Metabolic transit and in vivo effects of Maillard reaction products

These topics are considered in detail in an excellent review by Faist and Erbersdobler (2001) that has been used extensively to prepare this section. The two authors suggest dividing MRPs into three classes: melanoidin precursors (reactive low molecular weight compounds), premelanoidins (non-polymeric end products), and melanoidins. At the outset, it is important to underline that most data have been obtained by feeding experiments in rats, whereas only the Amadori compound fructosyllysine has been administered to humans (Erbersdobler et al, 1986; Lee and Erbersdobler, 1994).

11.6.1 Absorption

The intestinal absorption of the Amadori compounds occurs by passive diffusion (Faist and Erbersdobler, 2001). Amounts varying from 60 to 80% of ingested fructosyllysine is excreted in the urine, whereas only 1-3% undergoes faecal excretion (Faist and Erbersdobler, 2001). In humans trials (Erbersdobler et al, 1986; Lee and Erbersdobler, 1994) about 3% of orally administrated casein-bound fructosyllysine is excreted in urine, and only 1% via the faeces. Higher transit rates have been reported for infants (Niederweiser et al, 1975), as 16 and 55% of casein-bound fructosyllysine ingested from glucose-containing formula were excreted in the urine and faeces, respectively. The fate of most protein-bound fructosyllysine in humans remains completely obscure, indicating that its fate is probably metabolisation, degradation by intestinal microorganisms, or accumulation in different tissues. Microbiological degradation up to 80% has been demonstrated by Erbersdobler et al (1970).

Consistent amounts of CML are formed in foods containing milk protein which are severely treated and very small amounts of CML, detectable in the urine of human infants, are now considered normal constituents of urine (Wadman et al, 1975). Among the few other premelanoidins that have been investigated, furans and pyrroles are known to inhibit intestinal carboxypeptidases and aminopeptidases (Oste et al, 1986). HMF, by radio-labelling experiments, has been demonstrated to accumulate mainly in the kidney and less in the bladder and liver (Germond, 1987).

In conclusion, taking into account the data collected to date, it can be said that three different mechanisms are likely to be involved in the metabolic transit of early and advanced MRPs: (1) intestinal degradation by digestive or microbial enzymes and subsequent adsorption of the MRPs or their degradation products;

(2) metabolisation of MRPs themselves or their degradation products, probably neither acting as metabolically inert substance; (3) different retention mechanisms in various tissues and organs (Faist and Erbersdobler, 2001).

In the case of melanodins, studies indicate that they are partially absorbed in the intestine; the level is low for high molecular weight fractions, and high for low molecular weight fractions. Specific transport mechanisms are still unknown. It is speculated that the fractions absorbed are not used by the organism and are excreted slightly modified or unmodified with the urine. Kidneys retain these compounds more than do other organs, such as liver. For the nonabsorbable low molecular weight fractions, intestinal degradation by digestive or microbial enzymes may be postulated while the high molecular weight fraction is not degraded (O'Brien and Morrissey, 1989).

11.6.2 Antioxidant activity

In vivo effects of MRPs and melanoidins may be classified as primary, attributed to specific actions, and secondary, based on interaction with other nutrients (Faist and Erbersdobler, 2001). Most of the secondary nutritional effects may be corrected with a suitable dietary supplementation.

An important primary effect of browning is the formation of antioxidants, compounds that are able to delay or prevent oxidation processes, typically involving lipids. Such antioxidants greatly affect the shelf-life of foods but may also benefit health (Halliwel, 1996), especially in the prevention of cancer (Kim and Mason, 1996), cardiovascular disease (Maxwell and Lip, 1997) and ageing (Deschamps et al, 2001).

The formation of antioxidants in browning has been observed in several different systems, for example sugar/amino acids model systems (Lignert and Eriksson, 1981), model melanoidins (Hayase et al, 1990), and honey/lysine model systems (Antony et al, 2000). They have also been seen in heated or roasted foods, such as coffee brews (Nicoli et al, 1997). However, the processing conditions should be chosen very carefully: in coffee, for example, the antioxidant activity increases with roasting up to the medium-dark roasted stage, then decreases with further roasting (Nicoli et al, 1997). This experimental observation is explained by the partial decomposition of the antioxidant compounds.

11.6.3 Activation of xenobiotic enzymes

Much interest has been raised also by the possible activation of xenobiotic enzymes by MRPs. Induction of detoxifying enzymes, either by natural or synthetic substances, is still a promising chemopreventive strategy (Faist and Erbersdobler, 2001). Naturally occurring substances in foods have been shown to serve as antimutagens, which may function as chemical inactivators, enzymatic inducers, scavengers and antioxidants. The modulators can act through enzyme systems by inducing phase-I and phase-II enzymes or by altering the balance of different enzyme activities.

Phase-I metabolic transformations include reduction, oxidation and hydrolytic reactions in order to release or induce functional or reactive groups from or into the xenobiotic substances. Phase-II transformations are mostly conjugation reactions of the parent xenobiotics, or phase-I metabolites, with sulphur-containing amino acids or glutathione. The conjugation reactions facilitate transport and hence elimination. Thus the balance between phase-I and phase-II enzymes is very critical (Prochaska and Talalay, 1988). The most potent inducers of these enzymes in foods are phenolic compounds and antioxidants. Antimutagenic properties of MRPs have been noted by Kim et al (1986) and are attributed to the inhibition of mutagenic activation through enhanced detoxification of reactive intermediates (Kitts et al, 1993; Pintauro and Lucchina, 1987). Because several MPRs or melanoidins exhibit antioxidant properties, they may inhibit phase-I mutagenic activating enzymes and may induce detoxifying phase-II enzymes. CML-casein increases significantly the activity of phase-II glutathione-S-transferase in kidney isolates, whereas LAL-casein has no effect (Faist et al, 1998; Wenzel et al, 2000).

11.6.4 Other activities

Melanodins possess the ability to bind metals, such as copper and zinc (O'Brien and Morrissey, 1989; Andrieux et al, 1980 and 1984; Furniss et al, 1986).

Some antibiotic activity against both pathogenic or spoilage organisms, including Lactobacillus, Proteus, Salmonella and Streptococcus faecalis and others, has been observed in mixtures obtained by heating arginine and xylose or histidine and glucose (Einarsson et al, 1983, 1988).

An interesting topic, still to be investigated in detail, is the relationship of MRPs with products that derive from physiological protein glycation, especially in diabetic patients and that are involved in ageing and act as promoting agents in Alzheimer's disease. However, it has been suggested that dietary restriction of food MRPs may be useful to reduce the burden of AGEs in diabetic patients and possibly improve the prognosis of the disease (Koschinsky et al, 1997).

Losing Weight Without Starving

Losing Weight Without Starving

Tired of Trying To Loose Weight And It Never Works or You Have To Starve Yourself Well Here's A Weight Loss Plan That takes Care of Your Weight Problem And You Can Still Eat. In This Book, You’ll Learn How To Lose Weight And Not Feel Hungry! In An Easy Step-By-Step Process That Enables You To Feel Good About Loosing Weight As Well As Feeling Good Because Your Stomach Is Still Full.

Get My Free Ebook


Post a comment