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Trends Endocrinol Metab. 2016 Nov;27(11):796-806. doi: 10.1016/j.tem.2016.06.010. Epub 2016 Jul 19.

Amino Acid Sensing in Skeletal Muscle.

Author information

1
Department of Nutrition and Metabolism, University of Texas Medical Branch, Galveston, TX, USA; Sealy Center on Aging, University of Texas Medical Branch, Galveston, TX, USA.
2
Department of Internal Medicine, University of Iowa, Iowa City, IA, USA; Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA, USA; Iowa City Veterans Affairs Medical Center, Iowa City, IA, USA.
3
Department of Nutrition and Metabolism, University of Texas Medical Branch, Galveston, TX, USA; Sealy Center on Aging, University of Texas Medical Branch, Galveston, TX, USA. Electronic address: blrasmus@utmb.edu.

Abstract

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.

KEYWORDS:

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

PMID:
27444066
PMCID:
PMC5075248
DOI:
10.1016/j.tem.2016.06.010
[Indexed for MEDLINE]
Free PMC Article

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