ISSN 0371-0874, CN 31-1352/Q

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Research progress on the mechanism of leucine regulation of protein synthesis in aging skeletal muscle through LAT1

KE Yu1,2, DAI Zhi-Qiang3, YANG Ying1,2, WU Hui-Wen1,2, ZHAO Yan1,2, SHANG Hua-Yu4, XIA Zhi1,2,*

1 College of Physical Education and Health, Wenzhou University, Wenzhou 325035, China;2Key Lab of Biohealth Materials and Chemistry of Wenzhou, Wenzhou 325035, China;3School of Physical Education, Nanchang University, Nanchang 330031, China;4School of Sports Medicine and Health, Chengdu Sport University, Chengdu 610041, China

Abstract

Age-related sarcopenia is a degenerative disease characterized by the decline in skeletal muscle mass and function during the aging process. Anabolic resistance, which refers to the diminished response of skeletal muscle to anabolic stimulation from leucine and other nutrients, is a significant contributing factor to its development. Recent studies have suggested that large neutral amino acid-transporter 1 (LAT1/SLC7A5) may play an important role in enhancing leucine's effects on protein synthesis in aging skeletal muscle. In this paper, the structure and function of LAT1 and its key molecules regulating aging skeletal muscle protein synthesis were reviewed, and the potential relationship between LAT1, as a transmembrane transporter of leucine, and protein synthesis in aging skeletal muscle was analyzed. The aim is to explore new mechanisms and insights for prevention and treatment of age-related sarcopenia, and provide reference for the application of relevant targets in clinical translational medicine.

Key words: age-related sarcopenia; anabolic resistance; leucine; large neutral amino acid-transporter 1; skeletal muscle protein synthesis

Received:   Accepted:

Corresponding author: 夏志  E-mail:

Citing This Article:

KE Yu, DAI Zhi-Qiang, YANG Ying, WU Hui-Wen, ZHAO Yan, SHANG Hua-Yu, XIA Zhi. Research progress on the mechanism of leucine regulation of protein synthesis in aging skeletal muscle through LAT1. Acta Physiol Sin 2024; 76 (6): 1001-1018 (in Chinese with English abstract).