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dc.contributor.authorEscoté, Xabier
dc.contributor.authorGómez Zorita, Saioa
dc.contributor.authorLópez Yoldi, Miguel
dc.contributor.authorMilton Laskibar, Iñaki
dc.contributor.authorFernández Quintela, Alfredo
dc.contributor.authorMartínez, José Alfredo
dc.contributor.authorMoreno Aliaga, María J.
dc.contributor.authorPortillo Baquedano, María Puy
dc.date.accessioned2019-01-07T17:53:23Z
dc.date.available2019-01-07T17:53:23Z
dc.date.issued2017-08-15
dc.identifier.citationInternational Journal of Molecular Sciences 18(8) : (2017) // Article ID 1770es_ES
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/10810/30653
dc.description.abstractAdipose tissue releases bioactive mediators called adipokines. This review focuses on the effects of omentin, vaspin, cardiotrophin-1, Tumor necrosis factor-like Weak Inducer of Apoptosis (TWEAK) and nephroblastoma overexpressed (NOV/CCN3) on obesity and diabetes. Omentin is produced by the stromal-vascular fraction of visceral adipose tissue. Obesity reduces omentin serum concentrations and adipose tissue secretion in adults and adolescents. This adipokine regulates insulin sensitivity, but its clinical relevance has to be confirmed. Vaspin is produced by visceral and subcutaneous adipose tissues. Vaspin levels are higher in obese subjects, as well as in subjects showing insulin resistance or type 2 diabetes. Cardiotrophin-1 is an adipokine with a similar structure as cytokines from interleukin-6 family. There is some controversy regarding the regulation of cardiotrophin-1 levels in obese -subjects, but gene expression levels of cardiotrophin-1 are down-regulated in white adipose tissue from diet-induced obese mice. It also shows anti-obesity and hypoglycemic properties. TWEAK is a potential regulator of the low-grade chronic inflammation characteristic of obesity. TWEAK levels seem not to be directly related to adiposity, and metabolic factors play a critical role in its regulation. Finally, a strong correlation has been found between plasma NOV/CCN3 concentration and fat mass. This adipokine improves insulin actions.es_ES
dc.description.sponsorshipThis study was supported by grants from the Ministerio de Economia y Competitividad (AGL-2015-65719-FEDER-UE and BFU2015-65937-R), Government of the Basque Country (IT-572-13), University of the Basque Country (UPV/EHU) (ELDUNANOTEK UFI11/32), Linea Especial about Nutrition, Obesity and Health from the University of Navarra LE/97, Department of Health, Government of Navarra (67-2015) and Instituto de Salud Carlos III (CIBERobn). I. Milton-Laskibar is a PhD fellowship from the Basque Government and S. Gomez-Zorita is a post-doc fellowship from CIBERobn.es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/AGL-2015-65719-FEDER-UEes_ES
dc.relationinfo:eu-repo/grantAgreement/MINECO/BFU2015-65937-Res_ES
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectadipokineses_ES
dc.subjectomentines_ES
dc.subjectvaspines_ES
dc.subjectcardiotrophin-1es_ES
dc.subjectTWEAK and NOVes_ES
dc.subjectCCN3es_ES
dc.titleRole of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Developmentes_ES
dc.typeinfo:eu-repo/semantics/bookPartes_ES
dc.rights.holder© 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).es_ES
dc.rights.holderAtribución 3.0 España*
dc.relation.publisherversionhttps://www.mdpi.com/1422-0067/18/8/1770es_ES
dc.identifier.doi10.3390/ijms18081770
dc.departamentoesFarmacia y ciencias de los alimentoses_ES
dc.departamentoeuFarmazia eta elikagaien zientziakes_ES


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© 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Except where otherwise noted, this item's license is described as © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).