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Acute Effects of Enteral Leucine Supplementation of a Low Protein Diet on Muscle Protein Synthesis in Neonatal Pigs
Author(s) -
Murgas Torrazza Roberto,
Suryawan Agus,
Orellana Renan,
Gazzaneo Carolina,
Nguyen Hanh,
Almonaci Rose,
Davis Teresa
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.33.1
Subject(s) - protein biosynthesis , leucine , medicine , enteral administration , endocrinology , low protein diet , biology , amino acid , p70 s6 kinase 1 , skeletal muscle , phosphorylation , biochemistry , protein kinase b , parenteral nutrition
Protein synthesis and eukaryotic initiation factor (eIF) activation are increased in skeletal muscle of neonatal pigs parenterally infused with insulin and amino acids (AA), particularly leucine. We hypothesized that enteral Leu supplementation of a low protein diets in neonatal pigs will acutely increase muscle protein synthesis to a rate similar to that achieved by feeding a high protein (HP) diet. Fasted 5‐d‐old piglets (n=12) were gavage fed at 0 and 60 min either: 1) low protein diet (LP), 2) low protein diet supplemented with Leu (LP+L) to equal HP diet, or 3) HP diet. Diets were isocaloric and lactose was equal. Fractional protein synthesis rates and translational initiation control mechanisms were examined 90 min after feeding. Muscle protein synthesis increased in the LP+L group compared to the LP group alone and did not differ from the HP group. LP+L and HP increased the phosphorylation of S6K1, eIF4G, and 4E binding protein‐1 (4E‐BP1), decreased inactive 4E‐BP1▸eIF4E complex abundance, and increased active eIF4E▸eIF4G complex formation in muscle. There were no difference between groups in PKB phosphorylation. Our results suggest that low protein diets supplemented with leucine stimulates muscle protein synthesis to a rate similar to that achieved by high protein diets and this stimulation involves activation of mTOR downstream effectors. (Supported by Ajinomoto Amino Acid Research Program and USDA 58‐6250‐6‐001).

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