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Updated: Jan 21, 2026

Author Spotlight: Investigating the Mechanisms and Inducing Models of Polycystic Ovary Syndrome
Published on: July 5, 2024
Polycystic ovary syndrome dependency on mtDNA mutation; copy Number and its association with insulin resistance
Noor AlHuda Ali A H Saeed1, Israa Hussein Hamzah2,3, Samar Abdul Raheem Al-Gharrawi4
1Branch of Zoology, Biology Department, College of Science, Mustansiriyah University, POX 10422, Baghdad, Iraq.
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.
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