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Growth Hormone Reduces Inflammation in Postmenopausal Women with Abdominal Obesity: A 12-Month, Randomized, Placebo-Controlled Trial

Departments of Endocrinology (C.F., B.-Å.B., J.S., G.J.), Medicine (B.A.), and Diagnostic Radiology (L.L.), Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden

Address all correspondence and requests for reprints to: Celina Franco, M.D., Department of Endocrinology, Gröna Stråket 8, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden. E-mail: celina.franco{at}medic.gu.se.

Context: Abdominal obesity is associated with low GH secretion, elevated circulating markers of inflammation, and increased risk of cardiovascular disease.

Objective: The objective was to study the effect of GH treatment on inflammatory markers and vascular adhesion molecules in postmenopausal women with abdominal obesity.

Design: Forty women aged 51–63 yr received GH (0.67 mg/d) in a randomized, double-blind, placebo-controlled, 12-month trial. Measurements of inflammatory markers [highly sensitive C-reactive protein (CRP), IL-6, and amyloid polypeptideA] and markers of endothelial dysfunction (soluble E-selectin, vascular adhesion molecule-1, intercellular molecule-1, and matrix metalloproteinase-9) were performed at baseline and after 6 and 12 months of treatment.

Results: After 12 months, the mean IGF SD score was 0.9 ± 1.5 and –0.8 ± 0.6 in the GH and placebo groups, respectively. GH treatment reduced CRP and IL-6 levels compared with placebo (P = 0.03 and P = 0.05, respectively), whereas the markers of endothelial dysfunction were unaffected. Within the GH-treated group, a reduction was shown in CRP (4.3 ± 4 to 3.0 ± 3 mg/liter; P < 0.05) and in IL-6 (4.4 ± 2 to 3.3 ± 2 ng/liter; P < 0.01). In the GH-treated group, the decrease in CRP and IL-6 correlated with a reduction in visceral adipose tissue (r = 0.7, P < 0.001 and r = 0.5, P < 0.05, respectively).

Conclusion: GH treatment in postmenopausal women with abdominal obesity reduced serum markers of systemic inflammation. Circulating markers of endothelial dysfunction were unaffected by treatment.

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