Metabolic Transit and in vivo Effects of Melanoidins and Precursor Compounds Deriving from the Maillard Reaction

Abstract

Metabolic transit data on food-borne advanced MRPs (Maillard reaction products) termed melanoidins are yet not completely elucidated and it is still an open question whether isolated melanoidin structures undergo metabolic biotransformation and subsequently cause physiological effects in vivo. Advanced MRPs, acting as premelanoidins, and melanoidins are formed under severe heat treatment of foods and are ingested with the habitual diet at considerable amounts. Metabolic transit data are known for Amadori compounds classified as early MRPs, like, e.g., fructose-lysine. For rats and humans, the percentages of ingested free versus protein-bound fructose-lysine excreted in the urine were found within ranges of 60–80% and 3–10%, respectively. Balance studies on free advanced MRPs are still lacking, but protein-bound low-molecular-weight premelanoidins and high-molecular-weight melanoidins have already been investigated in animal experiments using ¹⁴C-tracer isotopes. The amount of ingested radioactivity absorbed and excreted in the urine was found at levels ranging from 16 to 30% and from 1 to 5% for premelanoidins and melanoidins, respectively. These different metabolic transit data of premelanoidins and melanoidins can be explained by the following mechanisms involved: (i) intestinal degradation by digestive and microbial enzymes; (ii) absorption of these compounds or their degradates, and (iii) tissue retention. Structure specific in vivo effects have been identified for protein-bound premelanoidins on intestinal microbial activity, xenobiotic biotransformation enzymes and further glycation reactions. The latter are hypothesized to be involved in the aging process and in the course of different diseases. Further investigations are needed to clarify synergistic in vivo effects of dietary ingested melanoidins and endogenously formed glycation products.

Mass spectrometric characterization of glycated β-lactoglobulin peptides derived from galacto-oligosaccharides surviving the in vitro gastrointestinal digestion

“…The resistance of some MRP to the gastrointestinal digestion environment has been proven [5][6][7], indicating that they could be available for gut microflora fermentation. However, little is known about their effects on the growth of these micro-organisms and consequently on chronic gut disorders.…”

“…Considering that Amadori compounds, the relatively stable products formed during the early stages of the Maillard reaction, can reach the distal regions of the gut [5][6][7], the conjugation between a prebiotic carbohydrate and a protein could potentially allow carbohydrate to reach the distal parts of the colon and be fermented slowly.…”

Profound Mishandling of Protein Glycation Degradation Products in Uremia and Dialysis

“…Proteins also suffer oxidative and nitrosative damage forming methionine sulfoxide (MetSO) (5) and 3-nitrotyrosine (3-NT) (6) (Figure 1f). Glycation adduct residues are formed by the physiologic glycation of endogenous cellular and extracellular proteins and are also present in ingested food (7). Glycation free adducts are found in plasma, urine, and other physiologic fluids.…”

Diabetic threesome (hyperglycaemia, renal function and nutrition) and advanced glycation end products: evidence for the multiple-hit agent?

“…pentosidine in the free adducts in brewed coffee v. that of pretzel sticks). In animal studies faecal excretion was reported to be £ 26-29 % for CML but only 1-3 % for fructoselysine (122,123) , which was considered to be an effect of the metabolisation of fructoselysine by colon microflora, e.g. Escherichia coli can degrade fructoselysine to glucose 6-phosphate and utilise it as a substrate (127) .…”