Toxic AGEs (TAGE) theory: a new concept for preventing the development of diseases related to lifestyle

Abstract

Background The habitual excessive intake of sugar (i.e., sucrose and high-fructose corn syrup), which has been implicated in the onset of diabetes mellitus, induces excessive production of glyceraldehyde, a metabolite produced during glucose and fructose metabolism, in hepatocytes, neuronal cells, and cardiomyocytes. Main text Toxic advanced glycation end-products (toxic AGEs, TAGE) are formed from reactions between glyceraldehyde and intracellular proteins, and their accumulation contributes to various cellular disorders. TAGE leakage from cells affects the surrounding cells and increases serum TAGE levels, promoting the onset and/or development of lifestyle-related diseases (LSRD). Therefore, serum TAGE levels have potential as a novel biomarker for predicting the onset and/or progression of LSRD, and minimizing the effects of TAGE might help to prevent the onset and/or progression of LSRD. Serum TAGE levels are closely related to LSRD associated with the excessive ingestion of sugar and/or dietary AGEs. Conclusions The TAGE theory is also expected to open new perspectives for research into numerous other diseases.

Effects of Vanadium Inhalation and Sweetened Beverage Ingestion in Mice: Morphological and Biochemical Changes in the Liver

“…Besides oxidative stress, the accumulation of AGES in hepatocytes induces necrosis and inflammation that affects the function of hepatic stellate cells predisposing to liver fibrosis. Serum levels of AGEs have been postulated as a biomarker of NALD and other lifestyle-related diseases, 24 so this mechanism may be studied in a further research with this model.…”

Trapa bispinosa Roxb. extract lowers advanced glycation end-products and increases live births in older patients with assisted reproductive technology: a randomized controlled trial

“…While MG-H1 and CMA are most sensitive to in vivo effects of Hishi, they do not necessarily dominate pathogenic processes compromising follicular function. Glycation/carbonyl stress generates various AGE in vivo , including less harmful AGE without direct cytotoxic effects such as CML, Pent, MG-H1, and pyrraline, as well as toxic, highly pathogenic AGE such as TAGE [ 3 ]. Some non-toxic AGE may be components of biologic defense mechanisms working against accumulation of toxic AGE [ 3 ].…”

“…Glycation/carbonyl stress generates various AGE in vivo , including less harmful AGE without direct cytotoxic effects such as CML, Pent, MG-H1, and pyrraline, as well as toxic, highly pathogenic AGE such as TAGE [ 3 ]. Some non-toxic AGE may be components of biologic defense mechanisms working against accumulation of toxic AGE [ 3 ]. MG-H1 and CMA were found to be elevated in diabetic patients [ 27 , 28 ], but implications for pathogenesis in diabetes remain unclear.…”

“…Advanced glycation end-products (AGE) are cross-linked molecules formed by nonenzymatic reactions of carbonyl groups with amino groups of proteins, lipids, or nucleic acids [ 1 ]. AGE participate in aging [ 2 ] and in conditions involving insulin resistance (IR) such as metabolic syndrome, type 2 diabetes, hypertension, atherosclerosis, dyslipidemia, polycystic ovary syndrome (PCOS), and central obesity [ 1 , 3 , 4 ]. AGE toxicity results directly from macromolecular trapping and cross-linking, and indirectly from binding to AGE receptors (RAGE) [ 1 , 5 ].…”

Food Contaminants Effects on an In Vitro Model of Human Intestinal Epithelium

“…As for the Maillard reaction, which generally occurs between reduced sugars and some amino acids [8], it leads to the production of several compounds among which are advanced glycation end products (AGEs). While their adverse effects on health are often suggested [9], it still remains difficult to confirm them [8]. For instance, the consumption of AGEs such as N ε -Carboxymethyllysine (CML) or of acrylamide has negative impacts on human health.…”