CAMP expression in adipocytes. Since cfDNA acts as a physiological TLR9 agonist, we additionally investigated TLR9-mediated CAMP regulation in adipocytes and adipose tissue. CAMP gene expression in murine 3T3-L1 and human SGBS adipocytes and in murine and human adipose tissues was quantified by real-time PCR. Adipocyte inflammation was induced in vitro by TNFα and cfDNA stimulation. Serum CAMP concentrations in TLR9 knockout (KO) and in wildtype mice were quantified by ELISA. In primary adipocytes of wildtype and TLR9 KO mice, CAMP gene expression was quantified by real-time PCR. CAMP gene expression was considerably increased in 3T3-L1 and SGBS adipocytes during differentiation. TNFα significantly induced CAMP gene expression in mature adipocytes, which was effectively antagonized by inhibition of PI3K signaling. Cell-free nucleic acids (cfDNA) significantly impaired CAMP gene expression, whereas synthetic agonistic and antagonistic TLR9 ligands had no effect. CAMP and TLR9 gene expression were correlated positively in murine and human subcutaneous but not in intra-abdominal/visceral adipose tissues. Male TLR9 knockout mice exhibited lower systemic CAMP concentrations than wildtype mice. CAMP gene expression levels in primary adipocytes did not significantly differ between wildtype and TLR9 KO mice. These findings suggest a regulatory role of inflammatory mediators, such as TNFα and cfDNA, in adipocytic CAMP expression as a novel putative molecular mechanism in adipose tissue innate immunity.

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Egger, Garry, John Stevens, Andrew Binns, and Bob Morgan. "Psychosocial Determinants of Chronic Disease: Implications for Lifestyle Medicine." American Journal of Lifestyle Medicine 13, no. 6 (May 9, 2019): 526–32. http://dx.doi.org/10.1177/1559827619845335.

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We have previously identified a number of “determinants” of chronic disease, using the acronym NASTIE ODOURS. These have been given the collective term “anthropogens,” in this journal and other publications, to help direct the management of modern chronic ailments to a monocausal focus, akin to that afforded infectious diseases by the “germ theory.” We suggested the acronym NASTIE ODOURS as a starting point for a taxonomy of lifestyle medicine determinants. In the current article, we add 3, less quantifiable, but currently increasingly more important psychosocial experiences to these: Lack of Meaning, Alienation, and Loss of culture, changing the previous acronym to NASTIE MAL ODOURS. As with other determinants, all have accumulating evidence of an underlying low-grade, systemic, inflammatory physiological base (“metaflammation”), but with the need for further research to solidify these findings.

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Riaz, Thoufiqul Alam, Raghu Patil Junjappa, Mallikarjun Handigund, Jannatul Ferdous, Hyung-Ryong Kim, and Han-Jung Chae. "Role of Endoplasmic Reticulum Stress Sensor IRE1α in Cellular Physiology, Calcium, ROS Signaling, and Metaflammation." Cells 9, no. 5 (May 8, 2020): 1160. http://dx.doi.org/10.3390/cells9051160.

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Inositol-requiring transmembrane kinase endoribonuclease-1α (IRE1α) is the most prominent and evolutionarily conserved unfolded protein response (UPR) signal transducer during endoplasmic reticulum functional upset (ER stress). A IRE1α signal pathway arbitrates yin and yang of cellular fate in objectionable conditions. It plays several roles in fundamental cellular physiology as well as in several pathological conditions such as diabetes, obesity, inflammation, cancer, neurodegeneration, and in many other diseases. Thus, further understanding of its molecular structure and mechanism of action during different cell insults helps in designing and developing better therapeutic strategies for the above-mentioned chronic diseases. In this review, recent insights into structure and mechanism of activation of IRE1α along with its complex regulating network were discussed in relation to their basic cellular physiological function. Addressing different binding partners that can modulate IRE1α function, UPRosome triggers different downstream pathways depending on the cellular backdrop. Furthermore, IRE1α are in normal cell activities outside the dominion of ER stress and activities under the weather of inflammation, diabetes, and obesity-related metaflammation. Thus, IRE1 as an ER stress sensor needs to be understood from a wider perspective for comprehensive functional meaning, which facilitates us with assembling future needs and therapeutic benefits.

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El-Ashmawy, Nahla E., Ghada M. Al-Ashmawy, and Asmaa A. Kamel. "Docosahexaenoic acid-flurbiprofen combination ameliorates metaflammation in rats fed on high-carbohydrate high-fat diet." Biomedicine & Pharmacotherapy 109 (January 2019): 233–41. http://dx.doi.org/10.1016/j.biopha.2018.10.049.

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Russo, Giorgio Ivan, Sebastiano Cimino, Tommaso Castelli, Vincenzo Favilla, Mauro Gacci, Marco Carini, Rosita A. Condorelli, et al. "Benign Prostatic Hyperplasia, Metabolic Syndrome and Non-Alcoholic Fatty Liver Disease: Is Metaflammation the Link?" Prostate 76, no. 16 (July 25, 2016): 1528–35. http://dx.doi.org/10.1002/pros.23237.

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Chen, Xide, Yuanli Yan, Zhiyan Weng, Chao Chen, Miaoru Lv, Qingwen Lin, Qiuxia Du, Ximei Shen, and Liyong Yang. "TAK-875 Mitigates β-Cell Lipotoxicity-Induced Metaflammation Damage through Inhibiting the TLR4-NF-κB Pathway." Journal of Diabetes Research 2019 (December 19, 2019): 1–11. http://dx.doi.org/10.1155/2019/5487962.

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Metabolic inflammatory damage, characterized by Toll-like receptor 4 (TLR4) signaling activation, is a major mechanism underlying lipotoxicity-induced β-cell damage. The present study is aimed at determining whether G protein-coupled receptor 4 (GPR40) agonist can improve β-cell lipotoxicity-induced damage by inhibiting the TLR4-NF-κB pathway. Lipotoxicity, inflammation-damaged β-cells, obese SD, and TLR4KO rat models were used in the study. In vitro, TAK-875 inhibited the lipotoxicity- and LPS-induced β-cell apoptosis in a concentration-dependent manner, improved the insulin secretion, and inhibited the expression of TLR4 and NF-κB subunit P65. Besides, silencing of TLR4 expression enhanced the protective effects of TAK-875, while TLR4 overexpression attenuated this protective effect. Activation of TLR4 or NF-κB attenuated the antagonism of TAK-875 on PA-induced damage. Moreover, the above process of TAK-875 was partially independent of GPR40 expression. TAK-875 reduced the body weight and inflammatory factors, rebalanced the number and distribution of α or β-cells, inhibited the apoptosis of islet cells, and inhibited the expression of TLR4 and NF-κB subunit P65 in obese rats. Further knockout of the rat TLR4 gene delayed the damage induced by the high-fat diet and synergy with the action of TAK-875. These data suggest that GPR40 agonists antagonized the lipotoxicity β-cell damage by inhibiting the TLR4-NF-κB pathway.

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Zayachkivska, Oksana, Oleg Revenko, Nazar Bula, Maryana Savytska, and Antonina Yaschenko. "Amelioration of metaflammation induced in rats by exogenous hydrogen sulfide: Focus on mesenteric adipocyte oxidative stress." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.06573.

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