An interventional study of Rosiglitazone and Acarbose in Polycystic Ovary Syndrome, sponsored by Jean-Patrice Baillargeon. Completed at 1 site in Canada. Open to female participants aged 18 Years to 40 Years, including healthy volunteers. Per ClinicalTrials.gov, last updated 2022-01-20.
Sponsored by Jean-Patrice Baillargeon · Not applicable, Interventional, and Basic science
The investigators hypothesis is that free fatty acids (FFA) accumulation in non fatty tissues would lead to insulin resistance and hyperandrogenism in PCOS women. Accordingly, Peroxisome Proliferator-Activated Receptor gamma (PPARγ) agonist (rosiglitazone) would be a great therapeutic option for PCOS as their activation induces transcription factors of gene implicated in fatty acids metabolism.
The aim is to verify if insulin-related hyperandrogenism can be reversed in women having polycystic ovary syndrome following an 8-week treatment with rosiglitazone compared to simple insulin reduction with acarbose.
For the purpose of this study, 14 lean women (BMI ≤ 25 kg/m2) and 36 obese women (BMI 30-39 kg/m2) with PCOS as well as 14 lean and 14 obese control women will be recruited to determine their insulin sensibility (insulin levels, M-value, metabolic clearance rate of glucose)and FFA metabolism (FFA levels, rythm of apparition and disapearance of FFA) during a 75g oral glucose tolerance test and a 2-step insulin-glucose clamp.
Polycystic ovary syndrome (PCOS) is a very common but complex endocrine disorder affecting 6 to 10% of childbearing age women. To diagnose PCOS, women must display two of these three symptoms: clinical or biochemical hyperandrogenism, oligoamenorrhea, and/or echographycally confirmed polycystic ovary. Many studies have also demonstrated that PCOS women are more insulin resistant than control women when matched for body mass index (BMI). Thus, insulin resistance (IR) and secondary hyperinsulinemia would be important premises in the development of PCOS. In fact, the prevalence of type 2 diabetes (T2D) is tripled in PCOS women.
Higher free fatty acid (FFA) concentrations were also observed in the circulation of PCOS women. As FFA accumulates in liver and muscle instead of fat cells, this could be an important cause of IR according to the theory of lipotoxicity. Some indirect evidences are suggesting that FFA accumulation in androgen secreting cells (ovary and adrenal gland) could enhance their androgen production. Based on these findings, our hypothesis is that FFA accumulation in non fatty tissues would lead to IR and hyperandrogenism in PCOS women. Accordingly, Peroxisome Proliferator-Activated Receptor gamma (PPARγ) agonist (rosiglitazone) would be a great therapeutic option for PCOS as their activation induces transcription factors of gene implicated in fatty acids metabolism.
The aim is to verify if insulin-related hyperandrogenism can be reversed in PCOS women following an 8-week treatment with rosiglitazone compared to simple insulin reduction with acarbose. For the purpose of this study, 14 lean women (BMI ≤ 25 kg/m2) and 36 obese women (BMI 30-39 kg/m2) with PCOS as well as 14 lean and 14 obese control women will be recruited to determine their insulin sensibility (insulin levels, M-value, metabolic clearance rate of glucose)and FFA metabolism (FFA levels, rythm of apparition and disapearance of FFA) during a 75g oral glucose tolerance test and a 2-step insulin-glucose clamp.
PCOS :
Health volunteers :
Exclusion Criteria:
Healthy volunteers :
Lean and obese PCOS women
Drug: Rosiglitazone
Obese PCOS women
Drug: Acarbose
Obese and lean healthy women evaluated only at baseline
4 mg twice daily for 8 weeks orally
Also known as: Avandia
100 mg three times daily for 8 weeks orally
Also known as: Prandase
Androgen hyper-responsiveness to insulin - Ratio
The calculated ratio of free testosterone to the area under the insulin curve during an OGTT
Time frame: 8 weeks
Androgen hyper-responsiveness to insulin - Relationship
Determined by the relationship between testosterone and insulin levels during an OGTT.
Time frame: 8 weeks
Insulin sensitivity
Determined by a 2-step insulin-glucose clamp
Time frame: 8 weeks
Insulin secretion
Determined by a 2-step insulin-glucose clamp
Time frame: 8 weeks
Hepatic glucose production
Determined by a 2-step insulin-glucose clamp
Time frame: 8 weeks
Plasma DCI-IPG during euglycemic-hyperinsulinemic clamp
Measured during steady-state
Time frame: 8 weeks
This study is completed, as verified in Jan 2022. You cannot join it, but the record below documents what was studied.
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