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      Role of gut microbiota in the modulation of the health effects of advanced glycation end‑products (Review)

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          Abstract

          <p xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" class="first" id="d1361777e235">The aim of the present review was to summarize the potential interactive effects between the gut microbiota and advanced glycation end-product (AGE) accumulation and toxicity in the host, and to reveal potential the mediatory effects of the gut microbiota on AGE-related health effects. The existing data demonstrate that dietary AGEs can have a significant impact on the richness and diversity of the gut microbiota, although the particular effect is dependent on the type of species, as well as the exposure dose. In addition, the gut microbiota may metabolize dietary AGEs. It has been also demonstrated that the characteristics of the gut microbiota, including its richness and relative abundance of certain taxa, is tightly associated with AGE accumulation in the host organism. In turn, a bilateral interplay between AGE toxicity and the modulation of the gut microbiota may contribute to pathogenesis of ageing and diabetes-associated diseases. Bacterial endotoxin lipopolysaccharide appears as the molecule that mediates the interactions between the gut microbiota and AGE toxicity, specifically via the modulation of the receptor for AGE signaling. Therefore, it is proposed that the modulation of the gut microbiota using probiotics or other dietary interventions may have a significant impact on AGE-induced glycative stress and systemic inflammation. </p>

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          Role of gut microbiota in type 2 diabetes pathophysiology

          A substantial body of literature has provided evidence for the role of gut microbiota in metabolic diseases including type 2 diabetes. However, reports vary regarding the association of particular taxonomic groups with disease. In this systematic review, we focused on the potential role of different bacterial taxa affecting diabetes. We have summarized evidence from 42 human studies reporting microbial associations with disease, and have identified supporting preclinical studies or clinical trials using treatments with probiotics. Among the commonly reported findings, the genera of Bifidobacterium, Bacteroides, Faecalibacterium, Akkermansia and Roseburia were negatively associated with T2D, while the genera of Ruminococcus, Fusobacterium, and Blautia were positively associated with T2D. We also discussed potential molecular mechanisms of microbiota effects in the onset and progression of T2D.
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            The influence of diet on the gut microbiota.

            Diet is a major factor driving the composition and metabolism of the colonic microbiota. The amount, type and balance of the main dietary macronutrients (carbohydrates, proteins and fats) have a great impact on the large intestinal microbiota. The human colon contains a dense population of bacterial cells that outnumber host cells 10-fold. Bacteroidetes, Firmicutes and Actinobacteria are the three major phyla that inhabit the human large intestine and these bacteria possess a fascinating array of enzymes that can degrade complex dietary substrates. Certain colonic bacteria are able to metabolise a remarkable variety of substrates whilst other species carry out more specialised activities, including primary degradation of plant cell walls. Microbial metabolism of dietary carbohydrates results mainly in the formation of short chain fatty acids and gases. The major bacterial fermentation products are acetate, propionate and butyrate; and the production of these tends to lower the colonic pH. These weak acids influence the microbial composition and directly affect host health, with butyrate the preferred energy source for the colonocytes. Certain bacterial species in the colon survive by cross-feeding, using either the breakdown products of complex carbohydrate degradation or fermentation products such as lactic acid for growth. Microbial protein metabolism results in additional fermentation products, some of which are potentially harmful to host health. The current 'omic era promises rapid progress towards understanding how diet can be used to modulate the composition and metabolism of the gut microbiota, allowing researchers to provide informed advice, that should improve long-term health status. Copyright © 2012 Elsevier Ltd. All rights reserved.
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              Advanced glycation end products (AGE) and diabetes: cause, effect, or both?

              Despite new and effective drug therapies, insulin resistance (IR), type 2 diabetes mellitus (T2D) and its complications remain major medical challenges. It is accepted that IR, often associated with over-nutrition and obesity, results from chronically elevated oxidant stress (OS) and chronic inflammation. Less acknowledged is that a major cause for this inflammation is excessive consumption of advanced glycation end products (AGEs) with the standard western diet. AGEs, which were largely thought as oxidative derivatives resulting from diabetic hyperglycemia, are increasingly seen as a potential risk for islet β-cell injury, peripheral IR and diabetes. Here we discuss the relationships between exogenous AGEs, chronic inflammation, IR, and T2D. We propose that under chronic exogenous oxidant AGE pressure the depletion of innate defense mechanisms is an important factor, which raises susceptibility to inflammation, IR, T2D and its complications. Finally we review evidence on dietary AGE restriction as a nonpharmacologic intervention, which effectively lowers AGEs, restores innate defenses and improves IR, thus, offering new perspectives on diabetes etiology and therapy.
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                Author and article information

                Journal
                International Journal of Molecular Medicine
                Int J Mol Med
                Spandidos Publications
                1107-3756
                1791-244X
                April 11 2023
                April 11 2023
                : 51
                : 5
                Affiliations
                [1 ]Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
                [2 ]Sechenov University (IM Sechenov First Moscow State Medical University), Moscow 119435, Russia
                [3 ]Institute of Cellular and Intracellular Symbiosis, Ural Branch of The Russian Academy of Sciences, Orenburg 460000, Russia
                [4 ]Laboratory of Excitatory Amino Acids/Laboratory of Molecular Neuropharmacology and Nanotechnology, National Institute of Neurology and Neurosurgery, Mexico City 14269, Mexico
                [5 ]Department of Biochemistry and Molecular Biology, CCNE, Federal University of Santa Maria, Santa Maria, RS 97105‑900, Brazil
                [6 ]Laboratory of Clinical Virology, Medical School, University of Crete, 71409 Heraklion, Greece
                [7 ]Yaroslavl State University, Yaroslavl 150003, Russia
                Article
                10.3892/ijmm.2023.5247
                c9963ad7-5bde-41ef-8ccb-41f9495d7d3d
                © 2023
                History

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