Growth Hormone Decreases Visceral Fat and Improves Cardiovascular Risk Markers in Women with Hypopituitarism: A Randomized, Placebo-Controlled Study

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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.


Our objective was to determine the effects of physiological GH replacement on cardiovascular risk markers and body composition in women with GH deficiency (GHD).


This was a 6-month, randomized, placebo-controlled, double-blind study.


The study was conducted at the General Clinical Research Center.

Study Participants:

43 women with GHD due to hypopituitarism were included in the study.


Study participants were randomized to receive GH (goal mid-normal serum IGF-1) or placebo.

Main Outcome Measures:

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.


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).


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.

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