TY - JOUR
T1 - Metabolic control of oocyte development
T2 - Linking maternal nutrition and reproductive outcomes
AU - Gu, Ling
AU - Liu, Honglin
AU - Gu, Xi
AU - Boots, Christina
AU - Moley, Kelle H.
AU - Wang, Qiang
N1 - Funding Information:
This work was funded by National Key Scientific Research Projects (2014CB943200), Natural Science Foundation of the Jiangsu Higher Education Institutions (13KJA310001), Fundamental Research Funds for the Central Universities (0606J0451) of China, the American Diabetes Association (KHM), and the NIH-NICHD (R01).
Publisher Copyright:
© 2014 Springer Basel.
PY - 2015/1
Y1 - 2015/1
N2 - Obesity, diabetes, and related metabolic disorders are major health issues worldwide. As the epidemic of metabolic disorders continues, the associated medical co-morbidities, including the detrimental impact on reproduction, increase as well. Emerging evidence suggests that the effects of maternal nutrition on reproductive outcomes are likely to be mediated, at least in part, by oocyte metabolism. Well-balanced and timed energy metabolism is critical for optimal development of oocytes. To date, much of our understanding of oocyte metabolism comes from the effects of extrinsic nutrients on oocyte maturation. In contrast, intrinsic regulation of oocyte development by metabolic enzymes, intracellular mediators, and transport systems is less characterized. Specifically, decreased acid transport proteins levels, increased glucose/lipid content and elevated reactive oxygen species in oocytes have been implicated in meiotic defects, organelle dysfunction and epigenetic alteration. Therefore, metabolic disturbances in oocytes may contribute to the diminished reproductive potential experienced by women with metabolic disorders. In-depth research is needed to further explore the underlying mechanisms. This review also discusses several approaches for metabolic analysis. Metabolomic profiling of oocytes, the surrounding granulosa cells, and follicular fluid will uncover the metabolic networks regulating oocyte development, potentially leading to the identification of oocyte quality markers and prevention of reproductive disease and poor outcomes in offspring.
AB - Obesity, diabetes, and related metabolic disorders are major health issues worldwide. As the epidemic of metabolic disorders continues, the associated medical co-morbidities, including the detrimental impact on reproduction, increase as well. Emerging evidence suggests that the effects of maternal nutrition on reproductive outcomes are likely to be mediated, at least in part, by oocyte metabolism. Well-balanced and timed energy metabolism is critical for optimal development of oocytes. To date, much of our understanding of oocyte metabolism comes from the effects of extrinsic nutrients on oocyte maturation. In contrast, intrinsic regulation of oocyte development by metabolic enzymes, intracellular mediators, and transport systems is less characterized. Specifically, decreased acid transport proteins levels, increased glucose/lipid content and elevated reactive oxygen species in oocytes have been implicated in meiotic defects, organelle dysfunction and epigenetic alteration. Therefore, metabolic disturbances in oocytes may contribute to the diminished reproductive potential experienced by women with metabolic disorders. In-depth research is needed to further explore the underlying mechanisms. This review also discusses several approaches for metabolic analysis. Metabolomic profiling of oocytes, the surrounding granulosa cells, and follicular fluid will uncover the metabolic networks regulating oocyte development, potentially leading to the identification of oocyte quality markers and prevention of reproductive disease and poor outcomes in offspring.
KW - Amino acid
KW - Biomarker
KW - Germ cell
KW - Glucose
KW - Lipid
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U2 - 10.1007/s00018-014-1739-4
DO - 10.1007/s00018-014-1739-4
M3 - Review article
C2 - 25280482
AN - SCOPUS:84921936276
SN - 1420-682X
VL - 72
SP - 251
EP - 271
JO - Cellular and Molecular Life Sciences
JF - Cellular and Molecular Life Sciences
IS - 2
ER -