Know your Enemy: The Rationale of Using Inositol in the Treatment of Polycystic Ovary Syndrome - PCOS Diva
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Know your Enemy: The Rationale of Using Inositol in the Treatment of Polycystic Ovary Syndrome

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Dr. Laganà has graciously allowed me to include his article on PCOS Diva.  For more information regarding his work researching myo-inositol and D-chiro- inositol you can also read this article.

Guest Post by Dr. Antonio Simone Laganà and Alfonsa Pizzo

Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Messina, Italy

The Polycystic Ovary Syndrome (PCOS) is defined, according to Rotterdam’s criteria proposed by the European Society for Human Reproduction and Embryology and the American Society for Reproductive Medicine [1,2], by the identification of two out of following parameters: oligo-anovulation; hyperandrogenism (clinical or biochemical); the presence of 12 or more follicles in each ovary measuring 2.9 mm in diameter, and/or an increased ovarian volume (>10 ml).

PCOS affects about 4-8% of the women in reproductive age [3], causing anovulatory cycles in the 74% of the cases, insulin- resistance in the 42% and hyperandrogenism in the 48% [4]. PCOS in our opinion could be considered as the result of concurrent endocrinological alterations, which affects each other. First of all, obesity affects the 35% of PCOS patients [5] and provoke multiple metabolic and endocrine dysfunctions: fatty tissue, in fact, behaves as non-classical endocrine organs and secretes specific cytokines and chemokines [6] which stimulate the androgens production by adrenal cortex and ovaries [7]; on the other hands, adipocytes’ mediators seems to alter thehypothalamus-hypophisis-gonads regulation system, causing high and constant production of Luteinizing Hormone (LH). This may accounts, at least in part, for the typical inhibition of the ovarian follicular maturation in PCOS patients [8]. Moreover, metabolic profile is strictly connected to gonadal function [9]: in PCOS patient’s insulin- resistance is commonly associated with hyperinsulinemia [10], and the latter acts synergistically with LH to enhance the androgen production of theca cells [11]. Furthermore, it is able to reduce circulating levels of Sex Hormone Binding Globulin (SHBG), leading to increased levels of free testosterone [12].Ovasitol

Considered altogether, these evidences led to the use of insulin sensitizing drugs to stem the symptoms of this pathology. To date, different Inositol isoforms seems to increase insulin action on various tissues and, in this way to improve the ovulatory function and to inhibit or limit the production of testosterone [13]. Moreover, the use of Inositol may improve the possibility of spontaneous ovulation and regular menstrual cycles, as well as to increase the production of progesterone in the luteal phase of female infertile patients with PCOS [14]. Inositol is a polyalcohol classified as insulin sensitizer and existing as nine stereoisomers, two of which, D-Chiro-inositol [15-18] and Myo-Inositol [14,19-22], are currently used in PCOS treatment.

Myo-Inositol, which is the most abundant form of inositol in humans, is converted to D-Chiro-inositol by an insulin-dependent epimerase [23]. These two stereoisomer showed an insulin-like action in vivo exerting the function of insulin mediators as inositolphosphoglycans (IPGs) [24]. In our experience, both Inositol isoforms are effective in improving ovarian function and metabolism of patients with PCOS, although Myo-Inositol shows the most marked effect on the metabolic profile, whereas D-Chiro-Inositol reduces more hyperandrogenism [25].


