Eicosapentaenoic Acid (EPA) Modulates Glucose Metabolism by Targeting AMP-Activated Protein Kinase (AMPK) Pathway
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Nami | - |
dc.contributor.author | Kang, Mi Sun | - |
dc.contributor.author | Nam, Miso | - |
dc.contributor.author | Kim, Shin Ae | - |
dc.contributor.author | Hwang, Geum-Sook | - |
dc.contributor.author | Kim, Hyeon Soo | - |
dc.date.accessioned | 2021-09-01T04:48:28Z | - |
dc.date.available | 2021-09-01T04:48:28Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2019-10 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/62593 | - |
dc.description.abstract | EPA, an omega-3 polyunsaturated fatty acid, exerts beneficial effects on human health. However, the molecular mechanisms underlying EPA function are poorly understood. The object was to illuminate molecular mechanism underlying EPA's role. Here, H-1-NMR-based metabolic analysis showed enhanced branched-chain amino acids (BCAAs) and lactate following EPA treatment in skeletal muscle cells. EPA regulated mitochondrial oxygen consumption rate. Furthermore, EPA induced calcium/calmodulin-dependent protein kinase kinase (CaMKK) through the generation of intracellular calcium. This induced the phosphorylation of AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (p38 MAPK) that led to glucose uptake, and the translocation of glucose transporter type 4 (GLUT4) in muscles. In conclusion, EPA exerts benign effects on glucose through the activation of AMPK-p38 MAPK signaling pathways in skeletal muscles. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.subject | CHAIN AMINO-ACIDS | - |
dc.subject | INSULIN-RESISTANCE | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | GLUT4 | - |
dc.subject | TRANSLOCATION | - |
dc.subject | ADIPONECTIN | - |
dc.subject | TRANSPORT | - |
dc.subject | METFORMIN | - |
dc.subject | LACTATE | - |
dc.title | Eicosapentaenoic Acid (EPA) Modulates Glucose Metabolism by Targeting AMP-Activated Protein Kinase (AMPK) Pathway | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Kim, Hyeon Soo | - |
dc.identifier.doi | 10.3390/ijms20194751 | - |
dc.identifier.scopusid | 2-s2.0-85072690745 | - |
dc.identifier.wosid | 000494798300092 | - |
dc.identifier.bibliographicCitation | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, v.20, no.19 | - |
dc.relation.isPartOf | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.title | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | - |
dc.citation.volume | 20 | - |
dc.citation.number | 19 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.subject.keywordPlus | CHAIN AMINO-ACIDS | - |
dc.subject.keywordPlus | INSULIN-RESISTANCE | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | GLUT4 | - |
dc.subject.keywordPlus | TRANSLOCATION | - |
dc.subject.keywordPlus | ADIPONECTIN | - |
dc.subject.keywordPlus | TRANSPORT | - |
dc.subject.keywordPlus | METFORMIN | - |
dc.subject.keywordPlus | LACTATE | - |
dc.subject.keywordAuthor | AMPK | - |
dc.subject.keywordAuthor | EPA | - |
dc.subject.keywordAuthor | GLUT4 | - |
dc.subject.keywordAuthor | oxygen consumption | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
(02841) 서울특별시 성북구 안암로 14502-3290-1114
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.