Polycystic ovary syndrome dependency on mtDNA mutation; copy Number and its association with insulin resistance

Abstract

Objective Study analyzes mutation in mtDNA (Mitochondrial DNA) among diabetic women with PCOS in non-diabetic diabetic women and compared with the healthy control. Women with known case of hyperandrogenism, ovulatory dysfunction and/or polycystic ovaries were selected and anthropometric and demographic variables were collected during their clinical visit. Biochemical estimation of glucose, FSH, LH, estradiol (E2), and insulin levels were analyzed. Mutational analysis of mt-tRNA genes of each individual was compared with the updated consensus Cambridge sequence. The mtDNA content was determined in triplicate using SYBR green PCR mastermix. Results The clinical and biochemical characteristics of participants showed no statistical difference in age and/or FSH, PRL, E2, PRGE or fasting glucose value between patients of different groups. Women with PCOS-D had significantly higher LH, LH/FSH, TT and fasting insulin levels and HOMA-IR with respect to the control group. Ten different type of mutation were seen in POCS group. Most of these mutations were confined to evolutionarily conserved region. The mtDNA copy numbers were considerably lower PCOS group irrespective of diabetic status. To conclude, the current study inferred that the mutations occur in the mitochondrial genome, mt-tRNA in specific, are the important causal factor in PCOS.

Mitochondrial DNA 4977 bp Deletion in Peripheral Blood is Associated with Polycystic Ovary Syndrome.

“…Lee et al provided the rst evidence of decreased peripheral mtDNA CN in PCOS patients [14]. Recently, another two studies indicated the same tendency, showing that mtDNA CN in the peripheral blood of PCOS patients was signi cantly lower than that in healthy controls matched by age and BMI [11,12]. However, this study revealed an elevated mtDNA CN in the peripheral blood of PCOS patients.…”

“…Mitochondrial DNA (mtDNA) copy number (CN) is a relative measure of the mitochondrial content or the mass of mitochondrion. Many studies have indicated that abnormal mtDNA is associated with the pathophysiology of PCOS [11][12][13][14][15]. However, due to the con icting results of these studies, the exact association of mtDNA content and PCOS remain undetermined.…”

Circulating levels of C1q/TNF‐α‐related protein 6 (CTRP6) in polycystic ovary syndrome

“…One proposed mechanism that could disrupt this balance is through mitochondrial dysfunction, characterized by mitochondrial DNA (mtDNA) depletion. It has been associated with the pathogenesis of PCOS, including hyperglycemia, insulin resistance, hyperandrogenism, and anovulation . mtDNA depletion downregulates adiponectin expression, while it stabilizes CTRP6 mRNA, inhibiting its decay .…”

Electroacupuncture alleviates polycystic ovary syndrome-like symptoms through improving insulin resistance, mitochondrial dysfunction, and endoplasmic reticulum stress via enhancing autophagy in rats

“…In addition, it was verified that mitochondrial dysfunction led to excess production of ROS and accelerated PCOS progression (Ding et al 2017 ). More importantly, the mitochondrial copy number was remarkably decreased in PCOS patient with insulin resistance, indicating that mitochondrial dysfunction corelated with PCOS-IR (Ding et al 2017 ; Saeed et al 2019 ). In the current study, EA treatment effectively attenuated mitochondrial dysfunction in the ovarian tissue of PCOS-like rats.…”