To evaluate the importance of protein digestion rate on protein deposition, we characterized leucine kinetics after ingestion of "protein" meals of identical amino acid composition and nitrogen contents but of different digestion rates. Four groups of five or six young men received an L-[1-13C]leucine infusion and one of the following 30-g protein meals: a single meal of slowly digested casein (CAS), a single meal of free amino acid mimicking casein composition (AA), a single meal of rapidly digested whey proteins (WP), or repeated meals of whey proteins (RPT-WP) mimicking slow digestion rate. Comparisons were made between "fast" (AA, WP) and "slow" (CAS, RPT-WP) meals of identical amino acid composition (AA vs. CAS, and WP vs. RPT-WP). The fast meals induced a strong, rapid, and transient increase of aminoacidemia, leucine flux, and oxidation. After slow meals, these parameters increased moderately but durably. Postprandial leucine balance over 7 h was higher after the slow than after the fast meals (CAS: 38 +/- 13 vs. AA: -12 +/- 11, P < 0.01; RPT-WP: 87 +/- 25 vs. WP: 6 +/- 19 micromol/kg, P < 0.05). Protein digestion rate is an independent factor modulating postprandial protein deposition.

In young men ingesting protein meals, slowly digested proteins (caseins: CAS) induce a higher protein gain than those that are rapidly digested (whey proteins: WP). Our aim was to assess whether or not this is true in elderly men receiving mixed meals. The effects of meals containing either CAS or two different amounts of WP (WP-iN: isonitrogenous with CAS, or WP-iL: providing the same amount of leucine as CAS) on protein metabolism (assessed by combining oral and intravenous leucine tracers) were compared in nine healthy, elderly (mean ± S.E.M. age 72 ± 1 years) and six young men (24 ± 1 years). In both age groups, WP-iL and WP-iN were digested faster than CAS (P < 0.001, ANOVA). Proteolysis was inhibited similarly whatever the meal and age groups (P = NS). Protein synthesis was higher with WP-iN than with CAS or WP-iL (P < 0.01), irrespective of age (P = NS). An age-related effect (P < 0.05) was found with postprandial leucine balance. Leucine balance was higher with CAS than with WP-iL (P < 0.01) in young men, but not in elderly subjects (P = NS). In isonitrogenous conditions, leucine balance was higher with WP-iN than with CAS (P < 0.001) in both age groups, but the magnitude of the differences was higher in the elderly men (P = 0.05). In conclusion, during aging, protein gain was greater with WP (rapidly digested protein), and lower with CAS (slowly digested protein). This suggests that a 'fast' protein might be more beneficial than a 'slow' one to limit protein losses during aging.

Chlorogenic acids (CGAs) are potent antioxidants found in certain foods and drinks, most notably in coffee. In recent years, basic and clinical investigations have implied that the consumption of chlorogenic acid can have an anti-hypertension effect. Mechanistically, the metabolites of CGAs attenuate oxidative stress (reactive oxygen species), which leads to the benefit of blood-pressure reduction through improved endothelial function and nitric oxide bioavailability in the arterial vasculature. This review article highlights the physiological and biochemical findings on this subject and highlights some remaining issues that merit further scientific and clinical exploration. In the framework of lifestyle modification for the management of cardiovascular risk factors, the dietary consumption of CGAs may hold promise for providing a non-pharmacological approach for the prevention and treatment of high blood pressure.

We determined whether the steady-state levels of intestinal mucins are more sensitive than total proteins to dietary threonine intake. For 14 d, male Sprague-Dawley rats (158 +/- 1 g, n = 32) were fed isonitrogenous diets (12.5% protein) containing 30% (group 30), 60% (group 60), 100% (control group), or 150% (group 150) of the theoretical threonine requirement for growth. All groups were pair-fed to the mean intake of group 30. The mucin and mucosal protein fractional synthesis rates (FSR) did not differ from controls in group 60. By contrast, the mucin FSR was significantly lower in the duodenum, ileum, and colon of group 30 compared with group 100, whereas the corresponding mucosal protein FSR did not differ. Because mucin mRNA levels did not differ between these 2 groups, mucin production in group 30 likely was impaired at the translational level. Our results clearly indicate that restriction of dietary threonine significantly and specifically impairs intestinal mucin synthesis. In clinical situations associated with increased threonine utilization, threonine availability may limit intestinal mucin synthesis and consequently reduce gut barrier function.

