WCRB2014 ORAL PRESENTATIONS Embryo (5 abstracts)
Restoring mitochondria in oocytes of obese mice normalizes embryo development
Linda Linyan Wu 1 , Darryl L Russell 1 , Miaoxin Cheng 1 , Mark A Febbraio 2 , Robert J Norman 1 & Rebecca L Robker 1
1The Robinson Institute, Adelaide, South Australia, Australia; 2Cellular and Molecular Metabolism Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Obesity in females causes altered fetal growth during pregnancy and permanently ‘programs’ the metabolism of offspring; however the origin of these changes and whether they are reversible is not known. We now show that in obese female mice the oocytes exhibit endoplasmic reticulum (ER) stress, high levels of intracellular lipid, reduced Ptx3 matrix production and fail to ovulate. The oocytes from obese mice contain normal levels of mtDNA but have reduced mitochondrial membrane potential and a high degree of autophagy compared to oocytes from lean mice. After IVF, the oocytes of obese female mice demonstrate their reduced developmental potential and they form blastocysts with reduced mtDNA. Analysis at e14.5 showed that obese oocytes gave rise to fetuses that were heavier than controls and had reduced liver and kidney mtDNA per cell indicating that maternal obesity altered the mitochondrial set-point of offspring. Treatment of the obese females with ER stress inhibitors for just 4 days prior to conception completely restored oocyte, embryo and fetal physiology to normal. These results show that obesity prior to conception imparts a legacy of mitochondrial loss in offspring due to ER stress that is reversible in the pre-conception period.
Volume 1
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