Rapid Sensing of Dietary Amino Acid Deficiency Does Not Require GCN2
Author(s) -
David E. Leib,
Zachary A. Knight
Publication year - 2016
Publication title -
cell reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.264
H-Index - 154
eISSN - 2639-1856
pISSN - 2211-1247
DOI - 10.1016/j.celrep.2016.08.022
Subject(s) - amino acid , kinase , piriform cortex , chemistry , biology , biochemistry , endocrinology , central nervous system
Animals are unable to synthesize the nine essential amino acids (EAAs) and consequently must obtain them from their food. In 2005, two papers proposed an extraordinary mechanism for dietary amino-acid sensing (Hao et al., 2005; Maurin et al., 2005). According to these reports, the consumption of food lacking a single EAA leads to the development of an amino-acid imbalance in the anterior piriform cortex (APC) within minutes. This amino acid imbalance was proposed to be sensed in the APC by activation of the protein kinase GCN2, enabling animals to reject the EAA-deficient food within the first hour of feeding.
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