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  4. Protective Effects of Glutamine and Leucine Supplementation on Sepsis-Induced Skeletal Muscle Injuries
 
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Protective Effects of Glutamine and Leucine Supplementation on Sepsis-Induced Skeletal Muscle Injuries

Journal
International journal of molecular sciences
Journal Volume
22
Journal Issue
23
Date Issued
2021-11-30
Author(s)
Hou, Yu-Chen
Pai, Man-Hui
JIN-MING WU  
PO-JEN YANG  
PO-CHU LEE  
KUEN-YUAN CHEN  
Yeh, Sung-Ling
MING-TSAN LIN  
DOI
10.3390/ijms222313003
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/604766
URL
https://scholars.lib.ntu.edu.tw/handle/123456789/604169
Abstract
This study investigated the effects of l-glutamine (Gln) and/or l-leucine (Leu) administration on sepsis-induced skeletal muscle injuries. C57BL/6J mice were subjected to cecal ligation and puncture to induce polymicrobial sepsis and then given an intraperitoneal injection of Gln, Leu, or Gln plus Leu beginning at 1 h after the operation with re-injections every 24 h. All mice were sacrificed on either day 1 or day 4 after the operation. Blood and muscles were collected for analysis of inflammation and oxidative damage-related biomolecules. Results indicated that both Gln and Leu supplementation alleviated sepsis-induced skeletal muscle damage by reducing monocyte infiltration, calpain activity, and mRNA expression levels of inflammatory cytokines and hypoxia-inducible factor-1α. Furthermore, septic mice treated with Gln had higher percentages of blood anti-inflammatory monocytes and muscle M2 macrophages, whereas Leu treatment enhanced the muscle expressions of mitochondrion-related genes. However, there were no synergistic effects when Gln and Leu were simultaneously administered. These findings suggest that both Gln and Leu had prominent abilities to attenuate inflammation and degradation of skeletal muscles in the early and/or late phases of sepsis. Moreover, Gln promoted the switch of leukocytes toward an anti-inflammatory phenotype, while Leu treatment maintained muscle bioenergetic function.
Subjects
calpain; hypoxia-inducible factor-1α; macrophage; mitochondria; monocyte
SDGs

[SDGs]SDG3

Publisher
MDPI
Type
journal article

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