p-Synephrine Suppresses Glucose Production but Not Lipid Accumulation in H4IIE Liver Cells
Identifieur interne : 000635 ( Pmc/Checkpoint ); précédent : 000634; suivant : 000636p-Synephrine Suppresses Glucose Production but Not Lipid Accumulation in H4IIE Liver Cells
Auteurs : Zhigang Cui ; Youngil Lee ; Youngki Lee ; Deokbae ParkSource :
- Journal of Medicinal Food [ 1096-620X ] ; 2015.
Abstract
Url:
DOI: 10.1089/jmf.2013.3133
PubMed: 25379695
PubMed Central: 4281838
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en"><italic>p</italic>-Synephrine Suppresses Glucose Production but Not Lipid Accumulation in H4IIE Liver Cells</title><author><name sortKey="Cui, Zhigang" sort="Cui, Zhigang" uniqKey="Cui Z" first="Zhigang" last="Cui">Zhigang Cui</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Lee, Youngil" sort="Lee, Youngil" uniqKey="Lee Y" first="Youngil" last="Lee">Youngil Lee</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Lee, Youngki" sort="Lee, Youngki" uniqKey="Lee Y" first="Youngki" last="Lee">Youngki Lee</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Park, Deokbae" sort="Park, Deokbae" uniqKey="Park D" first="Deokbae" last="Park">Deokbae Park</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25379695</idno><idno type="pmc">4281838</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4281838</idno><idno type="RBID">PMC:4281838</idno><idno type="doi">10.1089/jmf.2013.3133</idno><date when="2015">2015</date><idno type="wicri:Area/Pmc/Corpus">000C68</idno><idno type="wicri:Area/Pmc/Curation">000C67</idno><idno type="wicri:Area/Pmc/Checkpoint">000635</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main"><italic>p</italic>-Synephrine Suppresses Glucose Production but Not Lipid Accumulation in H4IIE Liver Cells</title><author><name sortKey="Cui, Zhigang" sort="Cui, Zhigang" uniqKey="Cui Z" first="Zhigang" last="Cui">Zhigang Cui</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Lee, Youngil" sort="Lee, Youngil" uniqKey="Lee Y" first="Youngil" last="Lee">Youngil Lee</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Lee, Youngki" sort="Lee, Youngki" uniqKey="Lee Y" first="Youngki" last="Lee">Youngki Lee</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Park, Deokbae" sort="Park, Deokbae" uniqKey="Park D" first="Deokbae" last="Park">Deokbae Park</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Medicinal Food</title><idno type="ISSN">1096-620X</idno><idno type="eISSN">1557-7600</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Abstract</title><p><italic>p</italic>-Synephrine, the primary protoalkaloid in the extract of bitter orange and other citrus species, has gained interest due to its lipolytic activity in adipose tissues. We previously found that <italic>p</italic>-synephrine stimulates glucose consumption via AMP-activated protein kinase (AMPK) in L6 skeletal muscle cells. This study investigated the effect of <italic>p</italic>-synephrine on glucose production and lipid accumulation in H4IIE rat liver cells. Glucose production was increased in H4llE cells that were incubated in glucose-free medium but decreased dose dependently (1–100 <italic>μ</italic>M) with <italic>p</italic>-synephrine treatment. Protein levels of glucose-6-phosphatase (G6Pase) and phosphoenol pyruvate carboxykinase (PEPCK) were also decreased by treatment (4 h) with <italic>p</italic>-synephrine. Antagonists against <italic>α</italic>- and <italic>β</italic>-adrenergic receptors (phentolamine and propranolol) and other inhibitors against signaling molecules did not interrupt <italic>p</italic>-synephrine-induced suppression in glucose production. However, H7 (an inhibitor of serine/threonine kinases PKA, PKC, and PKG) significantly blocked <italic>p</italic>-synephrine-induced suppression of glucose production and further increased basal glucose production. Unlike the suppressive effect on glucose production, <italic>p</italic>-synephrine failed to affect palmitic acid-induced cytoplasmic lipid accumulation. Protein levels of fatty acid synthase (FAS) and phosphorylation levels of AMPK and ACC were not changed by <italic>p</italic>-synephrine. Altogether, <italic>p</italic>-synephrine can suppress glucose production but does not affect lipid accumulation in H4IIE liver cells.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Med Food</journal-id><journal-id journal-id-type="iso-abbrev">J Med Food</journal-id><journal-id journal-id-type="publisher-id">jmf</journal-id><journal-title-group><journal-title>Journal of Medicinal Food</journal-title></journal-title-group><issn pub-type="ppub">1096-620X</issn><issn pub-type="epub">1557-7600</issn><publisher><publisher-name>Mary Ann Liebert, Inc.