Abstract
Chronic Low-Grade Inflammation (CLGI) is a non-overt inflammatory state characterized by a continuous activation of inflammation mediators associated with metabolic diseases. It has been linked to the overconsumption of Advanced Glycation End-Products (AGEs), and/or macronutrients which lead to an increase in local and systemic pro-inflammatory biomarkers in humans and animal models. This review provides a summary of research into biomarkers of diet-induced CLGI in murine models, with a focus on AGEs and obesogenic diets, and presents the physiological effects described in the literature. Diet-induced CLGI is associated with metabolic endotoxemia, and/or gut microbiota remodeling in rodents. The mechanisms identified so far are centered on pro-inflammatory axes such as the interaction between AGEs and their main receptor AGEs (RAGE) or increased levels of lipopolysaccharide. The use of murine models has helped to elucidate the local and systemic expression of CLGI mediators. These models have enabled significant advances in identification of diet-induced CLGI biomarkers and resultant physiological effects. Some limitations on the translational (murine → humans) use of biomarkers may arise, but murine models have greatly facilitated the testing of specific dietary components. However, there remains a lack of information at the whole-organism level of organization, as well as a lack of consensus on the best biomarker for use in CLGI studies and recommendations as to future research conclude this review.
Highlights
Diet plays a role in the induction and progression of Chronic Low-Grade Inflammation (CLGI) which has been associated with metabolic diseases such as obesity and diabetes [1].Some food contaminants such as the exogenous Advanced Glycation End-Products (AGEs), produced in thermally processed products, have been shown to contribute to the persistent inflammatory component of diabetes, aging, and heart failure [2]
Based on the data presented in this review, the involvement of diet in the induction and progression of CLGI has been clearly demonstrated in murine models
The murine models described in this review have shed significant light on CLGI, the importance of local measurements of CLGI biomarkers
Summary
Diet plays a role in the induction and progression of Chronic Low-Grade Inflammation (CLGI) which has been associated with metabolic diseases such as obesity and diabetes [1]. Compared to the chronic but severe inflammation present in arthritis or Crohn’s disease [15], metabolic disorders (such as obesity) and some age-related conditions (such as frailty) have only a CLGI component [16] This difference in the intensity of inflammation has orientated research seeking to characterize specific molecular patterns and biomarker clusters in order to develop predictive tools aimed at reducing the health and socioeconomic impacts of these pathologies. Based on the extensive literature currently published, CLGI can be formally defined as a pathological state lacking overt inflammation, but characterized by continuous and unresolved activation of inflammation mediators It results in increased production of cytokines, reactive oxygen species, macrophage infiltration, adipocyte imbalance, or vascular damage; these effects are associated with metabolically active tissues such as adipose tissue, skeletal muscle, and the liver, implicating CLGI in metabolic diseases [1,31]. A cluster or panel of biomarkers could best describe CLGI, and we present the biomarkers currently under investigation, with a brief description of those from human studies, and a focus on murine models
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