Biomedical subjects
Publications and source records attributed to M de Vrese.
Definitions of different pro-, pre-, and synbiotics suggested by different investigators are critically discussed. On the basis of this analysis, the probiotic concept is confined to effects exerted by viable microorganisms but is applicable independent of the site of action and route of administration. It therefore may include sites such as the oral cavity, the intestine, the vagina, and the skin.
Yogurt and other conventional starter cultures and probiotic bacteria in fermented and unfermented milk products improve lactose digestion and eliminate symptoms of intolerance in lactose maldigesters. These beneficial effects are due to microbial beta-galactosidase in the (fermented) milk product, delayed gastrointestinal transit, positive effects on intestinal functions and colonic microflora, and reduced sensitivity to symptoms. Intact bacterial cell walls, which act as a mechanical protection of lactase during gastric transit, and the release of the enzyme into the small intestine are determinants of efficiency. There is a poor correlation between lactose maldigestion and intolerance; in some studies, low hydrogen exhalation without significant improvement of clinical symptoms was observed. Probiotic bacteria, which by definition target the colon, normally promote lactose digestion in the small intestine less efficiently than do yogurt cultures. They may, however, alleviate clinical symptoms brought about by undigested lactose or other reasons.
Probiotics are nonpathogenic microorganisms that, when ingested, exert a positive influence on the health or physiology of the host. They can influence intestinal physiology either directly or indirectly through modulation of the endogenous ecosystem or immune system. The results that have been shown with a sufficient level of proof to enable probiotics to be used as treatments for gastrointestinal disturbances are 1) the good tolerance of yogurt compared with milk in subjects with primary or secondary lactose maldigestion, 2) the use of Saccharomyces boulardii and Enterococcus faecium SF 68 to prevent or shorten the duration of antibiotic-associated diarrhea, 3) the use of S. boulardii to prevent further recurrence of Clostridium difficile-associated diarrhea, and 4) the use of fermented milks containing Lactobacillus rhamnosus GG to shorten the duration of diarrhea in infants with rotavirus enteritis (and probably also in gastroenteritis of other causes). Effects that are otherwise suggested for diverse probiotics include alleviation of diarrhea of miscellaneous causes; prophylaxis of gastrointestinal infections, which includes traveler's diarrhea; and immunomodulation. Trials of gastrointestinal diseases that involve the ecosystem are currently being performed, eg, Helicobacter pylori infections, inflammatory bowel disease, and colon cancer.
Heat and alkali treatment of food may increase the concentrations of protein-bound D-amino acids and cross-links such as lysinoalanine (LAL). To examine how protein treatment affects digestibility, purified test meals [total protein 150 g/kg dry matter (DM), 0.44 MJ/(kg BW(0.75). d)] were prepared, containing (g/kg DM) casein, 75; beta-lactoglobulin, 50; or wheat protein, 40. Each was (15)N-labeled. Test proteins were used either in their native form or after treatment for 6 or 24 h at 65 degrees C, pH 10.5-11.5. Each meal was fed to nine adult miniature pigs (twofold complete cross-classification). Chyme was collected continuously over 33 h postprandially via T-fistulas in the terminal ileum, and digestibilities of test proteins and individual L- and D-amino acids were calculated on the basis of recovery of (15)N and the respective amino acids in the chyme. Treatment of casein, beta-lactoglobulin or wheat protein for 24 h increased levels of D-amino acid residues. L-Asparagine and aspartate (L-Asx) were particularly susceptible; 14. 7 +/- 0.4, 11.7 +/- 0.2 and 11.0 +/- 0.9%, respectively, underwent racemization. LAL levels increased in parallel; 11.7 +/- 0.3, 13.6 +/- 0 and 14.8 +/- 0.0%, respectively, of total lysine was converted to LAL. At the same time, prececal protein digestibility was decreased by 13.4 +/- 2.3, 15.3 +/- 1.4 and 17.8 +/- 1.2% units, respectively (P < 0.05; mean +/- SEM, n = 9). Digestibility of individual L-amino acids decreased by 10-15%, but L-amino acids prone to peptic cleavage, such as L-phenylalanine and L-tyrosine, were not affected. Digestibilities of D-amino acids and LAL were approximately 35%. It seems that mainly D-amino acids, and to a lesser extent LAL, were responsible for lower digestibility by interfering with peptic cleavage.
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The disaccharide lactose is naturally present as a component of foods in milk and dairy products. In the gastrointestinal tract, lactose is hydrolysed by the enzyme beta-galactosidase (lactase) into glucose and galactose. These components are absorbed. In most people lactase activity decreases at the age of approximately 2 years of age. After this lactose intake can cause symptoms of bloating, flatulence, abdominal pain and diarrhoea due to the lactose reaching the large intestine. This phenomenon is called lactose intolerance. It is generally recommended that these people abandon the consumption of milk and dairy products. However, most lactose-intolerant people are able to digest small amounts of milk (approximately 200 ml). They can also consume cheese without (hard and semi-hard cheese) or only low lactose content (only present in 10% of soft cheese). These products are a very important source of calcium.
