• Obesity
• Diabetes & Endocrinology Clinical Trials
• Hormone Therapy
• Menopause

Effects of Growth Hormone (GH) on Body Composition and Cardiovascular (CV) Risk Markers in Women with Visceral Adiposity was a 6-month randomized, double-blind, placebo-controlled trial to determine whether low-dose GH administration would reduce abdominal adiposity and CV risk markers in premenopausal women with reduced GH secretion due to abdominal obesity. Miriam Bredella, MD, Massachusetts General Hospital, Boston, Massachusetts, USA, presented findings from the study.

Abdominal adiposity confers a 3-fold increased risk for heart disease in women compared with accumulation of body fat in the gluteal femoral region [Rexrode KM et al. JAMA 1998]. Data also suggest that visceral adiposity may be associated with reduced endogenous growth hormone and that decreased growth hormone secretion may be associated with increased CV risk markers [Utz A et al. J Clin Endocrinol Metab 2008].

The study included 79 obese premenopausal women. The primary outcome measure was abdominal fat depots, including: visceral adipose tissue and the muscle area of the mid-thigh, as determined by computed tomography scan; fat and lean body mass, determined by dual-emission X-ray absorptiometry; intramyocellular (IMCL) and intrahepatic lipids (IHL), determined by proton magnetic resonance spectroscopy; high-sensitivity C-reactive protein (hs-CRP); total cholesterol, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C); apolipoprotein B (apo B); fibrinogen; tissue plasminogen activator (tPA); carotid intima-media thickness (CIMT); and endothelial function.

At 6 months, the mean GH dose was 1.7±0.6 mg/day. This resulted in a mean increase in the IGF-1 standard deviation score (SDS*) from −1.7±0.5 to −0.1±1.4 in the GH group. Compared with placebo, administration of GH led to an increase in muscle area (2.0±5.4 vs −3.0±6.8 cm²; p=0.03) and total lean mass (2.0±1.7 vs 0.1±2.1 kg; p=0.001), and a decrease in the trunk:extremity fat ratio (0.01±0.05 vs −0.03±0.06; p=0.006)

Change in IGF-1 level was associated with a 6-month decrease in visceral adipose tissue (VAT) (r=-0.56; p=0.002). This suggested that subjects with the greatest increases in IGF-1 levels had the greatest decreases in VAT. VAT decreased within the GH group, but the change was not significant when compared with placebo.

Compared with placebo, GH decreased hsCRP (−1.1±1.2 vs 0.07±1.2 mg/L; p=0.01), apo B (−9.1±17.9 vs 6.1± 17.5 mg/dL; p=0.005), apo B/LDL-C (a measure of LDL-C size and atherogenecity) (−0.009±0.1 vs 0.1±0.2; p=0.01), and tPA (−0.4±5.0 vs 4.5±10.3 ng/ml; p=0.03). Total cholesterol, LDL-C, HDL-C, fibrinogen, IMCL, and IHL did not change compared with placebo, but IMCL increased compared with baseline in the GH group. No effect on CIMT or endothelial function was observed.

GH increased fasting glucose (2.4±7.2 vs −0.9±3.6 mg/dL) and 2-hour glucose (18.6±32.8 vs −0.7±26.7 mg/dL) compared with placebo (p<0.05), with no difference in 2-hour glucose levels between groups at 6 months. Baseline fasting glucose predicted a 6-month change in 120 minute glucose levels within the growth GH (r=0.48; p=0.01). Five subjects had a 120-minute glucose level greater than 200 mg/dL, one of whom was on placebo. No subjects had fasting glucose levels ≥126 mg/dL. Additional side effects were limited.

Based on these findings, the authors concluded that GH replacement in viscerally obese premenopausal women has beneficial effects on markers of CV risk and body composition but is associated with a decrease in glucose tolerance in a minority of women.

• © 2011 MD Conference Express