Metabolic adaptation of short-living growth hormone transgenic mice to methionine restriction and supplementation.
Identifieur interne : 000242 ( Main/Exploration ); précédent : 000241; suivant : 000243Metabolic adaptation of short-living growth hormone transgenic mice to methionine restriction and supplementation.
Auteurs : Holly M. Brown-Borg [États-Unis] ; Sharlene Rakoczy [États-Unis] ; Joseph A. Wonderlich [États-Unis] ; Kurt E. Borg [États-Unis] ; Lalida Rojanathammanee [États-Unis, Thaïlande]Source :
- Annals of the New York Academy of Sciences [ 1749-6632 ] ; 2018.
Descripteurs français
- KwdFr :
- Adaptation physiologique (MeSH), Animaux (MeSH), Foie (enzymologie), Foie (métabolisme), Glutathion (métabolisme), Hormone de croissance (génétique), Longévité (MeSH), Mâle (MeSH), Méthionine (administration et posologie), Méthionine (métabolisme), Régime alimentaire (MeSH), Souris (MeSH), Souris transgéniques (MeSH).
- MESH :
- administration et posologie : Méthionine.
- enzymologie : Foie.
- génétique : Hormone de croissance.
- métabolisme : Foie, Glutathion, Méthionine.
- Adaptation physiologique, Animaux, Longévité, Mâle, Régime alimentaire, Souris, Souris transgéniques.
English descriptors
- KwdEn :
- MESH :
- chemical , administration & dosage : Methionine.
- chemical , genetics : Growth Hormone.
- chemical , metabolism : Glutathione, Methionine.
- enzymology : Liver.
- metabolism : Liver.
- Adaptation, Physiological, Animals, Diet, Longevity, Male, Mice, Mice, Transgenic.
Abstract
Extension of mammalian health and life span has been achieved using various dietary interventions. We previously reported that restricting dietary methionine (MET) content extends life span only when growth hormone signaling is intact (no life span increase in GH deficiency or GH resistance). To understand the metabolic responses of altered dietary MET in the context of accelerated aging (high GH), the current study evaluated MET and related pathways in short-living GH transgenic (GH Tg) and wild-type mice following 8 weeks of restricted (0.16%), low (0.43%), or enriched (1.3%) MET consumption. Liver MET metabolic enzymes were suppressed in GH Tg compared to diet-matched wild-type mice. MET metabolite levels were differentially affected by GH status and diet. SAM:SAH ratios were markedly higher in GH Tg mice. Glutathione levels were lower in both genotypes consuming 0.16% MET but reduced in GH Tg mice when compared to wild type. Tissue thioredoxin and glutaredoxin were impacted by diet and GH status. The responsiveness to the different MET diets is reflected across many metabolic pathways indicating the importance of GH signaling in the ability to discriminate dietary amino acid levels and alter metabolism and life span.
DOI: 10.1111/nyas.13687
PubMed: 29722030
PubMed Central: PMC7025433
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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We previously reported that restricting dietary methionine (MET) content extends life span only when growth hormone signaling is intact (no life span increase in GH deficiency or GH resistance). To understand the metabolic responses of altered dietary MET in the context of accelerated aging (high GH), the current study evaluated MET and related pathways in short-living GH transgenic (GH Tg) and wild-type mice following 8 weeks of restricted (0.16%), low (0.43%), or enriched (1.3%) MET consumption. Liver MET metabolic enzymes were suppressed in GH Tg compared to diet-matched wild-type mice. MET metabolite levels were differentially affected by GH status and diet. SAM:SAH ratios were markedly higher in GH Tg mice. Glutathione levels were lower in both genotypes consuming 0.16% MET but reduced in GH Tg mice when compared to wild type. Tissue thioredoxin and glutaredoxin were impacted by diet and GH status. The responsiveness to the different MET diets is reflected across many metabolic pathways indicating the importance of GH signaling in the ability to discriminate dietary amino acid levels and alter metabolism and life span.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29722030</PMID><DateCompleted><Year>2019</Year><Month>08</Month><Day>13</Day></DateCompleted><DateRevised><Year>2020</Year><Month>02</Month><Day>18</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1749-6632</ISSN><JournalIssue CitedMedium="Internet"><Volume>1418</Volume><Issue>1</Issue><PubDate><Year>2018</Year><Month>04</Month></PubDate></JournalIssue><Title>Annals of the New York Academy of Sciences</Title><ISOAbbreviation>Ann N Y Acad Sci</ISOAbbreviation></Journal><ArticleTitle>Metabolic adaptation of short-living growth hormone transgenic mice to methionine restriction and supplementation.