Please use this identifier to cite or link to this item: http://ri.uaemex.mx/handle20.500.11799/71083
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dc.contributor.authorAMADO ISRAEL DE LA CRUZ GALINDOen_EU
dc.contributor.authorJonnathan Guadalupe Santillán Benítezen_EU
dc.contributor.authorENRIQUE MORALES AVILAen_EU
dc.creatorAMADO ISRAEL DE LA CRUZ GALINDO-
dc.creatorJonnathan Guadalupe Santillán Benítez-
dc.creatorENRIQUE MORALES AVILA-
dc.date2017-09-13-
dc.identifierhttp://hdl.handle.net/20.500.11799/71083-
dc.descriptionRevisión bibliográfica de la relación entre adiponectina, obesidad y desarrollo de diferentes enfermedades-
dc.descriptionAdiponectin is an adipokine abundantly expressed in adipose tissue, which has been well characterized, demonstrating its beneficial effect on human health, circulates in the bloodstream in various isoforms, playing different roles in the balance of energy homeostasis. Adiponectin is an insulin sensitizing hormone that exerts its action through AdipoR1, AdipoR2 and T-cadherin receptors. AdipoR1 is abundantly expressed in muscle, whereas AdipoR2 is expressed predominantly in the liver. Adiponectin is inversely proportional to obesity, diabetes and other states of insulin resistance; this review presents current findings regarding regulation, production and biological effects. Adiponectin acts by activating AMPk (AMP-activated protein kinase) and thus the enzymatic modulation so that the signaling pathways play an important role in the regulation, in addition to the above it has been demonstrated that the deregulation in the biogenesis and function of the miRNAs contributes to the appearance and development of diverse diseases.-
dc.languageeng-
dc.publisherAnnual Research & Review in Biology-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/4.0-
dc.source2347-565X-
dc.subjectadiponectin-
dc.subjectadipokine-
dc.subjectobesity-
dc.subjectadipor1-
dc.subjectadipor2-
dc.subjectinfo:eu-repo/classification/cti/2-
dc.titleAdiponectin: Obesity and Development of Different Diseases-
dc.typearticle-
dc.audiencestudents-
dc.audienceresearchers-
item.fulltextNo Fulltext-
item.grantfulltextnone-
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