Regulating metabolic inflammation by nutritional modulation

被引:45
|
作者
Charles-Messance, Hugo [1 ,2 ]
Mitchelson, Kathleen A. J. [3 ,4 ]
Castro, Elena De Marco [3 ,4 ]
Sheedy, Frederick J. [1 ,2 ]
Roche, Helen M. [3 ,4 ,5 ]
机构
[1] Trinity Coll Dublin, Sch Biochem & Immunol, Macrophage Homeostasis Res Grp, Dublin, Ireland
[2] Trinity Coll Dublin, Trinity Biomed Sci Inst, Dublin, Ireland
[3] Univ Coll Dublin, Sch Publ Hlth Physiotherapy & Sports Sci, Nutrigen Res Grp, Dublin, Ireland
[4] Univ Coll Dublin, Conway Inst, Diabet Complicat Res Ctr, Inst Food & Hlth, Dublin, Ireland
[5] Queens Univ Belfast, Inst Global Food Secur, Belfast, Antrim, North Ireland
基金
爱尔兰科学基金会;
关键词
Metabolic inflammation; obesity; NAFLD; T2D; innate immunity; microbiota; trained immunity; SATURATED FATTY-ACIDS; ENDOPLASMIC-RETICULUM STRESS; BINDING CASSETTE TRANSPORTERS; FOAM CELL-FORMATION; YEAST BETA-GLUCAN; NLRP3; INFLAMMASOME; GUT MICROBIOTA; LIVER-DISEASE; MOLECULAR-MECHANISMS; INSULIN-RESISTANCE;
D O I
10.1016/j.jaci.2020.08.013
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
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-1 beta 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.
引用
收藏
页码:706 / 720
页数:15
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