Author | dc.contributor.author | Cabrera Cruz, Heidy | |
Author | dc.contributor.author | Oróstica, Lorena | |
Author | dc.contributor.author | Plaza Parrochia, Francisca | |
Author | dc.contributor.author | Torres Pinto, Ignacio | |
Author | dc.contributor.author | Romero, Carmen | |
Author | dc.contributor.author | Vega, Margarita | |
Admission date | dc.date.accessioned | 2020-05-11T22:24:50Z | |
Available date | dc.date.available | 2020-05-11T22:24:50Z | |
Publication date | dc.date.issued | 2020 | |
Cita de ítem | dc.identifier.citation | Am J Physiol Endocrinol Metab 318: E237–E248, 2020 | es_ES |
Identifier | dc.identifier.other | 10.1152/ajpendo.00162.2019 | |
Identifier | dc.identifier.uri | https://repositorio.uchile.cl/handle/2250/174663 | |
Abstract | dc.description.abstract | Polycystic ovary syndrome (PCOS) is an endocrine-metabolic disorder characterized by hyperandrogenism and ovulatory dysfunction but also obesity and hyperinsulinemia. These characteristics induce an insulin-resistant state in tissues such as the endometrium, affecting its reproductive functions. Myo-inositol (MYO) is an insulin-sensitizing compound used in PCOS patients; however, its insulin-sensitizing mechanism is unclear. To understand the relationship of MYO with insulin action in endometrial cells, sodium/myo-inositol transporter 1 (SMIT-1) (MYO-transporter), and MYO effects on protein levels related to the insulin pathway were evaluated. SMIT-1 was assessed in endometrial tissue from women with normal weight, obesity, insulin resistance, and PCOS; additionally, using an in vitro model of human endometrial cells exposed to an environment resembling hyperinsulinemic-obese-PCOS, MYO effect was evaluated on p-AMPK and GLUT-4 levels and glucose uptake by Western blot, immunocytochemistry, and confocal microscopy, respectively. SMIT-1 was detected in endometrial tissue from all groups and decreased in PCOS and obesity (P < 0.05 vs. normal weight). In the in vitro model, PCOS conditions decreased p-AMPK levels, while they were restored with MYO (P < 0.05). The diminished GLUT-4 protein levels promoted by PCOS environment were restored by MYO through SMIT-1 and p-AMPK-dependent mechanism (P < 0.05). Also, MYO restored glucose uptake in cells under PCOS condition through a p-AMPK-dependent mechanism. Finally, these results were similar to those obtained with metformin treatment in the same in vitro conditions. Consequently, MYO could be a potential insulin sensitizer through its positive effects on insulin-resistant tissues as PCOS-endometrium, acting through SMIT-1, provoking AMPK activation and elevated GLUT-4 levels and, consequently, increase glucose uptake by human endometrial cells. Therefore, MYO may be used as an effective treatment option in insulin-resistant PCOS women. | es_ES |
Patrocinador | dc.description.sponsorship | Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT), CONICYT FONDECYT: 1130053. | es_ES |
Lenguage | dc.language.iso | en | es_ES |
Publisher | dc.publisher | American Physiological Society | es_ES |
Type of license | dc.rights | Attribution-NonCommercial-NoDerivs 3.0 Chile | * |
Link to License | dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | * |
Source | dc.source | American Journal of Physiology-Endocrinology and Metabolism | es_ES |
Keywords | dc.subject | AMPK | es_ES |
Keywords | dc.subject | Endometrium | es_ES |
Keywords | dc.subject | GLUT-4 | es_ES |
Keywords | dc.subject | Myo-inositol | es_ES |
Keywords | dc.subject | Polycystic ovary syndrome | es_ES |
Título | dc.title | The insulin-sensitizing mechanism of myo-inositol is associated with AMPK activation and GLUT-4 expression in human endometrial cells exposed to a PCOS environment | es_ES |
Document type | dc.type | Artículo de revista | es_ES |
dcterms.accessRights | dcterms.accessRights | Acceso Abierto | |
Cataloguer | uchile.catalogador | rvh | es_ES |
Indexation | uchile.index | Artículo de publicación ISI | |
Indexation | uchile.index | Artículo de publicación SCOPUS | |