Maternal insulin resistance causes oxidative stress and mitochondrial dysfunction in mouse oocytes

Human Reproduction
Xiang-Hong OuQing-Yuan Sun

Abstract

Insulin resistance (IR) and hyperinsulinemia compromise fertility in females and are well-recognized characteristics of anovulatory women with polycystic ovary syndrome. Patients with IR and hyperinsulinemia undergoing ovarian stimulation for IVF are at increased risks of impaired oocyte developmental competence, implantation failure and pregnancy loss. However, the precise underlying mechanism remains unknown. We investigated how IR impairs oocyte quality and early embryonic development by an insulin-resistant mouse model. Oocyte quality, fertilization and embryonic development were analyzed. Furthermore, oxidant stress products and mitochondrial function were evaluated by quantitative real-time PCR and immunofluorescence. An imbalance between oxidants and antioxidants revealed by increased concentrations of reactive oxygen species, and a decreased concentration of glutathione (GSH) and a decreased GSH/GSSG ratio resulted in oxidative stress (OS) and impaired mitochondrial function in germinal vesicle (GV) and metaphase II (MII) oocytes of insulin-resistant mice. MII oocytes displayed a decrease in the ATP content and the mitochondrial DNA (mtDNA) copy number. In contrast, GV oocytes were characterized by a high ATP content co...Continue Reading

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