The disaccharide lactose is present as a natural component of foods only in milk and dairy products. In the gastrointestinal tract, lactose is hydrolysed by the enzyme beta-galactosidase (lactase) into glucose and galactose. These components are absorbed. With the exception of the caucasian race, the lactase activity decreases in most people at an age of 4 to 6 years. Lactose intake can cause symptoms of bloating, flatulence, abdominal pain, and diarrhea due to the lactose reaching the large intestine. This phenomenon is called lactose intolerance. It is generally recommended to those persons that they refrain from the consumption of milk and dairy products. However, most lactose intolerant people are able to digest small amounts of milk. They can also consume cheese that contains no (hard and semi-hard) or only small amounts of lactose (present in only 10% of soft cheeses). These products are very important sources of calcium. Compared to milk, the lactose content of yogurt is usually lower by about one third. Studies during the last 10 years have shown that in spite of its lactose content yogurt is very well tolerated by lactose intolerant persons. This advantage is ascribed to the presence of living lactic acid bacteria in fermented dairy products which survive passage through the stomach and also to the lactase present in these products.
Homoarginine labeling (guanidination) is used to calculate true prececal protein digestibility. A particular worry is that guanidination of proteins at alkaline pH might cause formation of D-amino acids. If D-amino acids show decreased protein digestibility in vivo, as seen in vitro, then the homoarginine method would underestimate protein digestibility. Therefore, the degree of protein racemization was measured during guanidination of casein at pH values between pH 9 and 11 and temperatures between 4 degrees and 65 degrees C. Optimal conditions for the guanidination reaction were 4 degrees C and pH 10.5-11 or 22 degrees C and pH 10. A higher pH value at 22 degrees C or temperatures above 22 degrees C at each pH leads to the formation of appreciable amounts of D-amino acids.
The effect of microbial beta-galactosidase (EC 3.2.1.23) activity on intestinal lactose digestion was estimated directly by following post-prandial venous plasma galactose concentrations. To avoid superimposing effects of free galactose, as with yogurt, fresh or heat-treated suspensions of mechanically disintegrated kefir grains in kefir, containing lactose but no free galactose, were fed to ten Göttingen minipigs. Each meal contained 101.1 (SEM 0.1) mmol lactose in kefir supplemented by either native or heat-treated kefir grains corresponding to a mean beta-galactosidase activity of either 72 (SEM 8) U or zero. Feeding kefir with beta-galactosidase activity resulted in a 30% enhancement of the mean post-prandial plasma galactose peak concentration from 33 (SEM 7) to 43 (SEM 12) mumol/l (n 10), as well as in 23% greater mean areas under the galactose-response curves (8.1 (SEM 1.5) v. 6.6 (SEM 1.2) mmol/min per l) if compared with kefir with heat-treated grains. Both differences were significant (P less than 0.05; paired Wilcoxon test by ranks). There was no induction of intestinal beta-galactosidase (EC 3.2.1.108) activity or intestinal lactose-hydrolysing bacteria by lactose feeding. These results give direct evidence of an enhanced lactose digestion and absorption in native fermented milk products due to the microbial beta-galactosidase activity.
The risk of D-lactic acidosis after consumption of yogurt was investigated in seven healthy volunteers. After ingestion of yogurt containing 1.06 mmol/kg body weight, D-lactic acid postprandial plasma D-lactate concentrations increased from 0.070 +/- 0.020 to a maximum of 0.200 +/- 0.010 mmol/l within 60 min. That was half the maximum concentration after the equivalent amount of D-lactate in the form of an aqueous solution of DL-lactate. The shape of the postprandial plasma D-lactate peak was flatter, but much broader after yogurt than after the aqueous solution, the peak areas being equal. When 0.64 mmol/kg body weight D-lactate were consumed as yogurt, plasma concentrations amounted to 0.086 +/- 0.030 mmol/l. Signs of a mild, transient, compensated metabolic acidosis, which was apparent in case of the aqueous lactic acid solution did not occur in case of yogurt. It is concluded that the consumption of foods containing D-lactic acid gives no reason for concern in healthy adults.
There were significant differences of postprandial plasma concentrations for 8 amino acids (Cys, Val, Met, Leu, Tyr, Lys, Trp, and Arg) depending on whether pigs consumed a meal containing casein or isolated soy protein. The postprandial plasma amino acid pattern conformed with the amino acid composition of the dietary protein (except for Ser). The data, however, do not allow to conclude unambiguously, whether specific amino acids are responsible for the difference of serum cholesterol following casein or soy protein intake. Significant differences between casein- and soy-fed rats were observed regarding total and free plasma thyroxine and triiodothyronine concentrations. This observation can explain the accompanying different serum cholesterol concentrations. The different thyroid hormone concentrations were not paralleled by differences in TSH levels suggesting that dietary proteins affect thyroid function at the thyroid gland.
There was a reversible inhibition of urea formation in the perfused rat liver caused by 2.25-27 mM lysine acting with a Ki of 10.8 mM in competition with ornithine. Urea formation in the presence of inhibitory concentrations of lysine ranged between 2.3 and 2.9 mumol X min-1 X (g, liver wet)-1 after addition of 1 mM of citrulline, argininosuccinate or arginine, whereas it amounted to 0.5 mumol X min-1 X (g, liver wet)-1 after addition of ornithine, showing that lysine inhibited the urea cycle between ornithine and citrulline. There was a rise of basal orotate formation of 0.03 +/- 0.02 mumol X h-1 X (g, liver wet)-1 towards a maximum of 0.6 +/- 0.04 mumol X h-1 X (g, liver wet)-1 after addition of 13.5 mM lysine, provided orotate utilization was blocked with allopurinol. Maximal rates of orotate formation were reached when ammonium concentrations exceeded 1 mM. We conclude that an inhibition of urea synthesis and a rise of orotate formation are caused by lysine in the isolated liver in vitro at rates observed in vivo. Hence, these metabolic alterations observed in the whole animal are most probably due to changes of liver metabolism.