  1. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group (2004) Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 81: 19-25.
  2. Rotterdam ESHRE/ASRM-Sponsored PCOS consensus workshop group (2004) Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod 19: 41-47.
  3. Azziz R, Woods KS, Reyna R, Key TJ, Knochenhauer ES, et al. (2004) The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab 89: 2745-2749.
  1. Kurdoglu Z, Ozkol H, Tuluce Y, Koyuncu I (2012) Oxidative status and its relation with insulin resistance in young non-obese women with polycystic ovary syndrome. J Endocrinol Invest 35: 317-321.
  2. Franks S (1989) Polycystic ovary syndrome: a changing perspective. Clin Endocrinol (Oxf) 31: 87-120.
  3. Schuring AN, Schulte N, Sonntag B, Kiesel L (2008) Androgens and insulin- -two key players in polycystic ovary syndrome. Recent concepts in the pathophysiology and genetics of polycystic ovary syndrome. Gynakol Geburtshilfliche Rundsch 48: 9-15.
  4. James RG, Krakower GR, Kissebah AH (1996) Influence of androgenicity on adipocytes and precursor cells in female rats. Obes Res 4: 463-470.
  5. Norman RJ (2000) Lifestyle factors in aetioloy and management. In: Polycystic Ovary Syndrome. (1st Edn), Cambridge University Press.
  6. Burghen GA, Givens JR, Kitabchi AE (1980) Correlation of hyperandrogenism with hyperinsulinism in polycystic ovarian disease. J Clin Endocrinol Metab 50: 113-116.
  7. Azziz R (2003) Androgen excess is the key element in polycystic ovary syndrome. Fertil Steril 80: 252-254.
  8. Baillargeon JP, Carpentier A (2007) Role of insulin in the hyperandrogenemia of lean women with polycystic ovary syndrome and normal insulin sensitivity. Fertil Steril 88: 886-893.
  9. 12.Baptiste CG, Battista MC, Trottier A, Baillargeon JP (2010) Insulin and hyperandrogenism in women with polycystic ovary syndrome. J Steroid Biochem Mol Biol 122: 42-52.
  10. 13. Baillargeon JP, Nestler JE, Ostlund RE, Apridonidze T, Diamanti-Kandarakis E (2008) Greek hyperinsulinemic women, with or without polycystic ovary syndrome, display altered inositols metabolism. Hum Reprod 23: 1439-1446.
  11. 14. Papaleo E, Unfer V, Baillargeon JP, De Santis L, Fusi F, et al. (2007) Myo- inositol in patients with polycystic ovary syndrome: a novel method for ovulation induction. Gynecol Endocrinol 23: 700-703.
  12. 15. Cheang KI, Baillargeon JP, Essah PA, Ostlund RE Jr, Apridonize T, et al. (2008) Insulin-stimulated release of D-chiro-inositol-containing inositolphosphoglycan mediator correlates with insulin sensitivity in women with polycystic ovary syndrome. Metabolism 57: 1390-1397.
  13. 16. Nordio M, Proietti E (2012) The combined therapy with myo-inositol and D-chiro-inositol reduces the risk of metabolic disease in PCOS overweight patients compared to myo-inositol supplementation alone. Eur Rev Med Pharmacol Sci 16: 575-581.
  14. 17. Nestler JE, Jakubowicz DJ, Reamer P, Gunn RD, Allan G (1999) Ovulatory and metabolic effects of D-chiro-inositol in the polycystic ovary syndrome. N Engl J Med 340: 1314-1320.
  15. 18. Iuorno MJ, Jakubowicz DJ, Baillargeon JP, Dillon P, Gunn RD, et al. (2002) Effects of d-chiro-inositol in lean women with the polycystic ovary syndrome. Endocr Pract 8: 417-423.
  16. Genazzani AD, Lanzoni C, Ricchieri F, Jasonni VM (2008) Myo-inositol administration positively affects hyperinsulinemia and hormonal parameters in overweight patients with polycystic ovary syndrome. Gynecol Endocrinol 24: 139-144.
  17. Gerli S, Papaleo E, Ferrari A, Di Renzo GC (2007) Randomized, double blind placebo-controlled trial: effects of myo-inositol on ovarian function and metabolic factors in women with PCOS. Eur Rev Med Pharmacol Sci 11: 347- 354.
  18. Costantino D, Minozzi G, Minozzi E, Guaraldi C (2009) Metabolic and hormonal effects of myo-inositol in women with polycystic ovary syndrome: a double-blind trial. Eur Rev Med Pharmacol Sci 13: 105-110.
  19. Papaleo E, Unfer V, Baillargeon JP, Chiu TT (2009) Contribution of myo-inositol to reproduction. Eur J Obstet Gynecol Reprod Biol 147: 120-123
  20.  Isabella R, Raffone E (2012) Does ovary need D-chiro-inositol? J Ovarian Res 5: 14.
  21. Larner J (2002) D-chiro-inositol–its functional role in insulin action and its deficit in insulin resistance. Int J Exp Diabetes Res 3: 47-60
  22. Laganà AS, Borrielli I, Barbaro L, Pizzo A (2013) Myo-Inositol Vs D-Chiro- Inositol: preliminary data on the comparison between their effects on ovarian function and metabolic factors in women with PCOS. Proceedings of The World Congress on Building Consensus out of Controversies in Gynecology, Infertility and Perinatology (BCGIP-cogi) (Istanbul, Turkey, 30th May – 2nd June 2013).

*Corresponding author: Antonio Simone Laganà, Department of Pediatric, Gynecological, Microbiological and Biomedical Sciences, University of Messina, Messina, Italy

Citation: Laganà AS, Pizzo A (2013) Know your Enemy: The Rationale of Using Inositol in the Treatment of Polycystic Ovary Syndrome. Endocrinol Metab Synd 2: e121. doi: 10.4172/2161-1017.1000e121

Copyright: © 2013 Laganà AS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Volume 2 • Issue 3 • 1000e121

Antonio Simone Laganà was born in Reggio Calabria (Italy) on 8th May 1986. During his university career he was trained in particular in histology and embryology (supervisor Prof. Domenico Puzzolo), Clinical Pharmacology (supervisor Prof. Edoardo Spina), Immunology and General Pathology (supervisors Prof. Vincenza Sofo, Dr. Francesca Maria Salmeri) and finally in Obstetrics and Gynecology. He attended also the Department of Interventional Radiology of the Virginia Commonwealth University (Richmond, Virginia –  USA), where he studied technique of uterine fibroids chemioembolization (supervisor Prof. Uma Prasad), and the Department of Obstetrics and Gynecology of the “Klinicky Centar”  (Belgrade – Serbia. Supervisor Prof.  Milan Terzic). He earned his graduation at University of Messina (Italy) and became Resident Medical Doctor in Obstetrics and Gynecology. He is of Member of the “Italian Association of Endometriosis” Expert Panel , In-Training Member of the “Society for Gynecologic Investigation”, Regular Member of  the “European Society of Human Reproduction and Embryology”, of the “International Society of Gynecological Endocrinology” and of Giorgio Pardi Foundation’s professional research team. He got a Master of “gynaecological minimally invasive and robotic surgery” (supervisor Prof. Vito Cela, University of Pisa).  His research interests are: Endometriosis, Reproductive Immunology, T cell subsets, Chronic Pelvic Pain, Organogenesis and Genetic of Mullerian-Derived Structures, Gynecological Endocrinology, Polycystic Ovarian Syndrome (PCOS), Laparoscopy, Hysteroscopy, Minimally invasive surgery in ob/gyn. He is author of many papers published in national and international peer-reviewed journals, and his presence is often requested as Invited Speaker in international congresses.
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