Obesity alters mitochondrial function in oocytes

Obesity and related metabolic issues are a major health issue worldwide (Igosheva, Abramov, Poston, Eckert, Fleming, Duchen & McConnell, 2010). By 2015, overweight and obesity is predicted to increase to 2.3 billion and 700 million respectively (Igosheva, Abramov, Poston, Eckert, Fleming, Duchen & McConnell, 2010). Evidence suggests that excessive body fat has a detrimental effect on female fertility and pregnancy (Igosheva, Abramov, Poston, Eckert, Fleming, Duchen & McConnell, 2010). In a recent study, researchers from the University of Southampton investigated the underlying mechanisms of obesity-induced reduced fertility (Igosheva, Abramov, Poston, Eckert, Fleming, Duchen & McConnell, 2010). This study was the first to show that maternal obesity prior to conception is associated with altered mitochondria in mouse oocytes and zygotes. It is proposed that because DNA located in mitochondria contains instructions for energy use by the cell, mitochondria dysfunction results in poor cellular health, and thus, less efficient mitochondrial potentil, mitochondrial DNA content and biogenesis (life forms arising from similar life forms). Moreover, altered mitochondria properties were associated with significant developmental impairment of the oocyte (immature female reproductive cell, pre-fertilisation) and embryo (organism in its earliest stages of development). This is not surprising, when we consider that previous research has confirmed, via in-vitro studies, the susceptibility of mitochondria within the oocyte and developing embryo to environmental stressors and that even low level acquired mitochondrial injuries may persist into embryonic lifeĀ (Igosheva, Abramov, Poston, Eckert, Fleming, Duchen & McConnell, 2010).

Igosheva, N., Abramov, A.Y., Poston, L., Eckert, J.J., Fleming, T.P., Duchen, M.R. & McConnell, J. 2010. Maternal diet-induced obesity alters mitochondiral activity and redox status in mouse oocytes and zygotes. PLoS, 5, 4, e10074.

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