Dietary arginine supplementation increases growth of neonatal pigs, but the underlying mechanisms are unknown. This study was conducted to test the hypothesis that the arginine treatment activates translation initiation factors and protein synthesis in skeletal muscle. Piglets were fed milk-based diets supplemented with 0 or 0.6% L-arginine between 7 and 14 d of age. Following a 7-d period of arginine supplementation, at 1 h after the last meal, jugular venous blood samples were obtained for metabolite analysis, whereas longissimus muscle and liver were collected to determine the abundance and phosphorylation state of the mammalian target of the rapamycin (mTOR), ribosomal protein S6 kinase 1 (S6K1), eukaryotic initiation factor (eIF) 4E-binding protein-1 (4E-BP1), eIF4E, and eIF4G. Fractional rates of protein synthesis were measured in muscle and liver using the [(3)H]phenylalanine flooding-dose technique. Arginine supplementation increased (P < 0.05) daily gain, the plasma insulin concentration, and protein synthesis in skeletal muscle but not in liver. The arginine treatment enhanced the formation of the active eIF4E x eIF4G complex but reduced the amount of the inactive 4E-BP1 x eIF4E complex in muscle. These changes were associated with elevated levels of phosphorylated mTOR and 4E-BP1 in muscle of arginine-supplemented piglets (P < 0.05). Neither the total amounts nor phosphorylation levels of the translation initiation factors in the liver differed between control and arginine-supplemented piglets. Collectively, these results suggest that dietary arginine supplementation increases mTOR signaling activity in skeletal muscle, but not in liver, of milk-fed neonatal pigs. The findings provide a molecular mechanism for explaining the previous observation that increased circulating arginine stimulated muscle protein synthesis and promoted weight gain in neonatal pigs.
Recent work with young pigs shows that reducing dietary protein intake can improve gut function after weaning but results in inadequate provision of essential amino acids for muscle growth. Because acute administration of L-leucine stimulates protein synthesis in piglet muscle, the present study tested the hypothesis that supplementing L-leucine to a low-protein diet may maintain the activation of translation initiation factors and adequate protein synthesis in multiple organs of post-weaning pigs. Eighteen 21-day pigs (Duroc×Landrace×Yorkshire) were fed low-protein diets (16.9% crude protein) supplemented with 0, 0.27 or 0.55% L-leucine (total leucine contents in the diets being 1.34, 1.61 or 1.88%, respectively). At 35 days of age, protein synthesis was determined using the [2H] phenylalanine flooding-dose technique. Additionally, total and phosphorylated levels of mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase 1 (S6K1), and eIF4E-binding protein-1 (4E-BP1) were measured in longissimus muscle and liver. Compared with the control group, dietary supplementation with 0.55% L-leucine for 2 weeks increased (P<0.05): (1) the phosphorylated levels of S6K1 and 4E-BP1; (2) protein synthesis in skeletal muscle, liver, the heart, kidney, pancreas, spleen, and stomach; and (3) daily weight gain by 61%. Dietary supplementation with 0.27% L-leucine enhanced (P<0.05) protein synthesis in proximal small intestine, kidney and pancreas. These novel findings provide a molecular basis for designing effective nutritional means to increase the efficiency of nutrient utilization for protein accretion in neonates.
This study was conducted to determine the effect of dietary supplementation of a low dose of chito-oligosaccharide (COS) on intestinal morphology, immune response, antioxidant capacity, and barrier function in weaned piglets. A total of 120 weaned pigs (21 d of age; 7.86 ± 0.22 kg average BW) were randomly assigned (6 pens/diet; 10 pigs/pen) to 2 dietary treatments consisting of a basal diet (negative control) or the basal diet supplemented with COS (30 mg/kg) for a 14-d period. Six randomly selected piglets from each treatment were killed for blood and tissue sampling. No significant differences were observed in ADG, ADFI, and G:F between treatment and the control group. Piglets fed the COS-supplemented diet had greater ( < 0.05) stomach pH than those fed the control diet on d 14 postweaning. Dietary supplementation with COS reduced villus height ( < 0.05) and villus height:crypt depth ( < 0.05) in the ileum. Dietary COS supplementation tended to reduce villus height in the duodenum ( = 0.065) and jejunum ( = 0.058). There was no effect on crypt depth in the intestinal segments of treatment group. Piglets fed the COS-supplemented diet increased ( < 0.05) the number of intraepithelial lymphocytes in duodenum or jejunum and goblet cells of ileum. However, COS decreased ( < 0.05) the number of intraepithelial lymphocytes in ileum of weaned piglets. The concentrations of IL-10 (duodenum, jejunum, and ileum) and secretory immunoglobulin (SIgA; duodenum and ileum) were higher in piglets fed the COS-supplemented diet compared with control ( < 0.05). Dietary COS supplementation reduced ( < 0.05) the concentration of total antioxidant capacity and superoxide dismutase of the jejunum or ileum. The mRNA expression of occludin in the ileum and ZO-1 in jejunum and ileum had a significant change in piglets fed the COS-supplemented diet compared with the control group ( < 0.05). In conclusion, these results indicated that dietary COS supplementation at 30 mg/kg had no effects on promoting growth performance and tended to reduce villus height in the duodenum or jejunum of weaned piglets. The results further showed that supplemental COS at this level may cause an immune and oxidative stress response in small intestine and have compromised the intestinal barrier integrity in weaned piglets. The research will provide guidance on the low dosage of COS supplementation on weaning pigs.
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