Amino Acid Sensing in Skeletal Muscle

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

Research output: Contribution to journalReview articlepeer-review

63 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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