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assay in quantifying CML in plasma, urine, and foods is given. Using the same analytical approach for quanti cation of AGEs, several papers reported on possible pathophysiological effects of dietary glycation compounds. For rats fed a high-AGE diet for 6 months, a decreased glucose and insulin response was found together with 1.5-fold increase in plasma AGEs (114). Improved insulin sensitivity and a prevention of diabetic nephropathy was observed for diabetic mice after a 2-month low-AGE diet (115, 116), whereas a diet high in AGEs was made responsible for impaired wound healing in genetically diabetic mice (117). For patients with renal failure, dietary glycation compounds were found to correlate with circulating AGEs (118). For dialysis patients on an AGE-free diet for 4 weeks, a signi cant decrease of in ammatory markers such as tumor necrosis factor- and C-reactive protein was observed (119, 120). Following ingestion of a single high-AGE meal by patients suffering from type 2 diabetes, impaired micro- and macrovascular function concomitant with an increase of markers for postprandial vascular dysfunction and oxidative stress was found (121). When reviewing reports presenting evidence for detrimental effect of dietary AGEs, one cannot overlook that most of the studies report biological phenomena without any chemical characterization of the stimulating agent. AGEs are generally taken as anonymous mixture of compounds, for which no reliable quantitative data are given. Most of the studies refer to the aforementioned database (73) when creating diets high or low in AGEs. In other words, up to now, there is no study showing unambiguously any toxicological effect of one single glycation compound based on accepted structure-function assays. Actual studies based on chemically characterized compounds are rare, however, in general report either on low bioavailability of glycation compounds or on quick elimination without accumulation in vivo. From peptidebound Amadori products such as N- -fructosyllysine or N- -lactulosyllysine, only 3% to 10% are resorbed and are rapidly excreted via the kidney (122 124). Even in dialysis patients, plasma concentrations of Amadori products did not rise following a diet high in N- -lactulosyllysine (125). Enzymes produced by the microbiota present in the colon of humans may be responsible for the degradation of Amadori products (126). For rats fed a diet high in N- -carboxymethyllysine, about half of the administered CML was recovered in the feces and the urine, whereas most of the compound was discussed to be metabolized by the colonic micro ora, as virtually no deposition of CML in organs was found (127). Using positron-emission tomography, rapid elimination without accumulation was found after intravenous injection of radioactively labeled CML (128). N- -fructoselysine and CML were the only glycation compounds for which a study was performed to investigate the intestinal transepithelial absorption in vitro and to determine whether these glycation compounds are substrates for physiologically occurring membrane transport proteins for amino acids and dipeptides. The transepithelial ux measured for these compounds was very low, indicating that resorption most probably occurs by simple diffusion (129). The metabolic fate
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of dietary pyrraline and pentosidine has been investigated in an intervention study with 18 healthy volunteers. It was found that peptide-bound pyrraline present in bakery products is rapidly proteolyzed and resorbed. Most of the ingested pyrrole derivative (ca. 80%) was found in the urine within 24 h after the diet. Similar data were obtained for free pentosidine in coffee, whereas the peptide-bound cross-link seems to be not available during digestion (130). In addition to the studies reporting on bioavailability and rapid elimination of individual compounds, several reports argue against adverse effects of AGEs and even discuss positive aspects. In a cross-sectional study with 312 hemodialysis patients, it was found that high serum AGEs are not linked to increased mortality (131). This observation was con rmed recently for 540 patients suffering from diabetes and nephropathy, for which serum CML content could not be identi ed as an independent risk factor for cardiovascular or renal outcomes (132). As already mentioned, the generally accepted role of RAGE as a speci c receptor for AGEs, which should trigger in ammatory responses on a cellular level, has come under debate. It was found that chemically de ned AGEs free of endotoxins do not bind to RAGE, and AGE RAGE interaction is not suf cient to induce in ammatory signals, thus arguing against a uniform role of AGEs in cellular activation (133 135). In this context, it should also be noted that despite the highly visible number of papers dealing with RAGE, to date, none of them has ever reported on an individual glycation compound as speci c ligand of RAGE. A paper in which CML is suggested to speci cally interact with RAGE must be handled with care, as binding could also result from unspeci c electrostatic interactions between the receptor protein, which due to its low isoelectric point is positively charged under the assay conditions, and negatively charged proteins containing CML residues (136). No controls with other proteins containing, for instance, high amounts of aspartic or glutamic acid were made in order to exclude such unspeci c ion-exchange mechanisms and to prove selective binding mechanisms. Finally, it shall be mentioned that more and more papers discuss possible bene ts of glycation compounds. A chemoprotective role of individual dietary AGEs may result from their antioxidative properties, which is well established for melanoidins from various food sources (137 139). Pronyllysine, which is present in bread crust melanoidins, may be one of the important antioxidants in this context (140). Melanoidins formed during baking of bread or caramelization of fructooligosaccharides may have a prebiotic effect on colonic microorganisms (141, 142). Several Maillard compounds identi ed as constituents of melanoidins were found to inhibit tumor cell growth (143).
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