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 methylation-specific 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, PPARGC1A promoter methylation and mitochondrial content were found to be potential biomarkers for the prediction of metabolic risk in women with PCOS.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.fertnstert.2016.10.039 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The transcriptional repressor HEY2 regulates mitochondrial oxidative respiration to maintain cardiac homeostasis.
Nat Commun
January 2025
Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Energy deprivation and metabolic rewiring of cardiomyocytes are widely recognized hallmarks of heart failure. Here, we report that HEY2 (a Hairy/Enhancer-of-split-related transcriptional repressor) is upregulated in hearts of patients with dilated cardiomyopathy. Induced Hey2 expression in zebrafish hearts or mammalian cardiomyocytes impairs mitochondrial respiration, accompanied by elevated ROS, resulting in cardiomyocyte apoptosis and heart failure.
View Article and Find Full Text PDFEffect of Short-Term Restraint Stress on the Expression of Genes Associated with the Response to Oxidative Stress in the Hypothalamus of Hypertensive ISIAH and Normotensive WAG Rats.
Antioxidants (Basel)
October 2024
Federal Research Center Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, 630090 Novosibirsk, Russia.
Normotensive and hypertensive organisms respond differently to stress factors; however, the features of the central molecular genetic mechanisms underlying the reaction of the hypertensive organism to stress have not been fully established. In this study, we examined the transcriptome profiles of the hypothalamus of hypertensive ISIAH rats, modeling a stress-sensitive form of arterial hypertension, and normotensive WAG rats at rest and after exposure to a single short-term restraint stress. It was shown that oxidative phosphorylation is the most significantly enriched process among metabolic changes in the hypothalamus of rats of both strains when exposed to a single short-term restraint stress.
View Article and Find Full Text PDFSirtuin1 Suppresses Calcium Oxalate Nephropathy via Inhibition of Renal Proximal Tubular Cell Ferroptosis Through PGC-1α-mediated Transcriptional Coactivation.
Adv Sci (Weinh)
December 2024
Tumor Precision Diagnosis and Treatment Technology and Translational Medicine, Hubei Engineering Research Center, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430071, China.
Calcium oxalate (CaOx) crystals induce renal tubular epithelial cell injury and subsequent nephropathy. However, the underlying mechanisms remain unclear. In the present study, single-cell transcriptome sequencing is performed on kidney samples from mice with CaOx nephrocalcinosis.
View Article and Find Full Text PDFAcetylcholine receptor-β inhibition by interleukin-6 in skeletal muscles contributes to modulating neuromuscular junction during aging.
Mol Med
October 2024
Department of Neurology, Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, P.R. China.
Article Synopsis
- The study investigates how aging affects muscle strength and identifies interleukin-6 (IL-6) as a key factor that inhibits acetylcholine receptor (AChR) expression, contributing to muscle decline in older adults.
- Using various experimental methods, the researchers found that increased IL-6 levels during aging lead to reduced AChR-β expression, and this effect can be countered by treatments like tocilizumab and PGC1α agonists.
- The findings reveal a specific pathway (IL-6/IL-6R-ERK1/2-PGC1α/MEF2C) that regulates AChR-β, suggesting potential strategies for early intervention in muscle deterioration related to aging
The bacterial quorum sensing signal 2'-aminoacetophenone rewires immune cell bioenergetics through the Ppargc1a/Esrra axis to mediate tolerance to infection.
Elife
September 2024
Department of Surgery, Massachusetts General Hospital, and Harvard Medical School, Boston, United States.
How bacterial pathogens exploit host metabolism to promote immune tolerance and persist in infected hosts remains elusive. To achieve this, we show that () a recalcitrant pathogen, utilizes the quorum sensing (QS) signal 2'-aminoacetophenone (2-AA). Here, we unveil how 2-AA-driven immune tolerization causes distinct metabolic perturbations in murine macrophages' mitochondrial respiration and bioenergetics.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!