Effect of Advanced Glycation End-Products and Excessive Calorie Intake on Diet-Induced Chronic Low-Grade Inflammation Biomarkers in Murine Models

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.

Mitochondria: It is all about energy

“…Modern life puts a real burden on the normal functioning of mitochondria in multiple organs. Factors such as sitting time ( Nogueira Silva Lima et al, 2021 ), high-calorie diet ( Nogueira Silva Lima et al, 2021 ), sleep disturbance ( Saner et al, 2021 ), and alcohol abuse ( Wang et al, 2010 ) and factors that are hardly evitable such as environmental pollution ( Grytting et al, 2022 ), light pollution ( Grytting et al, 2022 ) diesel exhaust and the use of multiple medicines, including NAISDs ( Tang et al, 2022 ), can produce a state of low-grade inflammation (LGI) associated with many chronic diseases ( de Punder and Pruimboom, 2015a ). LGI and mitochondrial dysfunction are two cross-connected mechanisms.…”

Reviving the mutual impact of SARS-COV-2 and obesity on patients: From morbidity to mortality

“…Higher intake of SFAs (saturated fatty acids) has been demonstrated to produce lipotoxicity, inflammation of adipose tissue, and enhance the innate immunity activity via TRL-4 activation (toll-like receptor-4) [66] . Increased production of TNF and interleukin-1 generated by lipopolysaccharide, and enhanced MCP-1 for macrophage permeation into lung tissue, are induced by a high-fat diet in the animal model [108] . Maintaining good immune function requires a satisfactory consumption of omega-3 fatty acids (polyunsaturated), iron, selenium, copper, zinc, folate, and vitamins (A, B 3/6/12 , D, E).…”

Exposure of Caenorhabditis elegans to Dietary Nε-Carboxymethyllysine Emphasizes Endocytosis as a New Route for Intestinal Absorption of Advanced Glycation End Products

“…Some experimental models, mainly murine, of renal insufficiency or metabolic disorders have confirmed the induction of inflammation and metabolic complications by dAGEs [20][21][22]. The pathophysiological effects of dAGEs were also observed in healthy animals, where they promote oxidative and inflammatory processes and impair metabolic homeostasis [23]. However, as with clinical studies, the use of different diets from one experimental study to another complicates the inter-study comparisons.…”