Effects of Toxic AGEs (TAGE) on Human Health

Takeuchi, Masayoshi; Sakasai-Sakai, Akiko; Takata, Takanobu; Takino, Junichi; Koriyama, Yoshiki

doi:10.3390/cells11142178

Cited by 23 publications

(33 citation statements)

References 122 publications

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“…Enhanced intake of sugars, in particular fructose along with abundant AGE-rich diet are associated with the formation of intracellular AGEs which cause induction of lipogenesis in addition to inflammation in crosstalk with ER stress [118]. Apart from the extravasation of AGEs as well as their crosstalk with RAGE has a correlation with formation besides evolution of different chronic diseases inclusive of steatosis along with CVD [119]. A correlation amongst escalated quantities of different kinds of AGEs along with NAFLD was illustrated in a recent meta-analysis [120].…”

Section: Atherogenic/cardiovascular Disease (Cvd) Along With Er Stres...mentioning

confidence: 99%

An Update on Mechanistic Modes in AGEs Stimulated & ER and Inflammatory Stress-Modulated Control of the GLUT4 expression (SLC2A4 promoted) and Atherogenesis in Diabetes Mellitus-A Narrative Review

Kaur¹,

Allahbadia²,

Singh³

2022

MJCH

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Earlier we had reviewed the role of herbal treatment, epigenetic modes, other mechanistic pathophysiological roles like macrophage polarization, epigenetics, role of adipokines &treatment using role of empagliflozin Extracellular Vesicles (ECV's), gut microbiota (GM) in Diabetes mellitus (DM) here we concentrated on more work on ER stress, inflammation, AGE's, Glut4 regulation by its gene. In the last 20 years complicated besides elegant pathways implicated in endoplasmic reticulum (ER) along with inflammatory stress reactions have been illustrated regarding taking part in the generation besides propagation of different diseases inclusive of Diabetes mellitus (DM). These pathways possess different actors taking part pointing to a complex crosstalk amongst ER along with inflammatory stress. Regarding DM, both ER and inflammatory stress are implicated in elimination of glycaemic regulation besides the generation of degenerative complications. Moreover, hyperglycemia enhanced the formation of advanced glycation end-products (AGE), that in turn further triggers the ER along with inflammatory stress, aiding in the inimical glycaemic homeostasis along with escalating the formation of DM complications. Here we conducted a narrative review utilizing search engines PubMed, Google Scholar; Web of Science; Embase; Cochrane review library utilizing the MeSH terms like AGEs; ER stress; inflammation) glucose transporter number 4(GLUT4); soluble carrier family 2 members 4(SLC2A4); glycaemic homeostasis; cardiovascular disease (CVD); atherogenesis from 1990-2022 till date. We found 300 articles out of which we used 130 articles for this review. Here we have highlighted role of AGEs-stimulated ER along with inflammatory stress in the control of GLUT4 expression besides atherogenesis in the form of commonest etiology regarding CVD generation, mortality along with morbidity in DM. Furthermore recently small molecule hampering

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Section: Atherogenic/cardiovascular Disease (Cvd) Along With Er Stres...mentioning

confidence: 99%

An Update on Mechanistic Modes in AGEs Stimulated & ER and Inflammatory Stress-Modulated Control of the GLUT4 expression (SLC2A4 promoted) and Atherogenesis in Diabetes Mellitus-A Narrative Review

Kaur¹,

Allahbadia²,

Singh³

2022

MJCH

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“…During the last century, several advanced glycation end-products (AGEs) have been identified and studied [1,2]. Many AGEs are produced in certain organs and tissues and circulate in the body through the bloodstream, whereas dietary AGEs are taken up by the body through food and drink consumption [1,2].…”

Section: Introductionmentioning

confidence: 99%

Is the Novel Slot Blot a Useful Method for Quantification of Intracellular Advanced Glycation End-Products?

