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The Effects of Central Adiposity on Growth Hormone (GH) Response to GH-Releasing Hormone-Arginine Stimulation Testing in Men

Program in Nutritional Metabolism and Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Hideo Makimura, M.D., Ph.D., Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, LON 211, Boston, Massachusetts 02114. E-mail: hmakimura{at}partners.org.

Context: The relative contribution of central adiposity vs. weight on GH response to stimulation testing in obesity is not known.

Objective: We aimed to assess the contribution of weight and specific measures of central and peripheral adiposity to GH response to GHRH-arginine testing in lean, overweight, and obese men.

Design: A total of 75 men [mean age, 44.3 ± 1.1 yr; body mass index (BMI), 28.8 ± 0.7 kg/m²] were investigated. Subjects were classified as lean (BMI < 25 kg/m²; n = 23), overweight (BMI 25 and <30 kg/m²; n = 28), or obese (BMI 30 kg/m²; n = 24). Subjects were also stratified by waist circumference (WC) (<102 cm, n = 47; 102 cm, n = 28). Body composition and regional adiposity were assessed by anthropometrics, dual-energy x-ray absorptiometry (DEXA), and abdominal computed tomography (CT) scans.

Results: Peak stimulated GH was 36.4 ± 5.4, 16.6 ± 2.9, and 7.6 ± 0.9 µg/liter among lean, overweight, and obese subjects, respectively (P < 0.001 for all comparisons). Peak stimulated GH was 26.9 ± 3.4 µg/liter among subjects with WC less than 102 cm compared to 7.9 ± 0.9 µg/liter among subjects with WC of 102 cm or greater (P < 0.0001). Separate multivariate models using anthropometric, DEXA, and CT-derived measures of central adiposity demonstrated strong associations between peak stimulated GH and measures of central adiposity including WC, trunk fat by DEXA, and visceral adiposity by CT, controlling for age, BMI, and more general measures of adiposity. WC was independently associated with peak GH response to GHRH-arginine in a model including age, BMI, and hip circumference. In this model, BMI was no longer significant, and peak GH was reduced 1.02 µg/liter for each 1 cm increase in WC (P = 0.02).

Conclusions: GH response to GHRH-arginine testing is reduced in both overweight and obese subjects and negatively associated with indices of central abdominal obesity including WC, trunk fat, and visceral adipose tissue. The use of waist circumference, as a surrogate for central adiposity, adds predictive information to the determination of GH response, independent of BMI.