HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 287/1/E63    most recent 00375.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Buijs, M. M. Articles by Pijl, H. Search for Related Content PubMed PubMed Citation Articles by Buijs, M. M. Articles by Pijl, H.

Glucose homeostasis in abdominal obesity: hepatic hyperresponsiveness to growth hormone action

Departments of ¹General Internal Medicine and ²Endocrinology, and ³Center for Human Drug Research, Leiden University Medical Center, 2300 RC Leiden; and ⁴Department of Clinical Chemistry, Laboratory of Endocrinology and Radiochemistry, and ⁵Department of Endocrinology and Metabolism, Academic Medical Center, 1100 DD Amsterdam, The Netherlands

Submitted 20 August 2003 ; accepted in final form 16 February 2004

It has been suggested that (abdominally) obese individuals are hypersensitive to growth hormone (GH) action. Because GH affects glucose metabolism, this may impact glucose homeostasis in abdominal obesity. Therefore, we studied the effect of GH on glucose metabolism in abdominally obese (OB) and normal-weight (NW) premenopausal women. A 1-h intravenous infusion of GH or placebo was randomly administered to six NW [body mass index (BMI) 21.1 ± 1.9 kg/m²] and six OB (BMI 35.5 ± 1.5 kg/m²) women in a crossover design. Insulin, glucagon, and GH secretion were suppressed by concomitant infusion of somatostatin. Glucose kinetics were measured using a 10-h infusion of [6,6-²H₂]glucose. In both groups, similar physiological GH peaks were reached by infusion of GH. GH strongly stimulated endogenous glucose production (EGP) in both groups. The percent increase was significantly greater in OB than in NW women (29.8 ± 11.3 vs. 13.3 ± 7.4%, P = 0.014). Accordingly, GH responsiveness, defined as the maximum response of EGP per unit GH, was increased in OB vs. NW subjects (6.0 ± 2.1 vs. 2.2 ± 1.5 µmol·min^–1·mU^–1·l^–1, P = 0.006). These results suggest that the liver is hyperresponsive to GH action in abdominally obese women. The role of the somatotropic ensemble in the control of glucose homeostasis in abdominal obesity is discussed.

hyperinsulinemia; hyposomatotropism; glucagon