Takata

2023

Metabolites

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Various types of advanced glycation end-products (AGEs) have been identified and studied. I have reported a novel slot blot analysis to quantify two types of AGEs, glyceraldehyde-derived AGEs, also called toxic AGEs (TAGE), and 1,5-anhydro-D-fructose AGEs. The traditional slot blot method has been used for the detection and quantification of RNA, DNA, and proteins since around 1980 and is one of the more commonly used analog technologies to date. However, the novel slot blot analysis has been used to quantify AGEs from 2017 to 2022. Its characteristics include (i) use of a lysis buffer containing tris-(hydroxymethyl)-aminomethane, urea, thiourea, and 3-[3-(cholamidopropyl)-dimetyl-ammonio]-1-propane sulfonate (a lysis buffer with a composition similar to that used in two-dimensional gel electrophoresis-based proteomics analysis); (ii) probing of AGE-modified bovine serum albumin (e.g., standard AGE aliquots); and (iii) use of polyvinylidene difluoride membranes. In this review, the previously used quantification methods of slot blot, western blot, immunostaining, enzyme-linked immunosorbent assay, gas chromatography–mass spectrometry (MS), matrix-associated laser desorption/ionization–MS, and liquid chromatography–electrospray ionization–MS are described. Lastly, the advantages and disadvantages of the novel slot blot compared to the above methods are discussed.

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“…Our recent findings showed that intracellular TAGE damaged not only liver cells [ 9 , 10 , 11 , 12 ], but also other cell types, including neuroblasts, pancreatic cancer cells, cardiomyocytes, myoblasts, pancreatic islet β-cells, osteoblasts, and cardiac fibroblasts [ 13 , 14 , 15 , 16 , 17 , 18 , 19 ]. The leakage of cytotoxic intracellular TAGE into the blood has been suggested to increase their concentration in circulating fluids [ 20 , 21 , 22 ]. Extracellular TAGE and receptor for AGEs (RAGE) interactions were found to affect intracellular signaling, gene expression, and the release of pro-inflammatory molecules and promoted reactive oxygen species (ROS) production in many cell types [ 23 , 24 , 25 , 26 , 27 ], and these changes collectively contribute to the development of NASH.…”

Section: Introductionmentioning

confidence: 99%

Involvement of Intracellular TAGE and the TAGE–RAGE–ROS Axis in the Onset and Progression of NAFLD/NASH

2023

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The repeated excessive intake of sugar, a factor that contributes to the onset of nonalcoholic fatty liver disease (NAFLD) and its progression to the chronic form of nonalcoholic steatohepatitis (NASH), markedly increases the hepatocyte content of glyceraldehyde (GA), a glucose/fructose metabolic intermediate. Toxic advanced glycation end-products (toxic AGEs, TAGE) are synthesized by cross-linking reactions between the aldehyde group of GA and the amino group of proteins, and their accumulation has been implicated in the development of NAFLD/NASH and hepatocellular carcinoma (HCC). Our previous findings not only showed that hepatocyte disorders were induced by the intracellular accumulation of TAGE, but they also indicated that extracellular leakage resulted in elevated TAGE concentrations in circulating fluids. Interactions between extracellular TAGE and receptor for AGEs (RAGE) affect intracellular signaling and reactive oxygen species (ROS) production, which may, in turn, contribute to the pathological changes observed in NAFLD/NASH. RAGE plays a role in the effects of the extracellular leakage of TAGE on the surrounding cells, which ultimately promote the onset and progression of NAFLD/NASH. This review describes the relationships between intracellular TAGE levels and hepatocyte and hepatic stellate cell (HSC) damage as well as the TAGE–RAGE–ROS axis in hepatocytes, HSC, and HCC cells. The “TAGE theory” will provide novel insights for future research on NAFLD/NASH.

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Effects of Toxic AGEs (TAGE) on Human Health

Cited by 23 publications

References 122 publications

An Update on Mechanistic Modes in AGEs Stimulated & ER and Inflammatory Stress-Modulated Control of the GLUT4 expression (SLC2A4 promoted) and Atherogenesis in Diabetes Mellitus-A Narrative Review

An Update on Mechanistic Modes in AGEs Stimulated & ER and Inflammatory Stress-Modulated Control of the GLUT4 expression (SLC2A4 promoted) and Atherogenesis in Diabetes Mellitus-A Narrative Review

Is the Novel Slot Blot a Useful Method for Quantification of Intracellular Advanced Glycation End-Products?

Involvement of Intracellular TAGE and the TAGE–RAGE–ROS Axis in the Onset and Progression of NAFLD/NASH

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