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Effects of Lysine deficiency and Lys‐Lys dipeptide on cellular apoptosis and amino acids metabolism
Author(s) -
Yin Jie,
Li Yuying,
Han Hui,
Zheng Jie,
Wang Lijian,
Ren Wenkai,
Chen Shuai,
Wu Fei,
Fang Rejun,
Huang Xingguo,
Li Chunyong,
Tan Bie,
Xiong Xia,
Zhang Yuzhe,
Liu Gang,
Yao Jiming,
Li Tiejun,
Yin Yulong
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600754
Subject(s) - dipeptide , lysine , apoptosis , metabolism , amino acid , chemistry , biochemistry , microbiology and biotechnology , biology
Scope Lysine (Lys) is a common limiting amino acids (AA) for humans and animals and plays an important role in cell proliferation and metabolism, while metabolism of Lys deficiency and its dipeptide is still obscure. Thus, this study mainly investigated the effects of Lys deficiency and Lys‐Lys dipeptide on apoptosis and AA metabolism in vitro and in vivo models. Methods and results Lys deficiency induced cell‐cycle arrest and apoptosis and upregulated Lys transporters in vitro and in vivo. SLC7A11, a cystine‐glutamate antiporter, was markedly upregulated by Lys deficiency and then further mediated cystine uptake and glutamate release, which was negatively regulated by cystine and glutamate transporters. Meanwhile, Lys deprivation upregulated pept1 expression, which might improve Lys‐Lys dipeptide absorption to compensate for the reduced Lys availability. Lys‐Lys dipeptide alleviated Lys deficiency induced cell‐cycle arrest and apoptosis and influenced AA metabolism. Furthermore, the mammalian target of rapamycin signal might be involved in sensing cellular Lys starvation and Lys‐Lys dipeptide. Conclusions Altogether, these studies suggest that Lys deficiency impairs AA metabolism and causes apoptosis. Lys‐Lys dipeptide serves as a Lys source and alleviates Lys deficiency induced cellular imbalance.