Processed foods drive intestinal barrier permeability and microvascular diseases

Snelson, Matthew; Tan, Sih Min; Clarke, Rachel E.; Pasquale, Cassandra de; Thallas‐Bonke, Vicki; Nguyen, Tuong-Vi; Penfold, Sally A.; Harcourt, Brooke E.; Sourris, Karly C.; Lindblom, Runa; Ziemann, Mark; Steer, David; El‐Osta, Assam; Davies, Michael J.; Donnellan, Leigh; Deo, Permal; Kellow, Nicole J.; Cooper, Mark E.; Woodruff, Trent M.; Mackay, Charles R.; Forbes, Josephine M.; Coughlan, Melinda T.

doi:10.1126/sciadv.abe4841

Cited by 90 publications

(83 citation statements)

References 61 publications

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“…A very recent paper adds a novel layer of complexity in the dAGE relationship with inflammation. Snelson et al have shown that long-term consumption of dAGEs leads to changes in intestinal barrier permeability in rodents [ 101 ]. This alteration increases innate immune complement activation and local inflammation (especially evident at the renal level), via generation of the pro-inflammatory effector molecule complement 5a (C5a).…”

Section: Mechanisms Of Cell/tissue Damage Induced By Agesmentioning

confidence: 99%

Dietary AGEs as Exogenous Boosters of Inflammation

et al. 2021

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Most chronic modern non-transmissible diseases seem to begin as the result of low-grade inflammation extending over prolonged periods of time. The importance of diet as a source of many pro-inflammatory compounds that could create and sustain such a low-grade inflammatory state cannot be ignored, particularly since we are constantly exposed to them during the day. The focus of this review is on specific components of the diet associated with inflammation, specifically advanced glycation end products (AGEs) that form during thermal processing of food. AGEs are also generated in the body in normal physiology and are widely recognized as increased in diabetes, but many people are unaware of the potential importance of exogenous AGEs ingested in food. We review experimental models, epidemiologic data, and small clinical trials that suggest an important association between dietary intake of these compounds and development of an inflammatory and pro-oxidative state that is conducive to chronic diseases. We compare dietary intake of AGEs with other widely known dietary patterns, such as the Mediterranean and the Dietary Approaches to Stop Hypertension (DASH) diets, as well as the Dietary Inflammation Index (DII). Finally, we delineate in detail the pathophysiological mechanisms induced by dietary AGEs, both direct (i.e., non-receptor-mediated) and indirect (receptor-mediated).

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Section: Mechanisms Of Cell/tissue Damage Induced By Agesmentioning

confidence: 99%

Dietary AGEs as Exogenous Boosters of Inflammation

et al. 2021

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“…Similar to observations in animals fed HFD, dAGEs may also play a role in remodeling of gut microbiota. Evidence from experiments on rats and C57BL/6 mice demonstrated that dietary MG-H1 had a pro-inflammatory effect as well as remodeling gut microbiota [ 39 , 75 ]. Diet-induced gut permeability was demonstrated to result from increased CML, CEL, and MG-H1 consumption on Sprague-Dawley male rats exposed to a baked chow diet for 24 weeks.…”

Section: High-age Diets and Clgi Initiation In Murine Modelsmentioning

confidence: 99%

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

et al. 2021

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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.

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“…An unhealthy diet, with suboptimal intake of fruits, vegetables, whole grains and a high consumption of processed food products high in saturated fat, with added sugar and salt, all major risk factors for poor health outcomes. Processed food (the key hallmark of Western diet) do not only cause excess of calorie intake [44] but also drive intestinal barrier permeability and microvascular disease [62]. Moreover, as it was recently reported that processed red meat, in contrast with unprocessed red meat, was linked to increased risk of incident dementia [63], it seems like the processing of food per se drive disease.…”

Section: Figure 1 Dietary Intake Tmao Metabolism and Disease Riskmentioning

confidence: 99%

A biomimetic natural sciences approach to understanding the mechanisms of ageing in burden of lifestyle diseases

et al. 2021

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The worldwide landscape of an ageing population and age-related disease brings with it huge socio-economic and public healthcare concerns across nations. Correspondingly, monumental human and financial resources have been invested in biomedical research, with a mission to decode the mechanisms of ageing and how these contribute to age-related disease. Multiple hallmarks of ageing have been identified that are common across taxa, highlighting their fundamental importance. These include dysregulated mitochondrial metabolism and telomeres biology, epigenetic modifications, cell–matrix interactions, proteostasis, dysregulated nutrient sensing, stem cell exhaustion, inflammageing and immuno-senescence. While our understanding of the molecular basis of ageing is improving, it remains a complex and multifactorial process that remains to be fully understood. A key aspect of the shortfall in our understanding of the ageing process lies in translating data from standard animal models to humans. Consequently, we suggest that a ‘biomimetic’ and comparative approach, integrating knowledge from species in the wild, as opposed to inbred genetically homogenous laboratory animals, can provide powerful insights into human ageing processes. Here we discuss some particularities and comparative patterns among several species from the animal kingdom, endowed with longevity or short lifespans and unique metabolic profiles that could be potentially exploited to the understanding of ageing and age-related diseases. Based upon lessons from nature, we also highlight several avenues for renewed focus in the pathophysiology of ageing and age-related disease (i.e. diet-microbiome-health axis, oxidative protein damage, adaptive homoeostasis and planetary health). We propose that a biomimetic alliance with collaborative research from different disciplines can improve our understanding of ageing and age-related diseases with long-term sustainable utility.

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Processed foods drive intestinal barrier permeability and microvascular diseases

Cited by 90 publications

References 61 publications

Dietary AGEs as Exogenous Boosters of Inflammation

Dietary AGEs as Exogenous Boosters of Inflammation

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

A biomimetic natural sciences approach to understanding the mechanisms of ageing in burden of lifestyle diseases

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