Role of glucagon on the control of hepatic protein synthesis and degradation in the rat in vivo.
Identifieur interne : 002412 ( PubMed/Corpus ); précédent : 002411; suivant : 002413Role of glucagon on the control of hepatic protein synthesis and degradation in the rat in vivo.
Auteurs : M S Ayuso-Parrilla ; A. Martín-Requero ; J. Pérez-Días ; R. ParrillaSource :
- The Journal of biological chemistry [ 0021-9258 ] ; 1976.
English descriptors
- KwdEn :
- MESH :
- chemical , blood : Urea.
- chemical , metabolism : Proteins, Valine.
- chemical , pharmacology : Glucagon.
- drug effects : Liver, Polyribosomes, Protein Biosynthesis.
- metabolism : Liver, Polyribosomes.
- ultrastructure : Polyribosomes.
- Animals, Kinetics, Male, Rats, Time Factors.
Abstract
The effect of glucagon on hepatic protein systhesis and proteolysis has been investigated. The intraperitoneal administration of 200 mug of glucagon produced an increase of the polypeptide chains completion time which was maximal 5 min after its administration and approached control values at 20 min. The increase of the polypeptides chains completion time observed at 5 min after the hormone administration represents a 38% inhibition of the hepatic protein synthetic rate. When glucagon was continuously supplied by intravascular infusion, maximal inhibition was attained throughout the experiment. This inhibition of protein synthesis brought about by glucagon was accompanied by an increase in the polyribosomal state of aggregation, indicating that the hormone acts mainly if not exclusively, on the elongation or termination step, or both. The administration of glucagon produced also a progressive increase in the hepatic valine concentration. This increase could not be accounted for the the decrease in plasma valine levels, suggesting that the rise in haptic valine concentration is an expression of hepatic proteolysis rather than the result of an accelerated transport of amino acids across the hepatocyte plasma membrane. The different time sequence in the glucagon-induced effects of protein synthesis and proteolysis suggests that both effects are independent and probably mediated by different mechanisms.
PubMed: 1002712
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pubmed:1002712Le document en format XML
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Parrilla</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1976">1976</date><idno type="RBID">pubmed:1002712</idno><idno type="pmid">1002712</idno><idno type="wicri:Area/PubMed/Corpus">002412</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Role of glucagon on the control of hepatic protein synthesis and degradation in the rat in vivo.</title><author><name sortKey="Ayuso Parrilla, M S" sort="Ayuso Parrilla, M S" uniqKey="Ayuso Parrilla M" first="M S" last="Ayuso-Parrilla">M S Ayuso-Parrilla</name></author><author><name sortKey="Martin Requero, A" sort="Martin Requero, A" uniqKey="Martin Requero A" first="A" last="Martín-Requero">A. Martín-Requero</name></author><author><name sortKey="Perez Dias, J" sort="Perez Dias, J" uniqKey="Perez Dias J" first="J" last="Pérez-Días">J. Pérez-Días</name></author><author><name sortKey="Parrilla, R" sort="Parrilla, R" uniqKey="Parrilla R" first="R" last="Parrilla">R. Parrilla</name></author></analytic><series><title level="j">The Journal of biological chemistry</title><idno type="ISSN">0021-9258</idno><imprint><date when="1976" type="published">1976</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Glucagon (pharmacology)</term><term>Kinetics</term><term>Liver (drug effects)</term><term>Liver (metabolism)</term><term>Male</term><term>Polyribosomes (drug effects)</term><term>Polyribosomes (metabolism)</term><term>Polyribosomes (ultrastructure)</term><term>Protein Biosynthesis (drug effects)</term><term>Proteins (metabolism)</term><term>Rats</term><term>Time Factors</term><term>Urea (blood)</term><term>Valine (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Urea</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Proteins</term><term>Valine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Glucagon</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Liver</term><term>Polyribosomes</term><term>Protein Biosynthesis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Liver</term><term>Polyribosomes</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Polyribosomes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Kinetics</term><term>Male</term><term>Rats</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effect of glucagon on hepatic protein systhesis and proteolysis has been investigated. The intraperitoneal administration of 200 mug of glucagon produced an increase of the polypeptide chains completion time which was maximal 5 min after its administration and approached control values at 20 min. The increase of the polypeptides chains completion time observed at 5 min after the hormone administration represents a 38% inhibition of the hepatic protein synthetic