title: Increased adiposity enhances intrafollicular estradiol levels in normoandrogenic ovulatory women receiving gonadotropin-releasing hormone analog/recombinant human follicle-stimulating hormone therapy for in vitro fertilization.
abstract: BACKGROUND
  Body mass index (BMI) reflects the amount of insulin in the human follicle and may enhance insulin action as a cogonadotropin.
  
  
  OBJECTIVE
  This study examined whether increased adiposity enhances intrafollicular steroidogenesis in normoandrogenic ovulatory women receiving GnRH analog/recombinant human FSH therapy for in vitro fertilization.
  
  
  METHODS
  Study participants were from an institutional practice and comprised 30 normoandrogenic ovulatory women who were lean (n=17; BMI<25 kg/m2) or overweight (n=13; BMI>or=25 kg/m2). Women received GnRH analog after basal serum hormone determinations and oral glucose tolerance testing, followed by recombinant human FSH therapy and human chorionic gonadotropin administration when two or more follicles 18 mm or larger in diameter were present.
  
  
  METHODS
  Follicle fluid was aspirated at oocyte retrieval from the first follicle of each ovary.
  
  
  METHODS
  Follicle fluid was assayed for estradiol (E2), progesterone, 17-hydroxyprogesterone, androstenedione, testosterone, dihydrotestosterone, insulin, glucose, and lactate.
  
  
  RESULTS
  Overweight women had hyperinsulinemia (P=0.03) with decreased serum SHBG (P=0.001) and increased serum free testosterone levels (P=0.02). Elevated intrafollicular insulin levels in overweight women (P=0.004) were accompanied by normal glucose and lactate levels. Intrafollicular E2 levels were greater in overweight vs. lean women (P=0.03), whereas the remaining intrafollicular steroid levels were similar in both female groups.
  
  
  CONCLUSIONS
  In normoandrogenic ovulatory women undergoing in vitro fertilization, increased adiposity elevates insulin and E2 levels in terminally differentiated follicles without altering intrafollicular androgen levels or luteinization. Additional studies are required to determine whether these abnormalities impair oocyte development.
authors.affiliation: National Primate Research Center, University of Wisconsin, Madison 53715, USA. danieldumesic@aol.com
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Dumesic
authors.forename: Timothy G
authors.initials: TG
authors.lastname: Lesnick
authors.forename: David H
authors.initials: DH
authors.lastname: Abbott
mesh_terms: D000328:Adult; D004958:Estradiol / Q000097:blood*; D005260:Female; D005300:Fertility Agents, Female / Q000627:therapeutic use; D005307:Fertilization in Vitro; D005640:Follicle Stimulating Hormone / Q000627:therapeutic use*; D006801:Humans; D016729:Leuprolide / Q000627:therapeutic use*; D006080:Ovarian Follicle / Q000187:drug effects / Q000502:physiology; D050177:Overweight; D010060:Ovulation / Q000502:physiology*; D011994:Recombinant Proteins / Q000627:therapeutic use; D013851:Thinness; D015430:Weight Gain
chemical_list: D005300:Fertility Agents, Female; D011994:Recombinant Proteins; D004958:Estradiol; D005640:Follicle Stimulating Hormone; D016729:Leuprolide