</publisher-name><publisher-loc>140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25379695</article-id><article-id pub-id-type="pmc">4281838</article-id><article-id pub-id-type="publisher-id">10.1089/jmf.2013.3133</article-id><article-id pub-id-type="doi">10.1089/jmf.2013.3133</article-id><article-categories><subj-group subj-group-type="heading"><subject>Full Communications</subject></subj-group></article-categories><title-group><article-title><italic>p</italic>-Synephrine Suppresses Glucose Production but Not Lipid Accumulation in H4IIE Liver Cells</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Cui</surname><given-names>Zhigang</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Youngil</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Youngki</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Park</surname><given-names>Deokbae</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><aff id="aff1"><label><sup>1</sup></label>Department of Histology and Embryology,<institution>Hainan Medical University</institution>, Haikou,<country>China</country>.</aff><aff id="aff2"><label><sup>2</sup></label><institution>Dankook University Medical College</institution>, Cheonan-Si, Korea.</aff><aff id="aff3"><label><sup>3</sup></label>Department of Histology, School of Medicine, Institute of Medical Science,<institution>Jeju National University</institution>, Jeju, Korea.</aff></contrib-group><author-notes><corresp><italic>Address correspondence to: Deokbae Park, PhD, Department of Histology, School of Medicine, Institute of Medical Science,</italic><institution><italic>Jeju National University</italic></institution><italic>, Jeju 690-756, Korea, E-mail:</italic><email xlink:href="mailto:parkdb@jejunu.ac.kr">parkdb@jejunu.ac.kr</email></corresp></author-notes><pub-date pub-type="ppub"><day>01</day><month>1</month><year>2015</year><pmc-comment>string-date: January 2015</pmc-comment>
</pub-date><volume>18</volume><issue>1</issue><fpage>76</fpage><lpage>82</lpage><history><date date-type="received"><day>17</day><month>12</month><year>2013</year><pmc-comment>string-date: Manuscript received 17 December 2013</pmc-comment>
</date><date date-type="accepted"><day>26</day><month>8</month><year>2014</year><pmc-comment>string-date: Revision accepted 26 August 2014</pmc-comment>
</date></history><permissions><copyright-statement>Copyright 2015, Mary Ann Liebert, Inc. and Korean Society of Food Science and Nutrition</copyright-statement><copyright-year>2015</copyright-year></permissions><self-uri content-type="pdf" xlink:type="simple" xlink:href="jmf.2013.3133.pdf"></self-uri><abstract><title>Abstract</title><p><italic>p</italic>-Synephrine, the primary protoalkaloid in the extract of bitter orange and other citrus species, has gained interest due to its lipolytic activity in adipose tissues. We previously found that <italic>p</italic>-synephrine stimulates glucose consumption via AMP-activated protein kinase (AMPK) in L6 skeletal muscle cells. This study investigated the effect of <italic>p</italic>-synephrine on glucose production and lipid accumulation in H4IIE rat liver cells. Glucose production was increased in H4llE cells that were incubated in glucose-free medium but decreased dose dependently (1–100 <italic>μ</italic>M) with <italic>p</italic>-synephrine treatment. Protein levels of glucose-6-phosphatase (G6Pase) and phosphoenol pyruvate carboxykinase (PEPCK) were also decreased by treatment (4 h) with <italic>p</italic>-synephrine. Antagonists against <italic>α</italic>- and <italic>β</italic>-adrenergic receptors (phentolamine and propranolol) and other inhibitors against signaling molecules did not interrupt <italic>p</italic>-synephrine-induced suppression in glucose production. However, H7 (an inhibitor of serine/threonine kinases PKA, PKC, and PKG) significantly blocked <italic>p</italic>-synephrine-induced suppression of glucose production and further increased basal glucose production. Unlike the suppressive effect on glucose production, <italic>p</italic>-synephrine failed to affect palmitic acid-induced cytoplasmic lipid accumulation. Protein levels of fatty acid synthase (FAS) and phosphorylation levels of AMPK and ACC were not changed by <italic>p</italic>-synephrine. Altogether, <italic>p</italic>-synephrine can suppress glucose production but does not affect lipid accumulation in H4IIE liver cells.</p></abstract><kwd-group kwd-group-type="author"><title><bold>Key Words:</bold> </title><kwd><italic>glucose production</italic></kwd><kwd><italic>H4IIE liver cells</italic></kwd><kwd><italic>lipid accumulation</italic></kwd><kwd><bold>p</bold><bold><italic>-synephrine</italic></bold></kwd></kwd-group><counts><fig-count count="4"></fig-count><ref-count count="30"></ref-count><page-count count="7"></page-count></counts></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Cui, Zhigang" sort="Cui, Zhigang" uniqKey="Cui Z" first="Zhigang" last="Cui">Zhigang Cui</name><name sortKey="Lee, Youngil" sort="Lee, Youngil" uniqKey="Lee Y" first="Youngil" last="Lee">Youngil Lee</name><name sortKey="Lee, Youngki" sort="Lee, Youngki" uniqKey="Lee Y" first="Youngki" last="Lee">Youngki Lee</name><name sortKey="Park, Deokbae" sort="Park, Deokbae" uniqKey="Park D" first="Deokbae" last="Park">Deokbae Park</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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