rate. When glucagon was continuously supplied by intravascular infusion, maximal inhibition was attained throughout the experiment. This inhibition of protein synthesis brought about by glucagon was accompanied by an increase in the polyribosomal state of aggregation, indicating that the hormone acts mainly if not exclusively, on the elongation or termination step, or both. The administration of glucagon produced also a progressive increase in the hepatic valine concentration. This increase could not be accounted for the the decrease in plasma valine levels, suggesting that the rise in haptic valine concentration is an expression of hepatic proteolysis rather than the result of an accelerated transport of amino acids across the hepatocyte plasma membrane. The different time sequence in the glucagon-induced effects of protein synthesis and proteolysis suggests that both effects are independent and probably mediated by different mechanisms.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">1002712</PMID><DateCreated><Year>1977</Year><Month>02</Month><Day>16</Day></DateCreated><DateCompleted><Year>1977</Year><Month>02</Month><Day>16</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0021-9258</ISSN><JournalIssue CitedMedium="Print"><Volume>251</Volume><Issue>24</Issue><PubDate><Year>1976</Year><Month>Dec</Month><Day>25</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J. Biol. Chem.</ISOAbbreviation></Journal><ArticleTitle>Role of glucagon on the control of hepatic protein synthesis and degradation in the rat in vivo.</ArticleTitle><Pagination><MedlinePgn>7785-90</MedlinePgn></Pagination><Abstract><AbstractText>The effect of glucagon on hepatic protein systhesis and proteolysis has been investigated. The intraperitoneal administration of 200 mug of glucagon produced an increase of the polypeptide chains completion time which was maximal 5 min after its administration and approached control values at 20 min. The increase of the polypeptides chains completion time observed at 5 min after the hormone administration represents a 38% inhibition of the hepatic protein synthetic rate. When glucagon was continuously supplied by intravascular infusion, maximal inhibition was attained throughout the experiment. This inhibition of protein synthesis brought about by glucagon was accompanied by an increase in the polyribosomal state of aggregation, indicating that the hormone acts mainly if not exclusively, on the elongation or termination step, or both. The administration of glucagon produced also a progressive increase in the hepatic valine concentration. This increase could not be accounted for the the decrease in plasma valine levels, suggesting that the rise in haptic valine concentration is an expression of hepatic proteolysis rather than the result of an accelerated transport of amino acids across the hepatocyte plasma membrane. The different time sequence in the glucagon-induced effects of protein synthesis and proteolysis suggests that both effects are independent and probably mediated by different mechanisms.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ayuso-Parrilla</LastName><ForeName>M S</ForeName><Initials>MS</Initials></Author><Author ValidYN="Y"><LastName>Martín-Requero</LastName><ForeName>A</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Pérez-Días</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Parrilla</LastName><ForeName>R</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011506">Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>8W8T17847W</RegistryNumber><NameOfSubstance UI="D014508">Urea</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-92-5</RegistryNumber><NameOfSubstance UI="D005934">Glucagon</NameOfSubstance></Chemical><Chemical><RegistryNumber>HG18B9YRS7</RegistryNumber><NameOfSubstance UI="D014633">Valine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005934">Glucagon</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007700">Kinetics</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008099">Liver</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011132">Polyribosomes</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000648">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014176">Protein Biosynthesis</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011506">Proteins</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051381">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013997">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014508">Urea</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014633">Valine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1976</Year><Month>12</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1976</Year><Month>12</Month><Day>25</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1976</Year><Month>12</Month><Day>25</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1002712</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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