Publication:
The Antagonist Effect of Arachidonic Acid on GLUT4 Gene Expression by Nuclear Receptor Type II Regulation.

dc.contributor.authorMoreno-Santos, Inmaculada
dc.contributor.authorGarcia-Serrano, Sara
dc.contributor.authorBoughanem, Hatim
dc.contributor.authorGarrido-Sanchez, Lourdes
dc.contributor.authorTinahones, Francisco José
dc.contributor.authorGarcia-Fuentes, Eduardo
dc.contributor.authorMacias-Gonzalez, Manuel
dc.date.accessioned2023-01-25T13:31:49Z
dc.date.available2023-01-25T13:31:49Z
dc.date.issued2019-02-22
dc.description.abstractObesity is a complex disease that has a strong association with diet and lifestyle. Dietary factors can influence the expression of key genes connected to insulin resistance, lipid metabolism, and adipose tissue composition. In this study, our objective was to determine gene expression and fatty acid (FA) profiles in visceral adipose tissue (VAT) from lean and morbidly obese individuals. We also aimed to study the agonist effect of dietary factors on glucose metabolism. Lean and low and high insulin resistance morbidly obese subjects (LIR-MO and HIR-MO) were included in this study. The gene expression of liver X receptor type alpha (LXR-α) and glucose transporter type 4 (GLUT4) and the FA profiles in VAT were determined. Additionally, the in vivo and in vitro agonist effects of oleic acid (OA), linoleic acid (LA), and arachidonic acid (AA) by peroxisome proliferator-activated receptor type gamma 2 (PPAR-γ2) on the activity of GLUT4 were studied. Our results showed a dysregulation of GLUT4 and LXR-α in VAT of morbidly obese subjects. In addition, a specific FA profile for morbidly obese individuals was found. Finally, AA was an PPAR-γ2 agonist that activates the expression of GLUT4. Our study suggests a dysregulation of LXR-α and GLUT4 expression in VAT of morbidly obese individuals. FA profiles in VAT could elucidate their possible role in lipolysis and adipogenesis. Finally, AA binds to PPAR-γ2 to activate the expression of GLUT4 in the HepG2 cell line, showing an alternative insulin-independent activation of GLUT4.
dc.identifier.doi10.3390/ijms20040963
dc.identifier.essn1422-0067
dc.identifier.pmcPMC6412497
dc.identifier.pmid30813326
dc.identifier.pubmedURLhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412497/pdf
dc.identifier.unpaywallURLhttps://www.mdpi.com/1422-0067/20/4/963/pdf?version=1550834977
dc.identifier.urihttp://hdl.handle.net/10668/13635
dc.issue.number4
dc.journal.titleInternational journal of molecular sciences
dc.journal.titleabbreviationInt J Mol Sci
dc.language.isoen
dc.organizationHospital Universitario Virgen de la Victoria
dc.organizationHospital Universitario Virgen de la Victoria
dc.organizationHospital Universitario Regional de Málaga
dc.organizationInstituto de Investigación Biomédica de Málaga-IBIMA
dc.pubmedtypeJournal Article
dc.rightsAttribution 4.0 International
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectGLUT4
dc.subjectLXR-α
dc.subjectPPAR-γ2
dc.subjectarachidonic acid
dc.subjectfatty acids
dc.subjectinsulin resistance
dc.subjectobesity
dc.subject.meshAdult
dc.subject.meshArachidonic Acid
dc.subject.meshDNA
dc.subject.meshDown-Regulation
dc.subject.meshFemale
dc.subject.meshGene Expression Regulation
dc.subject.meshGlucose Transporter Type 4
dc.subject.meshHep G2 Cells
dc.subject.meshHumans
dc.subject.meshInsulin Resistance
dc.subject.meshIntra-Abdominal Fat
dc.subject.meshLigands
dc.subject.meshLiver X Receptors
dc.subject.meshMale
dc.subject.meshObesity, Morbid
dc.subject.meshPPAR gamma
dc.subject.meshRNA, Messenger
dc.subject.meshRNA, Small Interfering
dc.subject.meshThinness
dc.titleThe Antagonist Effect of Arachidonic Acid on GLUT4 Gene Expression by Nuclear Receptor Type II Regulation.
dc.typeresearch article
dc.type.hasVersionVoR
dc.volume.number20
dspace.entity.typePublication

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