| Autor: |
Hernández-Jiménez JL; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Ciudad de México, México., Barrera D; Departamento de Biología de la Reproducción 'Dr. Carlos Gual Castro', Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Ciudad de México, México., Espinoza-Simón E; Departamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Coyoacán, Ciudad de México, México., González J; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Ciudad de México, México., Ortíz-Hernández R; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Ciudad de México, México., Escobar L; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Ciudad de México, México., Echeverría O; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Ciudad de México, México., Torres-Ramírez N; Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México. Avenida Universidad 3000, Ciudad de México, México. |
| Abstrakt: |
Polycystic ovary syndrome (PCOS) is a disease whose diagnosis is based on the detection of hyperandrogenism (HA) and ovulatory dysfunction. Women with PCOS frequently develop insulin resistance (IR), which generates a metabolic condition that involves a decrease in the action of insulin at the cellular level and is linked to compensatory hyperinsulinemia (HI). In PCOS, the ovary remains sensitive to the action of insulin. Additionally, it has been observed that the main effect of insulin in the ovary is the stimulation of androgen synthesis, resulting in HA, one of the fundamental characteristics of the PCOS. In this sense, the excess of androgens favors the development of IR, thus perpetuating the cycle of IR-HI-HA, and therefore PCOS. Moreover, mitochondrial dysfunction is present in PCOS patients and is a common feature in both IR and HA. This review places electron transfer as a key element in HA and IR development, with emphasis on the relationship between androgen biosynthesis and mitochondrial function. Indeed, metformin has been involved in repair mitochondrial dysfunction, decrease of oxidative stress, reduction of androgens levels and the enhancing of insulin sensitivity. Therefore, we propose that treatment with metformin could decrease HI and consequently HA, restoring, at least in part, the metabolic and hormonal disorders of PCOS. |
