Endothelial function and insulin resistance in polycystic ovary syndrome: the effects of medical therapy

Autor: Sophia Zoungas, Caroline Meyer, Barry P McGrath, Samantha K. Hutchison, Lisa J. Moran, Helena J. Teede
Rok vydání: 2010
Předmět:
Blood Glucose
Time Factors
medicine.medical_treatment
Ethinyl Estradiol
chemistry.chemical_compound
Sex hormone-binding globulin
Sex Hormone-Binding Globulin
Insulin
Medicine
Glucose homeostasis
Testosterone
biology
Obstetrics and Gynecology
General Medicine
Lipids
Polycystic ovary
Metformin
Vasodilation
Contraceptives
Oral
Combined
C-Reactive Protein
Treatment Outcome
Drug Therapy
Combination
Female
Inflammation Mediators
Polycystic Ovary Syndrome
medicine.drug
Adult
medicine.medical_specialty
Arginine
Contraceptives
Oral
Hormonal
Insulin resistance
Internal medicine
Plasminogen Activator Inhibitor 1
von Willebrand Factor
Humans
Hypoglycemic Agents
Cyproterone Acetate
business.industry
Hyperandrogenism
medicine.disease
Endocrinology
Reproductive Medicine
chemistry
biology.protein
Endothelium
Vascular
Insulin Resistance
business
Asymmetric dimethylarginine
Biomarkers
Zdroj: Fertility and Sterility. 93:184-191
ISSN: 0015-0282
Popis: Objective To assess the interaction between insulin resistance and endothelial function and the optimal treatment strategy addressing cardiovascular risk in polycystic ovary syndrome. Design Randomized controlled trial. Setting Controlled clinical study. Patient(s) Overweight age- and body mass index–matched women with polycystic ovary syndrome. Intervention(s) Six months metformin (1 g two times per day, n=36) or oral contraceptive pill (OCP) (35 μg ethinyl E 2 –2 mg cytoproterone acetate, n=30). Main Outcome Measure(s) Fasting and oral glucose tolerance test glucose and insulin levels, endothelial function (flow-mediated dilation, asymmetric dimethylarginine, plasminogen activator inhibitor-1, von Willebrand factor), inflammatory markers (high-sensitivity C-reactive protein), lipids, and hyperandrogenism. Result(s) The OCP increased levels of glucose and insulin on oral glucose tolerance test, high-sensitivity C-reactive protein, triglycerides, and sex-hormone binding globulin and decreased levels of low-density lipoprotein cholesterol and T. Metformin decreased levels of fasting insulin, oral glucose tolerance test insulin, high-density lipoprotein cholesterol, and high-sensitivity C-reactive protein. Flow-mediated dilation increased only with metformin (+2.2% ± 4.8%), whereas asymmetric dimethylarginine decreased equivalently for OCP and metformin (−0.3 ± 0.1 vs. −0.1 ± 0.1 mmol/L). Greater decreases in plasminogen activator inhibitor-1 occurred for the OCP than for metformin (−1.8 ± 1.6 vs. −0.7 ± 1.7 U/mL). Conclusion(s) In polycystic ovary syndrome, metformin improves insulin resistance, inflammatory markers, and endothelial function. The OCP worsens insulin resistance and glucose homeostasis, inflammatory markers, and triglycerides and has neutral or positive endothelial effects. The effect of the OCP on cardiovascular risk in polycystic ovary syndrome is unclear.
Databáze: OpenAIRE
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