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Reproduction (2010) 139 685-695
DOI: 10.1530/REP-09-0345
Copyright © 2010 Society for Reproduction and Fertility
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REVIEW

The pivotal role of glucose metabolism in determining oocyte developmental competence

Melanie L Sutton-McDowall, Robert B Gilchrist and Jeremy G Thompson

School of Paediatrics and Reproductive Health, The Robinson Institute, Research Centre for Reproductive Health, The University of Adelaide, Adelaide, South Australia 5005, Australia

Correspondence should be addressed to M L Sutton-McDowall; Email: melanie.mcdowall{at}adelaide.edu.au

The environment that the cumulus oocyte complex (COC) is exposed to during either in vivo or in vitro maturation (IVM) can have profound effects on the success of fertilisation and subsequent embryo development. Glucose is a pivotal metabolite for the COC and is metabolised by glycolysis, the pentose phosphate pathway (PPP), the hexosamine biosynthesis pathway (HBP) and the polyol pathway. Over the course of oocyte maturation, a large proportion of total glucose is metabolised via the glycolytic pathway to provide substrates such as pyruvate for energy production. Glucose is also the substrate for many cellular functions during oocyte maturation, including regulation of nuclear maturation and redox state via the PPP and for the synthesis of substrates of extracellular matrices (cumulus expansion) and O-linked glycosylation (cell signalling) via the HBP. However, the oocyte is susceptible to glucose concentration-dependent perturbations in nuclear and cytoplasmic maturation, leading to poor embryonic development post-fertilisation. For example, glucose concentrations either too high or too low result in precocious resumption of nuclear maturation. This review will discuss the relevant pathways of glucose metabolism by COCs during in vivo maturation and IVM, including the relative contribution of the somatic and gamete compartments of the COC to glucose metabolism. The consequences of exposing COCs to abnormal glucose concentrations will also be examined, either during IVM or by altered maternal environments, such as during hyperglycaemia induced by diabetes and obesity.







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