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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, et al. "GGPP depletion initiates metaflammation through disequilibrating CYB5R3-dependent eicosanoid metabolism." Journal of Biological Chemistry 295, no. 47 (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 wit

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2

Embgenbroich, Maria, Hendrik J. P. van der Zande, Leonie Hussaarts, et al. "Soluble mannose receptor induces proinflammatory macrophage activation and metaflammation." Proceedings of the National Academy of Sciences 118, no. 31 (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 weigh

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3

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

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4

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 ot

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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 (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

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6

Egger, Garry, and John Dixon. "Obesity and chronic disease: always offender or often just accomplice?" British Journal of Nutrition 102, no. 8 (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

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7

Tufanli, Ozlem, Pelin Telkoparan Akillilar, Diego Acosta-Alvear, et al. "Targeting IRE1 with small molecules counteracts progression of atherosclerosis." Proceedings of the National Academy of Sciences 114, no. 8 (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

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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 (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 year

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9

Paccoud, Romain, Céline Saint-Laurent, Enzo Piccolo, et al. "SHP2 drives inflammation-triggered insulin resistance by reshaping tissue macrophage populations." Science Translational Medicine 13, no. 591 (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 p

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10

Kanbay, Mehmet, Aslihan Yerlikaya, Alan A. Sag, et al. "A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease." Clinical Kidney Journal 12, no. 6 (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

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11

Meiliana, Anna, and Andi Wijaya. "Metaflammation, NLRP3 Inflammasome Obesity and Metabolic Disease." Indonesian Biomedical Journal 3, no. 3 (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

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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 (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 h

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13

Christ, Anette, and Eicke Latz. "The Western lifestyle has lasting effects on metaflammation." Nature Reviews Immunology 19, no. 5 (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 (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, et al. "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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17

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, po

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18

Kuryłowicz, Alina, and Krzysztof Koźniewski. "Anti-Inflammatory Strategies Targeting Metaflammation in Type 2 Diabetes." Molecules 25, no. 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 c

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19

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 (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 sy

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20

Yang, Soo Jin, and Yunsook Lim. "Resveratrol ameliorates hepatic metaflammation and inhibits NLRP3 inflammasome activation." Metabolism 63, no. 5 (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 (2017): e1-e3. http://dx.doi.org/10.17140/droj-3-e008.

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22

Ghosh, Amrit Raj, Roopkatha Bhattacharya, Shamik Bhattacharya, et al. "Adipose Recruitment and Activation of Plasmacytoid Dendritic Cells Fuel Metaflammation." Diabetes 65, no. 11 (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, et al. "Hematopoietic IKBKE limits the chronicity of inflammasome priming and metaflammation." Proceedings of the National Academy of Sciences 112, no. 2 (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 inhibit

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24

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

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25

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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26

Fu, Wei, Yujin Ma, Liping Li, et al. "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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27

Sánchez-Sánchez, Marina A., Adelaida Sara Minia Zepeda-Morales, Lucrecia Carrera-Quintanar, et al. "Alliin, An Allium sativum Nutraceutical, Reduces Metaflammation Markers in DIO Mice." Nutrients 12, no. 3 (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

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28

Prattichizzo, Francesco, Valeria De Nigris, Rosangela Spiga, et al. "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 (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 physiolo

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Collotta, Debora, William Hull, Raffaella Mastrocola, 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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31

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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32

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

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33

Jais, Alexander, Elisa Einwallner, Omar Sharif, et al. "Heme Oxygenase-1 Drives Metaflammation and Insulin Resistance in Mouse and Man." Cell 158, no. 1 (2014): 25–40. http://dx.doi.org/10.1016/j.cell.2014.04.043.

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34

Reginato, Andressa, Alana Carolina Costa Veras, Mayara da Nóbrega Baqueiro, et al. "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 (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 develop

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35

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

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36

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 (2016): 2099–114. http://dx.doi.org/10.1194/jlr.r066514.

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37

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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38

Pejnovic, Nada N., Jelena M. Pantic, Ivan P. Jovanovic, et al. "Galectin-3 is a regulator of metaflammation in adipose tissue and pancreatic islets." Adipocyte 2, no. 4 (2013): 266–71. http://dx.doi.org/10.4161/adip.24881.

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39

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 (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, et al. "Mitochondrial Methionyl-tRNA Formyltransferase Deficiency Alleviates Metaflammation by Modulating Mitochondrial Activity in Mice." International Journal of Molecular Sciences 24, no. 6 (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

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Wang, Guisheng, Rongrong Hua, Xiaoxia Chen, 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

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43

Liu, Lunhua, Karen Etsuko Inouye, Windy Rose Allman, et al. "TACI-Deficient Macrophages Protect Mice Against Metaflammation and Obesity-Induced Dysregulation of Glucose Homeostasis." Diabetes 67, no. 8 (2018): 1589–603. http://dx.doi.org/10.2337/db17-1089.

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Höpfinger, Alexandra, Andreas Schmid, Leonie Schweitzer та ін. "Regulation of Cathelicidin Antimicrobial Peptide (CAMP) Gene Expression by TNFα and cfDNA in Adipocytes". International Journal of Molecular Sciences 24, № 21 (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 adip

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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 (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

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46

Riaz, Thoufiqul Alam, Raghu Patil Junjappa, Mallikarjun Handigund, Jannatul Ferdous, Hyung-Ryong Kim та Han-Jung Chae. "Role of Endoplasmic Reticulum Stress Sensor IRE1α in Cellular Physiology, Calcium, ROS Signaling, and Metaflammation". Cells 9, № 5 (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

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47

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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48

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

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49

Chen, Xide, Yuanli Yan, Zhiyan Weng та ін. "TAK-875 Mitigates β-Cell Lipotoxicity-Induced Metaflammation Damage through Inhibiting the TLR4-NF-κB Pathway". Journal of Diabetes Research 2019 (19 грудня 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 in

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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 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.06573.

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