title: An analysis of the relationship between insulin resistance and the activity of steroid C17,20-lyase and 3beta-hydroxysteroid dehydrogenase in ovaries and adrenals in women with polycystic ovary syndrome.
abstract: Polycystic ovary syndrome (PCOS) is connected with insulin resistance (IR), and often with the hypersecretion of adrenal androgens. Mutual relationships between IR and adrenal and ovarian steroidogenesis were investigated in the group of 19 oligo/amenorhoeic women with PCOS. The age and body mass index (BMI) of the patients were 21+/-4.7 years and 26.4+/-5 kg/m2 (average+/-SD), respectively. All underwent a 60-minute adrenocorticotrophic hormone (ACTH) stimulation test, a gonadoliberin analogue (GnRHa) test with buserelin and an oral glucose tolerance test (oGTT) in the early follicular phase of the menstrual cycle. When absolute stimulated steroid levels after GnRHa were studied, a significant positive correlation between DHEA and area under curve during oGTT for C peptide (AUC-CP) (r=0.477, p= 0.039) and a borderline negative correlation (r=-0.404, p= 0.087) between AUC-CP and 17-OH progesterone, were found. Considering steroid values after ACTH, a significant positive correlation of IR index was found only with 17-OH-progesterone (r=0.499, p= 0.03). When stimulated enzymatic activities (expressed as product/ precursor ratios) were analyzed using factor analysis, a positive relationship between IR and ovarian C17,20-lyase in both delta4 and delta5 pathway was revealed. On the other hand, no relationship was confirmed between IR and enzymatic activities in the adrenals. The authors conclude that insulin resistance and/or hyperinsulinemia is probably not the primary factor responsible for the exaggerated adrenal androgen secretion found in a great number of patients with PCOS.
authors.affiliation: Institute of Endocrinology, Prague, Czech Republic. jvrbikova@endo.cz
authors.forename: J
authors.initials: J
authors.lastname: Vrbíklová
authors.forename: M
authors.initials: M
authors.lastname: Hill
authors.forename: L
authors.initials: L
authors.lastname: Stárka
authors.forename: K
authors.initials: K
authors.lastname: Vondra
authors.forename: J
authors.initials: J
authors.lastname: Sulcová
authors.forename: M
authors.initials: M
authors.lastname: Snajderová
authors.forename: D
authors.initials: D
authors.lastname: Cibula
authors.forename: Z
authors.initials: Z
authors.lastname: Pobisová
authors.forename: B
authors.initials: B
authors.lastname: Bendlová
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D015096:3-Hydroxysteroid Dehydrogenases / Q000378:metabolism*; D000311:Adrenal Glands / Q000201:enzymology*; D000324:Adrenocorticotropic Hormone; D000328:Adult; D000728:Androgens / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002096:C-Peptide / Q000097:blood; D003687:Dehydroepiandrosterone / Q000097:blood; D005163:Factor Analysis, Statistical; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007333:Insulin Resistance; D010053:Ovary / Q000201:enzymology*; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000201:enzymology / Q000503:physiopathology*; D012016:Reference Values; D013254:Steroid 17-alpha-Hydroxylase / Q000378:metabolism*
chemical_list: D000728:Androgens; D001786:Blood Glucose; D002096:C-Peptide; D003687:Dehydroepiandrosterone; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D015096:3-Hydroxysteroid Dehydrogenases; D013254:Steroid 17-alpha-Hydroxylase; D006854:Hydrocortisone