Nutritional and toxicological aspects of the Maillard browning reaction in foods

Abstract

The Maillard, or nonenzymatic, browning reaction between carbonyl and amino groups is a common reaction in foods which undergo thermal processing. The Maillard reaction is a desirable consequence of many industrial and domestic processes and is responsible for the attractive flavor and brown color of some cooked foods. An early recognized consequence of the Maillard reaction was the destruction of some essential amino acids, such as lysine. More recently, research interest has focused on the production of toxic and antinutritive compounds. This review examines the nutritional and toxicological consequences of the Maillard reaction in light of the findings of such research. In particular, the effect of Maillard reaction products on the digestion, absorption, and excretion of nutrients is considered. The cytotoxicity, mutagenicity, and immunochemical aspects of selected Maillard reaction products are also examined and suggestions are made for future areas of investigation.

Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy

“…Current dietary strategies center on nutrients, or caloric restriction, but not on risk-associated processing methods (1)(2)(3). An unrecognized risk factor for diabetic complications is the heat-generated group of advanced glycation end products (AGEs) which form in common foods during the spontaneous reactions between reducing sugars and proteins or lipids (4)(5)(6)(7)(8)(9).…”

High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model

“…Advanced glycation end products AGEs are long known to form in foods during heating (Lee et al ., 1981; O'Brien & Morrissey, 1989; Koschinsky et al ., 1997). There are two well‐characterized compounds, N ‐carboxy methyl‐lysine (CML) and methyl‐glyoxal (MG), derivatives of glucose–protein or glucose–lipid interactions, which serve as markers for AGEs (Dyer et al ., 1992; Vlassara & Palace, 2002).…”

High Levels of Dietary Advanced Glycation End Products Transform Low-Dersity Lipoprotein Into a Potent Redox-Sensitive Mitogen-Activated Protein Kinase Stimulant in Diabetic Patients

“…7 Several advanced glycoxidation end products (AGEs) and lipoxidation derivatives, such as ⑀N-(carboxymethyl)lysine (CML) 8 and 4-hydroxy-nonenal (HNE), 9 have been identified as having proatherogenic properties, 3,7 involving cell surface AGE receptors, redox-dependent oxidant stress, and activation of mitogen-activated protein kinase (MAPK) signaling and nuclear factor (NF)-B transcription factor pathways. 10 -15 AGE formation can be vastly accelerated as a function of degree and time of exposure to heat 16 and can be introduced into the body with heat-processed foods. 17 Two thirds of the absorbed AGEs (Ϸ10% of ingested) are integrated within tissue and blood components, including LDL.…”