EC Gynaecology

Short Communication Volume 12 Issue 7 - 2023

Advancements in the Etiopathogenesis, Pathophysiology and Treatment of Polycystic Ovary Syndrome (PCOS)

Kulvinder Kochar Kaur*

Scientific Director Cum Owner Dr Kulvinder Kaur Centre for Human Reproduction, Jalandhar, Punjab, India

*Corresponding Author: Kulvinder Kochar Kaur, Scientific Director Cum Owner Dr Kulvinder Kaur Centre for Human Reproduction, Jalandhar, Punjab, India.
Received: May 27, 2023; Published: June 17, 2023



The polycystic ovary syndrome (PCOS) portrays an endocrine impairment correlated with numerous metabolic conditions, inclusive of, insulin resistance (IR), type 2 diabetes mellitus (T2DM), metabolic syndrome (MetS), NAFLD, non alcoholic steatohepatitis (NASH), along with enhanced infertility rate. Recently PCOS has been considered to be a condition with low grade chronic inflammation (LGF) [1,2]. As summarised by Dabravolski., et al. [3] mitochondrial impairment is substantially responsible for PCOS generation and propagation [3].

Mitochondrial mutations, impaired mitophagy, diminished ATP generation and liberated ROS further aids in the related symptoms, primarily IR, MetS and obesity generation. Future investigations might focus on acquisition of a greater advantageous insight of the etiological part of nuclear and mitochondrial gene mutations, epigenetic, environmental apart from lifestyle factors on the aetiopathogenesis of PCOS and the associated symptoms.

  1. Kulvinder Kochar Kaur., et al. “Will exploration for role of kisspeptins answer the modes by which transgenerational transmission of Polycystic ovary syndrome (PCOS) occurs to find a way of avoidance of inheritance of PCOS? A Short Communication”. MAR Case Reports1 (2023): 1-17.
  2. Kulvinder Kochar Kaur., et al. “Identification of Women of Polycystic Ovary Syndrome (PCOS) At Risk for Generation of Metabolic Disease in Normal Weight PCOS: Is There a Role of Flutamide?- A Short Communication”. CPQ Medicine2 (2021): 01-06.
  3. Dabravolski SA., et al. “Mitochondrial Dysfunction and Chronic Inflammation in Polycystic Ovary Syndrome”. International Journal of Molecular Sciences 8 (2021): 3923.
  4. Finsterer J and Zarrouk-Mahjoub S. “Polycystic Ovary Syndrome in Mitochondrial Disorders Due MtDNA or NDNA Variants”. American Journal of Translational Research 10 (2018): 13-15.
  5. Zhu Y., et al. “Pathogenicity of the Homoplasmic C3275T, T4363C and A8343G Variant Requires Confirmation”. Gene 680 (2019): 97-98.
  6. Bozdag G., et al. “The Prevalence and Phenotypic Features of Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis”. Human Reproduction 31 (2016): 2841-2855.
  7. Muscogiuri G., et al. “Current Insights in to Inositol Isoforms, Mediterranean and Ketogenic Diets for Polycystic Ovary Syndrome: From Bench to Bedside”. Current Pharmaceutical Design 36 (2016): 5554-5557.
  8. Kulvinder Kochar Kaur., et al. “Mediterranean diet still holds a place in obesity treatment despite the considerable effectiveness of the very low-calorie ketogenic diet: A short communication”. Obesity Research and Clinical Practice Journal 1 (2023): 1-5.
  9. , et al. “Ketogenic diets as medical prescription for women with Polycystic Ovary Syndrome”. Current Nutrition Reports 12.1 (2023): 56-64.
  10. Cicione IR., et al. “Short term effects of Ketogenic diets or modestly hypocaloric diets Mediterranean diet on overweight and obese women with Polycystic Ovary Syndrome”. Journal of Endocrinological Investigation 4 (2023): 769-777.

Kulvinder Kochar Kaur. Advancements in the Etiopathogenesis, Pathophysiology and Treatment of Polycystic Ovary Syndrome (PCOS). EC Gynaecology 12.7 (2023): 20-23.