Amino Acid Sensing in Skeletal Muscle

Tatiana Moro, Scott M. Ebert, Christopher M. Adams, Blake B. Rasmussen

Research output: Contribution to journalReview article

27 Scopus citations


Aging impairs skeletal muscle protein synthesis, leading to muscle weakness and atrophy. However, the underlying molecular mechanisms remain poorly understood. Here, we review evidence that mammalian/mechanistic target of rapamycin complex 1 (mTORC1)-mediated and activating transcription factor 4 (ATF4)-mediated amino acid (AA) sensing pathways, triggered by impaired AA delivery to aged skeletal muscle, may play important roles in skeletal muscle aging. Interventions that alleviate age-related impairments in muscle protein synthesis, strength, and/or muscle mass appear to do so by reversing age-related changes in skeletal muscle AA delivery, mTORC1 activity, and/or ATF4 activity. An improved understanding of the mechanisms and roles of AA sensing pathways in skeletal muscle may lead to evidence-based strategies to attenuate sarcopenia.

Original languageEnglish (US)
Pages (from-to)796-806
Number of pages11
JournalTrends in Endocrinology and Metabolism
Issue number11
StatePublished - Nov 1 2016


  • activating transcription factor 4
  • general control nonderepressible 2
  • leucine
  • mammalian/mechanistic target of rapamycin complex 1
  • tomatidine
  • ursolic acid

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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