Journal
FERTILITY AND STERILITY
Volume 107, Issue 2, Pages 467-+Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.fertnstert.2016.10.039
Keywords
ATPIII; BMI; lipid profile; metabolic risk; mitochondrial biogenesis
Categories
Funding
- Ministry of Science and Technology of China Grants (973 program) [2014CB943203]
- Reproductive health and major birth defects prevention and control research specific project [2016YFC1000601]
- National Natural Science Funds [31371521, 81571400, 81471427, 81300457, 31501201, 81300543]
- Beijing Nova Program [xxjh2015A011]
- Science and Technology Innovation Base Cultivation and Development [Z151100001615023]
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Objective: To investigate PPARGC1A promoter methylation and mitochondria DNA (mtDNA) content in the leukocytes of women with polycystic ovary syndrome (PCOS) and analyze the relationship between these indices and metabolic risk for women with PCOS. Design: Cross-sectional study. Setting: University hospital. Patient(s): A total of 175 women with PCOS and 127 healthy controls. Intervention(s): None. Main Outcome Measure(s): Women with and without PCOS classified using the typical metabolic risk criteria of the National Cholesterol Education Program's Adult Treatment Panel III report (ATPIII), methylation of PPARGC1A promoter tested by methylationspecific polymerase chain reaction, and mtDNA content confirmed by quantitative polymerase chain reaction (PCR). Result(s): PPARGC1A promoter methylation was specifically increased, but mtDNA content was specifically decreased in women with PCOS compared with the control women after adjustment for body mass index. Moreover, in women with PCOS who have increased metabolic risk, the differences in PPARGC1A promoter methylation and mitochondrial content were aggravated. Conclusion(s): In conclusion, PPARGC1Apromotermethylation and mitochondrial content were found to be potential biomarkers for the prediction ofmetabolic risk inwomen with PCOS. (C) 2016 TheAuthors. Published by Elsevier Inc. on behalf of theAmerican Society for ReproductiveMedicine.
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