The Transcriptomic Landscape of Age-Induced Changes in Human Visceral Fat and the Predicted Omentum-Liver Connectome in Males

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dc.contributor.authorMoraes, Diogo de [UNESP]
dc.contributor.authorMousovich-Neto, Felippe
dc.contributor.authorCury, Sarah Santiloni [UNESP]
dc.contributor.authorOliveira, Jakeline [UNESP]
dc.contributor.authorSouza, Jeferson dos Santos [UNESP]
dc.contributor.authorFreire, Paula Paccielli [UNESP]
dc.contributor.authorDal-Pai-Silva, Maeli [UNESP]
dc.contributor.authorMori, Marcelo Alves da Silva
dc.contributor.authorFernandez, Geysson Javier
dc.contributor.authorCarvalho, Robson Francisco [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidad de Antioquia (UdeA)
dc.date.accessioned2023-07-29T16:15:37Z
dc.date.available2023-07-29T16:15:37Z
dc.date.issued2023-05-01
dc.description.abstractAging causes alterations in body composition. Specifically, visceral fat mass increases with age and is associated with age-related diseases. The pathogenic potential of visceral fat accumulation has been associated with its anatomical location and metabolic activity. Visceral fat may control systemic metabolism by secreting molecules that act in distal tissues, mainly the liver, through the portal vein. Currently, little is known about age-related changes in visceral fat in humans. Aiming to identify molecular and cellular changes occurring with aging in the visceral fat of humans, we analyzed publicly available transcriptomic data of 355 omentum samples from the Genotype-Tissue Expression portal (GTEx) of 20–79-year-old males and females. We identified the functional enrichment of genes associated with aging, inferred age-related changes in visceral fat cellularity by deconvolution analysis, profiled the senescence-associated secretory phenotype of visceral adipose tissue, and predicted the connectivity of the age-induced visceral fat secretome with the liver. We demonstrate that age induces alterations in visceral fat cellularity, synchronous to changes in metabolic pathways and a shift toward a pro-inflammatory secretory phenotype. Furthermore, our approach identified candidates such as ADIPOQ-ADIPOR1/ADIPOR2, FCN2-LPR1, and TF-TFR2 to mediate visceral fat-liver crosstalk in the context of aging. These findings cast light on how alterations in visceral fat with aging contribute to liver dysfunction and age-related disease etiology.en
dc.description.affiliationDepartment of Structural and Functional Biology Institute of Biosciences of Botucatu Sao Paulo State University UNESP, SP
dc.description.affiliationDepartment of Biochemistry and Tissue Biology University of Campinas, Monteiro Lobato St., 255, SP
dc.description.affiliationObesity and Comorbidities Research Center (OCRC) University of Campinas, SP
dc.description.affiliationExperimental Medicine Research Cluster (EMRC) University of Campinas, SP
dc.description.affiliationGrupo Biologia y Control de Enfermedades Infeciosas (BCEI) Facultad de Ciencias Exactas y Naturales Universidad de Antioquia (UdeA)
dc.description.affiliationUnespDepartment of Structural and Functional Biology Institute of Biosciences of Botucatu Sao Paulo State University UNESP, SP
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipIdCAPES: 001
dc.identifierhttp://dx.doi.org/10.3390/biomedicines11051446
dc.identifier.citationBiomedicines, v. 11, n. 5, 2023.
dc.identifier.doi10.3390/biomedicines11051446
dc.identifier.issn2227-9059
dc.identifier.scopus2-s2.0-85160782180
dc.identifier.urihttp://hdl.handle.net/11449/250023
dc.language.isoeng
dc.relation.ispartofBiomedicines
dc.sourceScopus
dc.subjectage-related diseases
dc.subjectaging
dc.subjectfat-liver crosstalk
dc.subjectobesity
dc.subjectvisceral adipose tissue
dc.titleThe Transcriptomic Landscape of Age-Induced Changes in Human Visceral Fat and the Predicted Omentum-Liver Connectome in Malesen
dc.typeArtigo
unesp.author.orcid0000-0002-8245-9450[2]
unesp.author.orcid0000-0002-4129-8769[5]
unesp.author.orcid0000-0003-0649-8279[6]
unesp.author.orcid0000-0001-7269-9197[7]
unesp.author.orcid0000-0002-8493-1587[9]
unesp.author.orcid0000-0002-4901-7714[10]

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