title: Glucose action and adrenocortical biosynthesis in women with polycystic ovary syndrome.
abstract: OBJECTIVE
  To determine if insulin or glucose action plays a role in adrenocortical steroidogenesis in the polycystic ovary syndrome (PCOS).
  
  
  METHODS
  Prospective cohort study.
  
  
  METHODS
  Academic medical center.
  
  
  METHODS
  Nine reproductive-aged patients with PCOS and nine age-, race-, and body mass index-matched controls.
  
  
  METHODS
  Insulin-modified frequently sampled intravenous glucose tolerance testing and an acute 60-minute ACTH-(1-24) stimulation test. From the glucose tolerance test, glucose and insulin were measured and the insulin sensitivity index, glucose effectiveness, and acute insulin response to glucose were determined. Dehydroepiandrosterone sulfate (DHEAS) basally and 17-hydroxypregnenolone, 17-hydroxyprogesterone, DHEA, androstenedione, and cortisol during ACTH testing at 0 and 60 minute (steroid(0) and steroid(60)) were determined. The net change in steroid during the ACTH test was calculated.
  
  
  RESULTS
  The insulin sensitivity index had limited correlation with adrenocortical variables in both groups. In patients with PCOS, glucose effectiveness was positively associated with DHEAS, cortisol(0), cortisol(60), change in cortisol, DHEA(0), DHEA(60), change in DHEA, 17-hydroxyprenenolone(60), change in 17-hydroxypregnenolone, DHEA(0), androstenedione(0), 17-hydroxyprenenolone(0), 17-hydroxyprogesterone(0), 17-hydroxyprenenolone(60), and 17-hydroxyprogesterone(60).
  
  
  CONCLUSIONS
  Adrenocortical biosynthesis, basally and in response to ACTH, appears to be closely associated with glucose effectiveness in PCOS. A common factor determining both the effectiveness of glucose to control its own production or uptake and adrenocortical biosynthesis may be aberrant in PCOS.
authors.affiliation: Department of Obstetrics and Gynecology, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
authors.forename: Lisa
authors.initials: L
authors.lastname: Farah-Eways
authors.forename: Rosario
authors.initials: R
authors.lastname: Reyna
authors.forename: Eric S
authors.initials: ES
authors.lastname: Knochenhauer
authors.forename: Alfred A
authors.initials: AA
authors.lastname: Bartolucci
authors.forename: Ricardo
authors.initials: R
authors.lastname: Azziz
mesh_terms: D006907:17-alpha-Hydroxypregnenolone / Q000097:blood; D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000302:Adrenal Cortex / Q000378:metabolism; D000305:Adrenal Cortex Hormones / Q000096:biosynthesis* / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000378:metabolism / Q000494:pharmacology; D000328:Adult; D000735:Androstenedione / Q000097:blood; D016022:Case-Control Studies; D015331:Cohort Studies; D003687:Dehydroepiandrosterone / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007333:Insulin Resistance; D011085:Polycystic Ovary Syndrome / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D011446:Prospective Studies; D013739:Testosterone / Q000097:blood
chemical_list: D000305:Adrenal Cortex Hormones; D006907:17-alpha-Hydroxypregnenolone; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D005947:Glucose; D006854:Hydrocortisone