</ArticleTitle><Pagination><MedlinePgn>118-136</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/nyas.13687</ELocationID><Abstract><AbstractText>Extension of mammalian health and life span has been achieved using various dietary interventions. We previously reported that restricting dietary methionine (MET) content extends life span only when growth hormone signaling is intact (no life span increase in GH deficiency or GH resistance). To understand the metabolic responses of altered dietary MET in the context of accelerated aging (high GH), the current study evaluated MET and related pathways in short-living GH transgenic (GH Tg) and wild-type mice following 8 weeks of restricted (0.16%), low (0.43%), or enriched (1.3%) MET consumption. Liver MET metabolic enzymes were suppressed in GH Tg compared to diet-matched wild-type mice. MET metabolite levels were differentially affected by GH status and diet. SAM:SAH ratios were markedly higher in GH Tg mice. Glutathione levels were lower in both genotypes consuming 0.16% MET but reduced in GH Tg mice when compared to wild type. Tissue thioredoxin and glutaredoxin were impacted by diet and GH status. The responsiveness to the different MET diets is reflected across many metabolic pathways indicating the importance of GH signaling in the ability to discriminate dietary amino acid levels and alter metabolism and life span.</AbstractText><CopyrightInformation>© 2018 New York Academy of Sciences.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brown-Borg</LastName><ForeName>Holly M</ForeName><Initials>HM</Initials><Identifier Source="ORCID">0000-0001-7415-4617</Identifier><AffiliationInfo><Affiliation>Department of Biomedical Sciences, University of North Dakota School of Medicine & Health Sciences, Grand Forks, North Dakota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rakoczy</LastName><ForeName>Sharlene</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, University of North Dakota School of Medicine & Health Sciences, Grand Forks, North Dakota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wonderlich</LastName><ForeName>Joseph A</ForeName><Initials>JA</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, University of North Dakota School of Medicine & Health Sciences, Grand Forks, North Dakota.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychology, George Mason University, Fairfax, Virginia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Borg</LastName><ForeName>Kurt E</ForeName><Initials>KE</Initials><AffiliationInfo><Affiliation>Education Resources, University of North Dakota School of Medicine & Health Sciences, Grand Forks, North Dakota.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rojanathammanee</LastName><ForeName>Lalida</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biomedical Sciences, University of North Dakota School of Medicine & Health Sciences, Grand Forks, North Dakota.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Sports Science, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, Thailand.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K02 AG038509</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AG034206</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Ann N Y Acad Sci</MedlineTA><NlmUniqueID>7506858</NlmUniqueID><ISSNLinking>0077-8923</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9002-72-6</RegistryNumber><NameOfSubstance UI="D013006">Growth Hormone</NameOfSubstance></Chemical><Chemical><RegistryNumber>AE28F7PNPL</RegistryNumber><NameOfSubstance UI="D008715">Methionine</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><MeshHeadingList><MeshHeading><DescriptorName UI="D000222" MajorTopicYN="Y">Adaptation, Physiological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004032" MajorTopicYN="N">Diet</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013006" MajorTopicYN="N">Growth Hormone</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008136" MajorTopicYN="N">Longevity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008715" MajorTopicYN="N">Methionine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">aging</Keyword><Keyword MajorTopicYN="Y">amino acid</Keyword><Keyword MajorTopicYN="Y">glutathione</Keyword><Keyword MajorTopicYN="Y">hormones</Keyword><Keyword MajorTopicYN="Y">metabolomics</Keyword><Keyword MajorTopicYN="Y">mice</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>09</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2018</Year><Month>02</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2018</Year><Month>02</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2018</Year><Month>5</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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