Show simple item record

Authordc.contributor.authorBasualto Alarcón, Carla
Authordc.contributor.authorLlanos Vidal, Paola
Authordc.contributor.authorGarcía Rivas, Gerardo
Authordc.contributor.authorTroncoso Magñin, Mayarling Francisca
Authordc.contributor.authorLagos, Daniel
Authordc.contributor.authorBarrientos Briones, Genaro Christian
Authordc.contributor.authorEstrada, Manuel
Cita de ítemdc.identifier.citationInternational Journal of Endocrinology Volume 2021, Article ID 5527973, 13 pageses_ES
Abstractdc.description.abstractIn men, 70% of circulating testosterone binds with high affinity to plasma sex hormone binding globulin (SHBG), which determines its bioavailability in their target cells. In recent years, a growing body of evidence has shown that circulating SHBG not only is a passive carrier for steroid hormones but also actively regulates testosterone signaling through putative plasma membrane receptors and by local expression of androgen-binding proteins apparently to reach local elevated testosterone concentrations in specific androgen target tissues. Circulating SHBG levels are influenced by metabolic and hormonal factors, and they are reduced in obesity and insulin resistance, suggesting that SHBG may have a broader clinical utility in assessing the risk for cardiovascular diseases. Importantly, plasma SHBG levels are strongly correlated with testosterone concentrations, and in men, low testosterone levels are associated with an adverse cardiometabolic profile. Although obesity and insulin resistance are associated with an increased incidence of cardiovascular disease, whether they lead to abnormal expression of circulating SHBG or its interaction with androgen signaling remains to be elucidated. SHBG is produced mainly in the liver, but it can also be expressed in several tissues including the brain, fat tissue, and myocardium. Expression of SHBG is controlled by peroxisome proliferator-activated receptor gamma (PPAR gamma) and AMP-activated protein kinase (AMPK). AMPK/PPAR interaction is critical to regulate hepatocyte nuclear factor-4 (HNF4), a prerequisite for SHBG upregulation. In cardiomyocytes, testosterone activates AMPK and PPARs. Therefore, the description of local expression of cardiac SHBG and its circulating levels may shed new light to explain physiological and adverse cardiometabolic roles of androgens in different tissues. According to emerging clinical evidence, here, we will discuss the potential mechanisms with cardioprotective effects and SHBG levels to be used as an early metabolic and cardiovascular biomarker in men.es_ES
Patrocinadordc.description.sponsorshipComision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) CONICYT FONDECYT 1151118 1190406 21180537 21191304es_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
Link to Licensedc.rights.uri*
Sourcedc.sourceInternational Journal of Endocrinologyes_ES
Keywordsdc.subjectTestosterone deficiencyes_ES
Keywordsdc.subjectMetabolic syndromees_ES
Keywordsdc.subjectShbg genees_ES
Keywordsdc.subjectPostmenopausal womenes_ES
Keywordsdc.subjectControls transcriptiones_ES
Keywordsdc.subjectSerum concentrationses_ES
Títulodc.titleClassic and novel sex hormone binding globulin effects on the cardiovascular system in menes_ES
Document typedc.typeArtículo de revistaes_ES
dc.description.versiondc.description.versionVersión publicada - versión final del editores_ES
dcterms.accessRightsdcterms.accessRightsAcceso abiertoes_ES
Indexationuchile.indexArtículo de publícación WoSes_ES

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivs 3.0 United States
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 United States