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