Regulating metabolic inflammation by nutritional modulation - 05/10/20
Abstract |
Metabolic inflammation (metaflammation) is characteristic of obesity-related metabolic disorders, associated with increased risk of development of type 2 diabetes, nonalcoholic fatty liver disease (NAFLD), or cardiovascular disease. Metaflammation refers to a chronic, low-grade systemic inflammation as opposed to the classical transient and acute inflammatory responses of the innate immune system. Metaflammation is driven by a range of adverse dietary factors, including saturated fatty acids and some sugars, suggesting that certain dietary triggers may be particularly relevant beyond simple excessive dietary intake presenting as obesity. Importantly, obese patients with diabetes have a higher risk of infection and display gut microbiota profiles characteristic of dysfunctional immunity. Targeting metaflammation has also emerged as a strategy to attenuate metabolic disease. In this review we explore how different nutrition interventions may reconfigure disrupted metabolic inflammation in type 2 diabetes and nonalcoholic fatty liver disease by reestablishing a conventional proinflammatory program in innate immune cells and/or correcting dysbiosis to dampen systemic inflammation. We begin by reviewing concepts of metabolic inflammation relating to IL-1β inflammation and how it is induced by dietary and/or metabolic stressors. We then explore whether and how dietary interventions may attenuate processes pertaining to metaflammation, either directly or indirectly via the microbiome. Hence, we hope to bring new perspectives to alleviate the metaflammation typifying metabolic disease.
Le texte complet de cet article est disponible en PDF.Key words : Metabolic inflammation, obesity, NAFLD, T2D, innate immunity, microbiota, trained immunity
Abbreviations used : AA, AMPK, ATF6, CVD, DAMP, DHA, EPA, ER, FA, FFa, GPCR, HFD, HSPC, IRE1, JNK, LA, LC, LDL, MUFA, n-3, n-6, NAFLD, NASH, NF-κB, NLR, NLRP3, oxLDL, PRR, PUFA, ROS, SCFA, SFA, T2D, TAG, TLR, UPR, WD
Plan
H.C.-M. is funded by the Irish Research Council Postdoctoral Fellowship Programme (GOIPD/2019/807). K.A.J.M. is funded by the Irish Department of Agriculture, Food and the Marine (14/F/828 ImmunoMet Programme) and Precision Oncology Ireland (18/SPP/3522), which is partly funded by the Science Foundation Ireland Strategic Partnership Programme. E.D.M.C. is supported by the Irish Research Council PhD Scholarship Scheme (EBPPG/2018/137). H.M.R. is funded by the Irish Department of Agriculture, Food and the Marine (14/F/828 “ImmunoMet” Programme) and Precision Oncology Ireland (18/SPP/3522), which is part funded by the Science Foundation Ireland Strategic Partnership Programme. F.J.S. and H.M.R. are supported by the Science Foundation Ireland Frontiers Award Programme (SFI 19/FFP/6625). H.C.-M. and F.J.S. are supported by the Enterprise Ireland Innovation Partnership Programme (IP/2018/0710). |
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Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest. |
Vol 146 - N° 4
P. 706-720 - octobre 2020 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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