| Autor: |
Aburto-Hernández C; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Barrera D; Departamento de Biología de la Reproducción, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Av. Vasco de Quiroga No. 15, Col. Belisario Domínguez, Sección XVI, Mexico City 14080, Mexico., Ortiz-Hernández R; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Espinoza-Simón E; Departamento de Bioquímica y Biología Estructural, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Parra-Gámez L; Departamento de Anatomía, Facultad de Medicina, Universidad Nacional Autónoma de México, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., González J; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Escobar ML; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Vázquez-Nin GH; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Echeverría-Martínez O; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico., Torres-Ramírez N; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de Mexico, Avenida Universidad 3000, Cd. Universitaria, Coyoacán, Mexico City 04510, Mexico. |
| Abstrakt: |
Polycystic ovary syndrome (PCOS) is an endocrine-metabolic disorder of unknown etiology. Hyperandrogenism (HA) is the main diagnostic criteria for PCOS, in addition to being a risk factor for developing several disorders throughout the patient's life, including pregnancy. However, the impact on offspring is little known. Therefore, the aim of this work was to evaluate the effect of maternal HA on glucose metabolism and hepatic lipid accumulation in adult offspring. We used Balb/c mice treated with dehydroepiandrosterone (DHEA) for 20 consecutive days. The ovary of DHEA-treated mice showed hemorrhagic bodies, an increased number of atretic follicles, and greater expression of genes related to meiotic cell cycle and DNA repair. The DHEA offspring (O-DHEA) had low birth weight, and some pups showed malformations. However, O-DHEA individuals gained weight rapidly, and the differences between them and the control group became significantly greater in adulthood. Moreover, O-DHEA presented higher serum glucose after a 6 h fast and a larger area under glucose, insulin, and pyruvate tolerance test curves. Oil Red O staining showed a more significant accumulation of fat in the liver but no changes in serum cholesterol and triacylglycerol levels. In summary, our results show that HA, induced by DHEA, affects gene expression in oocyte, which in turn generates defects in embryonic development, insulin resistance, and alteration in hepatic gluconeogenesis and lipid metabolism in O-DHEA, thereby increasing the risk of developing metabolic diseases. |
