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Higher Leucine Content in an Essential Amino Acid Solution Enhances Human Skeletal Muscle mTOR Signaling
Author(s) -
Glynn Erin Leigh,
Fry Christopher S,
Timmerman Kyle L,
Dhanani Shaheen,
Drummond Micah J,
Volpi Elena,
Rasmussen Blake B
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.227.3
Subject(s) - leucine , p70 s6 kinase 1 , pi3k/akt/mtor pathway , ingestion , phosphorylation , amino acid , essential amino acid , skeletal muscle , medicine , rptor , endocrinology , signal transduction , biochemistry , biology , chemistry
Essential amino acid (EAA) ingestion stimulates mammalian target of rapamycin (mTOR) signaling in humans. This effect appears to be largely due to the branched‐chain amino acid leucine. We hypothesized that increasing the leucine content of an EAA solution would enhance mTOR signaling to a greater extent as compared to an EAA solution with leucine content typical of high‐quality proteins. Subjects were randomized into two groups, each ingesting 10 grams of EAA but with differing amounts of leucine (18% or 1.8g in EAA group, n=6; 35% or 3.5g in LEU group, n=6). Muscle biopsies were taken at baseline, 1‐, 2‐ and 3‐hr post‐ingestion, and blood was sampled throughout. mTOR signaling was assessed by immunoblotting of biopsies. Phosphorylation of mTOR was increased 1‐hr following nutrient ingestion in both groups, however, the increase tended to be higher in the LEU group. mTOR signaling to downstream effectors S6K1 and 4E‐BP1 was also increased in both groups, though the time course differed between groups. Phosphorylation of eEF2 tended to decrease more at 1‐hr post‐ingestion in the LEU group, and remained dephosporylated 2‐ and 3‐hr post, indicating enhancement of translation elongation. We conclude that increasing leucine content in an EAA solution appears to alter the time course and enhance skeletal muscle mTOR signaling in young human subjects. Supported by NIH/NIAMS grant RO1 AR049877 & NIH/NIA P30 AG024832