Systemic low-grade inflammation does not decrease skeletal muscle mass and protein synthesis in old rats.

Age-associated low-grade systemic inflammation may contribute to sarcopenia. We hypothesized that skeletal muscle mass and protein synthesis rate would be reduced in old rats exhibiting persistent low-grade inflammation compared to age-matched controls. Male 24-month-old Wistar rats exhibiting a low-grade systemic inflammation for at least one month (LGI group) were compared to non-inflamed rats (C group). Tissue protein synthesis rates were quantified using the L-[1-(13)C]-valine flooding dose method. Body weight, gastrocnemius muscle and spleen weights were not significantly different between groups, but liver and small intestine weights were 13 and 14% higher in LGI than in C. Fractional and absolute protein synthesis rates were not significantly different between groups for gastrocnemius, spleen and small intestine, but higher for liver in LGI than in C. Despite an increase in liver protein synthesis, low-grade inflammation did not reduce skeletal muscle mass, suggesting that age-associated low-grade systemic inflammation occurs independently of sarcopenia.

Neither glutamine nor arginine supplementation of diets increase glutamine body stores in healthy growing rats.

The aim of the work was to resolve whether glutamine and arginine supplemented diets affect plasma and tissue (muscle, liver and intestinal mucosa) glutamine concentrations, as well as glutaminase and glutamine synthetase specific activities. The trial was performed in growing rats fed 10% protein diets for 3 weeks. Protein sources were: whey proteins (W); whey proteins+free glutamine (WG); whey proteins+arginine (WA); and casein+wheat protein hydrolysate+acid whey (39:39:22), as source containing protein-bound glutamine (CGW). Rats fed the control diet (6.4% glutamine) (W) showed comparable glutamine body stores to those of rats fed the WG diet. In fact, glutamine sup- plementation down-regulated the hepatic glutamine synthetic capacity of growing rats (W/WG: 6.8+/-0.3 vs 6.0+/-0.2 nmol/min/mg protein). Arginine supplementation of the diet (up to 9% of the protein content) resulted in a decrease in plasma and tissue glutamine concentrations (W/WA: plasma, 1218+/-51 vs 1031+/-48 micromol/L; liver 7.5+/-0.4 vs 6.5+/-0.2 micromol/g; muscle: 5.7+/-0.2 vs 4.0+/-0.2 micromol/g). These data suggest that glutamine supplementation of the diet does not increase plasma and tissue glutamine concentrations in healthy growing rats, while the addition of arginine to the diet decreases glutamine body stores.

Protein hydrolysate vs free amino acid-based diets on the nutritional recovery of the starved rat.

BACKGROUND AND AIMS: To test the hypothesis that a peptide-based enteral product was equivalent to a low-fat, free amino acid-based formula in the nutritional and functional recovery of the starved rat. METHODS: Sixteen male Wistar rats were starved for 3 days. Then, rats were randomised to a whey protein hydrolysate-based diet or a free amino acid-based diet and refed for 3 days. The experiment was designed to provide the same energy intake in both groups. The parameters studied included body weight gain, nitrogen retention, plasma free amino acid concentrations, muscle glutamine concentrations and glutathione levels in gut mucosa and liver. RESULTS: Weight gain was statistically higher on the peptide-based diet than on the elemental diet after the refeeding period. This difference in weight gain was associated with a statistically higher nitrogen retention. Plasma and muscle free glutamine concentrations were higher in rats fed the whey protein hydrolysate-based diet than those in rats refed the free amino acid-based diet, even though the glutamine intake was higher in the latter group. Glutathione concentrations in liver and gut mucosa were similar in the groups. CONCLUSION: We conclude that enteral diets containing peptides were more effective than a diet containing free amino acids in the nutritional recovery of the starved rat.

Food deprivation and refeeding influence growth, nutrient retention and functional recovery of rats.

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.