Polycystic ovary syndrome and mitochondrial dysfunction

Zhang, Jingshun; Bao, Yi-Gang; Zhou, Xu; Zheng, Lan

doi:10.1186/s12958-019-0509-4

Cited by 165 publications

(152 citation statements)

References 189 publications

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“…The change in mtDNA-CN was also uncorrelated with most other clinical variables, including BMI, which was implicated in previous studies [9,42]. Only testosterone appears to be statistically related to the change in mtDNA-CN, signifying that the changes in mtDNA-CN and testosterone were correspondent during treatment with metformin.…”

Section: Discussionsupporting

confidence: 64%

Changes in peripheral mitochondrial DNA copy number in metformin-treated women with polycystic ovary syndrome: a longitudinal study

Yang

Chou

Chang

et al. 2020

Reprod Biol Endocrinol

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Background: Patients with polycystic ovarian syndrome (PCOS) are associated with known alterations in mitochondria DNA copy number (mtDNA-CN). The aim of this study is to study the change in mtDNA-CN in patients with PCOS who were treated with metformin. Methods: This is a prospective cohort of patients with PCOS, who received metformin for one year. From 2009 to 2015, 88 women diagnosed with PCOS, based on the Rotterdam criteria, were enrolled. Serial measurements of mtDNA-CN, 8-hydroxydeoxyguanosine (8-OHdG), anthropometric, metabolic, endocrine, and inflammatory markers were obtained before and after 3, 6, and 12 months of treatment. Results: A significant decrease in mtDNA-CN was seen over the course of one year. Other markers, including 8-OHdG, testosterone, free androgen index, blood pressure and liver enzymes, also decreased in the same interval. On regression analysis, there was a significant association between the change in mtDNA-CN and serum total testosterone, and no association between mtDNA-CN and metabolic factors. Conclusions: Treatment with metformin is associated with a time-dependent decrease in mtDNA-CN in patients with PCOS who are treated over the course of one year. This may signify a reduction in mitochondria dysfunction. The change in mtDNA-CN corresponds to a similar change in serum total testosterone, and suggests a possible relationship between mtDNA-CN and testosterone.

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Section: Discussionsupporting

confidence: 64%

Changes in peripheral mitochondrial DNA copy number in metformin-treated women with polycystic ovary syndrome: a longitudinal study

Yang

Chou

Chang

et al. 2020

Reprod Biol Endocrinol

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“…However, the existence of an autonomous mitochondrial epigenetic regulation has been the subject of a long debate over the years with controversial reports stating the presence or absence of mtDNA methylation (Patil et al, 2019). With the improvement of detection techniques, recent studies proposed that similarly to nuclear DNA, mtDNA is also subjected to epigenetic modifications that can influence mitochondrial biogenesis, gene expression and function (Zhang et al, 2019a). A recent study demonstrated non-random patterns of mtDNA methylation, predominantly in a non-CpG context when comparing normal versus liver and breast cancer cells (Patil et al, 2019).…”

Section: Mitochondrial Dna Methylation/demethylationmentioning

confidence: 99%

Erasing gametes to write blastocysts: metabolism as the new player in epigenetic reprogramming

et al. 2020

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Understanding preimplantation embryonic development is crucial for the improvement of assisted reproductive technologies and animal production. To achieve this goal, it is important to consider that gametes and embryos are highly susceptible to environmental changes. Beyond the metabolic adaptation, the dynamic status imposed during follicular growth and early embryogenesis may create marks that will guide the molecular regulation during prenatal development, and consequently impact the offspring phenotype. In this context, metaboloepigenetics has gained attention, as it investigates the crosstalk between metabolism and molecular control, i.e., how substrates generated by metabolic pathways may also act as players of epigenetic modifications. In this review, we present the main metabolic and epigenetic events of pre-implantation development, and how these systems connect to open possibilities for targeted manipulation of reproductive technologies and animal production systems.

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“…In the reproductive environment, mtDNA copy number can be used as a means of detecting embryo viability . In addition, markers of abnormal mitochondrial metabolism such as ROS, advanced oxidation protein products, catalase, and superox-ide dismutase (SOD) are associated with PCOS (Zhang et al, 2019a).…”

Section: Mitochondria Structure and Functionmentioning

confidence: 99%

Mitochondrial Dysfunction in Polycystic Ovary Syndrome

Zeng

Huang

Long

et al. 2020

DNA and Cell Biology

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Polycystic ovary syndrome (PCOS) is one of the most common female reproductive metabolisms. It is an endocrine disease that affects reproductive women and often exhibits with hyperandrogenemia, insulin resistance (IR), low inflammation, and an increased risk of type 2 diabetes mellitus, metabolic syndrome, and cardiovascular events such as hypertension and dyslipidemia in patients. However, the molecular mechanism of PCOS is still unclear. Recently, an increasing number of studies have shown that the oxidative stress induced by mitochondrial dysfunction has negative effects on IR, lipid metabolism, and follicular development, suggesting that mitochondrial dysfunction plays an essential role in the development of PCOS. Abnormal mitochondrial DNA copy number in patients with PCOS, and mitochondrial gene mutations, has been the focus of research in recent years, and functional mitochondrial diseases have been gradually accepted as a related factor in PCOS. This review is intended to summarize and discuss previous and recent studies and findings on the connections between mitochondrial dysfunction and PCOS.

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Polycystic ovary syndrome and mitochondrial dysfunction

Cited by 165 publications

References 189 publications

Changes in peripheral mitochondrial DNA copy number in metformin-treated women with polycystic ovary syndrome: a longitudinal study

Changes in peripheral mitochondrial DNA copy number in metformin-treated women with polycystic ovary syndrome: a longitudinal study

Erasing gametes to write blastocysts: metabolism as the new player in epigenetic reprogramming

Mitochondrial Dysfunction in Polycystic Ovary Syndrome

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