Amino acid homeostasis and signalling in mammalian cells and organisms

Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved through exchange of essential amino acids with non-essential amino acids and the transfer of amino groups from oxidised amino acids to amino aci...

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Veröffentlicht in:	Biochemical journal Jg. 474; H. 12; S. 1935
Hauptverfasser:	Bröer, Stefan, Bröer, Angelika
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England 15.06.2017
Schlagworte:	Activating Transcription Factor 4 - metabolism Amino Acids - metabolism Animals Appetite Regulation Autophagy Biological Transport Central Nervous System - metabolism Central Nervous System - secretion Diet - adverse effects Fasting - metabolism Gene Expression Regulation Homeostasis Humans Malnutrition - etiology Malnutrition - metabolism Mechanistic Target of Rapamycin Complex 1 Models, Biological Multiprotein Complexes - metabolism Neurons - metabolism Neurons - secretion Oxidation-Reduction Postprandial Period Protein-Serine-Threonine Kinases - metabolism Signal Transduction TOR Serine-Threonine Kinases - metabolism amino acid transporters amino acid metabolism starvation signalling
ISSN:	1470-8728, 1470-8728
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Abstract	Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved through exchange of essential amino acids with non-essential amino acids and the transfer of amino groups from oxidised amino acids to amino acid biosynthesis. This homeostatic condition is maintained through an active mTORC1 complex. Under amino acid depletion, mTORC1 is inactivated. This increases the breakdown of cellular proteins through autophagy and reduces protein biosynthesis. The general control non-derepressable 2/ATF4 pathway may be activated in addition, resulting in transcription of genes involved in amino acid transport and biosynthesis of non-essential amino acids. Metabolism is autoregulated to minimise oxidation of amino acids. Systemic amino acid levels are also tightly regulated. Food intake briefly increases plasma amino acid levels, which stimulates insulin release and mTOR-dependent protein synthesis in muscle. Excess amino acids are oxidised, resulting in increased urea production. Short-term fasting does not result in depletion of plasma amino acids due to reduced protein synthesis and the onset of autophagy. Owing to the fact that half of all amino acids are essential, reduction in protein synthesis and amino acid oxidation are the only two measures to reduce amino acid demand. Long-term malnutrition causes depletion of plasma amino acids. The CNS appears to generate a protein-specific response upon amino acid depletion, resulting in avoidance of an inadequate diet. High protein levels, in contrast, contribute together with other nutrients to a reduction in food intake.
AbstractList	Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved through exchange of essential amino acids with non-essential amino acids and the transfer of amino groups from oxidised amino acids to amino acid biosynthesis. This homeostatic condition is maintained through an active mTORC1 complex. Under amino acid depletion, mTORC1 is inactivated. This increases the breakdown of cellular proteins through autophagy and reduces protein biosynthesis. The general control non-derepressable 2/ATF4 pathway may be activated in addition, resulting in transcription of genes involved in amino acid transport and biosynthesis of non-essential amino acids. Metabolism is autoregulated to minimise oxidation of amino acids. Systemic amino acid levels are also tightly regulated. Food intake briefly increases plasma amino acid levels, which stimulates insulin release and mTOR-dependent protein synthesis in muscle. Excess amino acids are oxidised, resulting in increased urea production. Short-term fasting does not result in depletion of plasma amino acids due to reduced protein synthesis and the onset of autophagy. Owing to the fact that half of all amino acids are essential, reduction in protein synthesis and amino acid oxidation are the only two measures to reduce amino acid demand. Long-term malnutrition causes depletion of plasma amino acids. The CNS appears to generate a protein-specific response upon amino acid depletion, resulting in avoidance of an inadequate diet. High protein levels, in contrast, contribute together with other nutrients to a reduction in food intake.Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved through exchange of essential amino acids with non-essential amino acids and the transfer of amino groups from oxidised amino acids to amino acid biosynthesis. This homeostatic condition is maintained through an active mTORC1 complex. Under amino acid depletion, mTORC1 is inactivated. This increases the breakdown of cellular proteins through autophagy and reduces protein biosynthesis. The general control non-derepressable 2/ATF4 pathway may be activated in addition, resulting in transcription of genes involved in amino acid transport and biosynthesis of non-essential amino acids. Metabolism is autoregulated to minimise oxidation of amino acids. Systemic amino acid levels are also tightly regulated. Food intake briefly increases plasma amino acid levels, which stimulates insulin release and mTOR-dependent protein synthesis in muscle. Excess amino acids are oxidised, resulting in increased urea production. Short-term fasting does not result in depletion of plasma amino acids due to reduced protein synthesis and the onset of autophagy. Owing to the fact that half of all amino acids are essential, reduction in protein synthesis and amino acid oxidation are the only two measures to reduce amino acid demand. Long-term malnutrition causes depletion of plasma amino acids. The CNS appears to generate a protein-specific response upon amino acid depletion, resulting in avoidance of an inadequate diet. High protein levels, in contrast, contribute together with other nutrients to a reduction in food intake. Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved through exchange of essential amino acids with non-essential amino acids and the transfer of amino groups from oxidised amino acids to amino acid biosynthesis. This homeostatic condition is maintained through an active mTORC1 complex. Under amino acid depletion, mTORC1 is inactivated. This increases the breakdown of cellular proteins through autophagy and reduces protein biosynthesis. The general control non-derepressable 2/ATF4 pathway may be activated in addition, resulting in transcription of genes involved in amino acid transport and biosynthesis of non-essential amino acids. Metabolism is autoregulated to minimise oxidation of amino acids. Systemic amino acid levels are also tightly regulated. Food intake briefly increases plasma amino acid levels, which stimulates insulin release and mTOR-dependent protein synthesis in muscle. Excess amino acids are oxidised, resulting in increased urea production. Short-term fasting does not result in depletion of plasma amino acids due to reduced protein synthesis and the onset of autophagy. Owing to the fact that half of all amino acids are essential, reduction in protein synthesis and amino acid oxidation are the only two measures to reduce amino acid demand. Long-term malnutrition causes depletion of plasma amino acids. The CNS appears to generate a protein-specific response upon amino acid depletion, resulting in avoidance of an inadequate diet. High protein levels, in contrast, contribute together with other nutrients to a reduction in food intake.
Author	Bröer, Angelika Bröer, Stefan
Author_xml	– sequence: 1 givenname: Stefan surname: Bröer fullname: Bröer, Stefan email: stefan.broeer@anu.edu.au organization: Research School of Biology, Australian National University, Linnaeus Way 134, Canberra, ACT 2601, Australia stefan.broeer@anu.edu.au – sequence: 2 givenname: Angelika surname: Bröer fullname: Bröer, Angelika organization: Research School of Biology, Australian National University, Linnaeus Way 134, Canberra, ACT 2601, Australia
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/28546457$$D View this record in MEDLINE/PubMed
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Snippet	Cells have a constant turnover of proteins that recycle most amino acids over time. Net loss is mainly due to amino acid oxidation. Homeostasis is achieved...
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SubjectTerms	Activating Transcription Factor 4 - metabolism Amino Acids - metabolism Animals Appetite Regulation Autophagy Biological Transport Central Nervous System - metabolism Central Nervous System - secretion Diet - adverse effects Fasting - metabolism Gene Expression Regulation Homeostasis Humans Malnutrition - etiology Malnutrition - metabolism Mechanistic Target of Rapamycin Complex 1 Models, Biological Multiprotein Complexes - metabolism Neurons - metabolism Neurons - secretion Oxidation-Reduction Postprandial Period Protein-Serine-Threonine Kinases - metabolism Signal Transduction TOR Serine-Threonine Kinases - metabolism
Title	Amino acid homeostasis and signalling in mammalian cells and organisms
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