Dietary effects on the intestinal microflora have gained increasing interest because of the evidence that a balanced micro ecology in the gut is important for health and well being. The aim of the present study was to evaluate the effect of different diets on faecal counts of bifidobacteria and Clostridium perfringens in dogs. Two extruded, dry diets, one supplemented with 3% chicory (1.5% inulin), a non-digestible oligosaccharide (NDO) and the other with 3% glucose (GLU) were compared with a protein rich diet (PR+) based on low quality animal derived protein sources (NDO 265, GLU 259, PR+ 726 g crude protein/kg dry matter; greaves meal and bovine lung as protein sources in PR+). Nine adult beagles were subjected to a consecutive cross-over trial. All dogs started with diet PR+, after which groups of four dogs (group A) received GLU and the other five dogs (group B) received NDO. After an intermediate wash-out period with diet PR+ for 3 weeks the A dogs were switched to diet NDO and B dogs to GLU. In the final period all dogs were fed with diet PR+. Faecal samples were collected during each period for dry matter and pH measurements. Faecal bifidobacteria and Cl. perfringens were quantified in fresh samples at the end of each feeding period and additionally on the first days after feed change from the dry diets to diet PR+. Diets NDO and GLU increased faecal dry matter and reduced faecal pH from 6.9 to 7.4 with the high protein diet to 5.9-6.5. The dry diets induced a firmer faecal consistency and a lower faecal pH, with no significant difference between NDO or GLU. Clostridium perfringens was found in all faecal specimens after feeding PR+ with counts of log 8.2-8.8 colony forming units (cfu)/g faeces. Both dry diets reduced the counts of Cl. perfringens significantly (log 3.3-4.0 cfu/g faeces). Switching from the dry diets to the high protein diet induced an increase of Cl. perfringens within 1 day, independent of the previous diet. In dogs fed PR+, bifidobacteria were detected in only four faecal samples and exclusively in the initial feeding period. During the remainder of the experiment the counts fell below the detection limit (log 6 cfu/g faeces). The faecal concentrations of bifidobacteria increased with both dry diets. Slightly higher concentrations (log 9.6-9.7 cfu/g faeces) were obtained from dogs fed the dry diet containing NDO compared with the diet containing glucose (log 9.3-9.4 cfu/g faeces). The increase was small which may be related to the level of total fermentable carbohydrates in both diets which alone increase remarkably the total counts of bifidobacteria. In conclusion, distinct dietary effects on the faecal counts of Cl. perfringens and bifidobacteria with a clear antagonistic pattern were observed. The main factor was the protein source and level in the diet. In this case, NDO favoured the concentrations of bifidobacteria to a limited degree. Further studies are needed to evaluate time effects, metabolic consequences and the potential implication for health promotion in pets.

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The objective of this work was to determine the effects of starvation and refeeding on growth, nutritional recovery and intestinal repair in starved rats. Male Wistar rats, weighing 200 g, were starved for 3 d, then refed a soy-based diet for another 3 d. Normally fed rats were given the same diet and used as controls. The variables assessed were as follows: body weight gain and nitrogen retention during recovery after starvation; muscle glutamine concentration; tissue protein content; gut mucosa and liver glutathione levels; intestinal permeability to ovalbumin, lactulose and mannitol; and intestinal tissue apoptosis. Starvation was associated with lower muscle glutamine levels and intestinal mucosa impairment, including a lower content of mucosal protein, a higher level of oxidized glutathione, enhanced permeability to macromolecules and greater numbers of apoptotic cells. Refeeding for 3 d resulted in rapid repair of gut atrophy and normalization of not only intestinal permeability but also of the majority of metabolic markers assessed in other tissues. In conclusion, with the use of severely starved rats, we have established a reversible experimental animal model of malnutrition that might prove useful in comparing the effectiveness of different enteral diets.

Maternal feeding of DHA significantly prevented prenatal stress-induced impairment of learning and memory and normalized the biomarkers of oxidative damage, apoptosis, and mitochondrial metabolism in the hippocampus of both male and female offspring. These results suggest that maternal feeding of DHA exerts preventive effects on prenatal stress-induced brain dysfunction and that modulation of mitochondrial metabolism may play critical role in DHA protection.