title: Growth hormone decreases visceral fat and improves cardiovascular risk markers in women with hypopituitarism: a randomized, placebo-controlled study.
abstract: BACKGROUND
  Data regarding gender-specific efficacy of GH on critical endpoints are lacking. There are no randomized, placebo-controlled studies of physiological GH therapy solely in women.
  
  
  OBJECTIVE
  Our objective was to determine the effects of physiological GH replacement on cardiovascular risk markers and body composition in women with GH deficiency (GHD).
  
  
  METHODS
  This was a 6-month, randomized, placebo-controlled, double-blind study.
  
  
  METHODS
  The study was conducted at the General Clinical Research Center.
  
  
  METHODS
  43 women with GHD due to hypopituitarism were included in the study.
  
  
  METHODS
  Study participants were randomized to receive GH (goal mid-normal serum IGF-1) or placebo.
  
  
  METHODS
  Cardiovascular risk markers, including high-sensitivity C-reactive protein, tissue plasminogen activator, and body composition, including visceral adipose tissue by cross-sectional computed tomography, were measured.
  
  
  RESULTS
  Mean daily GH dose was 0.67 mg. The mean IGF-1 sd score increased from -2.5 +/- 0.3 to -1.4 +/- 0.9 (GH) (P < 0.0001 vs. placebo). High-sensitivity C-reactive protein decreased by 38.2 +/- 9.6% (GH) vs.18.2 +/- 6.0% (placebo) (P = 0.03). Tissue plasminogen activator and total cholesterol decreased, and high-density lipoprotein increased. Homeostasis model assessment-insulin resistance and other markers were unchanged. Body fat decreased [-5.1 +/- 2.0 (GH) vs. 1.9 +/- 1.0% (placebo); P = 0.002] as did visceral adipose tissue [-9.0 +/- 5.9 (GH) vs. 4.3 +/- 2.7% (placebo); P = 0.03]. Change in IGF-1 level was inversely associated with percent change in visceral adipose tissue (r = -0.61; P = 0.002), total body fat (r = -0.69; P < 0.0001), and high-sensitivity C-reactive protein (r = -0.51; P = 0.003).
  
  
  CONCLUSIONS
  Low-dose GH replacement in women with GHD decreased total and visceral adipose tissue and improved cardiovascular markers, with a relatively modest increase in IGF-1 levels and without worsening insulin resistance.
authors.affiliation: Neuroendocrine Unit, Massachusetts General Hospital, Boston, MA 02114, USA.
authors.forename: Catherine
authors.initials: C
authors.lastname: Beauregard
authors.forename: Andrea L
authors.initials: AL
authors.lastname: Utz
authors.forename: Amber E
authors.initials: AE
authors.lastname: Schaub
authors.forename: Lisa
authors.initials: L
authors.lastname: Nachtigall
authors.forename: Beverly M K
authors.initials: BM
authors.lastname: Biller
authors.forename: Karen K
authors.initials: KK
authors.lastname: Miller
authors.forename: Anne
authors.initials: A
authors.lastname: Klibanski
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001823:Body Composition / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology* / Q000378:metabolism; D004311:Double-Blind Method; D005260:Female; D005947:Glucose / Q000378:metabolism; D013006:Growth Hormone / Q000172:deficiency; D019382:Human Growth Hormone / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D007018:Hypopituitarism / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D050152:Intra-Abdominal Fat / Q000187:drug effects* / Q000473:pathology; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008875:Middle Aged; D010919:Placebos; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D008055:Lipids; D008074:Lipoproteins; D010919:Placebos; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D005947:Glucose