Maternal diet-induced obesity alters mitochondrial activity and redox status in mouse oocytes and zygotes.

Abstract

The negative impact of obesity on reproductive success is well documented but the stages at which development of the
conceptus is compromised and the mechanisms responsible for the developmental failure still remain unclear. Recent
findings suggest that mitochondria may be a contributing factor. However to date no studies have directly addressed the
consequences of maternal obesity on mitochondria in early embryogenesis. Using an established murine model of
maternal diet induced obesity and a live cell dynamic fluorescence imaging techniques coupled with molecular biology we
have investigated the underlying mechanisms of obesity-induced reduced fertility. Our study is the first to show that
maternal obesity prior to conception is associated with altered mitochondria in mouse oocytes and zygotes. Specifically,
maternal diet-induced obesity in mice led to an increase in mitochondrial potential, mitochondrial DNA content and
biogenesis. Generation of reactive oxygen species (ROS) was raised while glutathione was depleted and the redox state
became more oxidised, suggestive of oxidative stress. These altered mitochondrial properties were associated with
significant developmental impairment as shown by the increased number of obese mothers who failed to support
blastocyst formation compared to lean dams. We propose that compromised oocyte and early embryo mitochondrial
metabolism, resulting from excessive nutrient exposure prior to and during conception, may underlie poor reproductive
outcomes frequently reported in obese women

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