Maternal obesity, infertility and mitochondrial dysfunction: potential mechanisms emerging from mouse model systems.

Abstract

Obesity is associated with ovulatory disorders, decreased rates of conception, infertility, early pregnancy loss and congenital abnormalities. Poor oocyte quality and reduced IVF success have also been reported in obese women. Recent attempts to understand the mechanism by which these defects occur have focused on mitochondria, essential organelles that are critical for oocyte maturation and subsequent embryo development. The oocyte relies on maternally supplied mitochondria until the resumption of mitochondrial replication in the peri-implantation period. Here we review current literature addressing the roles of mitochondria in oocyte function and how mitochondrial dysfunction can lead to fertility problems. The relationship between mitochondrial dysfunction and oocyte function is evaluated by examining the following examples of environmental exposures: tobacco smoke, aging, caloric restriction and hyperglycemia. Finally, we present new data from a mouse model of obesity that has demonstrated that oocyte mitochondria play a key role in obesity-associated reproductive disorders.