Growth hormone decreases visceral fat and improves cardiovascular risk markers in women with hypopituitarism: a randomized, placebo-controlled study.
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.
Beauregard
Catherine
C
Neuroendocrine Unit, Massachusetts General Hospital, Boston, MA 02114, USA.
Utz
Andrea L
AL
Schaub
Amber E
AE
Nachtigall
Lisa
L
Biller
Beverly M K
BM
Miller
Karen K
KK
Klibanski
Anne
A
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
D015415:Biomarkers; D008055:Lipids; D008074:Lipoproteins; D010919:Placebos; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D005947:Glucose