help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2004-0501
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
90/2/1061    most recent
Author Manuscript (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gleeson, H. K.
Right arrow Articles by Shalet, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gleeson, H. K.
Right arrow Articles by Shalet, S. M.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Substance via MeSH
Medline Plus Health Information
*Nutrition
*Obesity
Related Collections
Right arrow Neuroendocrinology and Pituitary
Right arrow Obesity
The Journal of Clinical Endocrinology & Metabolism Vol. 90, No. 2 1061-1067
Copyright © 2005 by The Endocrine Society

Insulin-Like Growth Factor-I Response to a Single Bolus of Growth Hormone Is Increased in Obesity

Helena K. Gleeson, Catherine A. Lissett and Stephen M. Shalet

Department of Endocrinology, Christie Hospital, Manchester M20 4BX, United Kingdom

Address all correspondence and requests for reprints to: Professor S. M. Shalet, Department of Endocrinology, Christie Hospital, Wilmslow Road, Withington, Manchester M20 4BX, United Kingdom. E-mail: helena.gleeson{at}christie-tr.nwest.nhs.uk.

Reduced GH levels are found in obesity; despite which IGF-I levels are reported as low normal or normal. Previously peripheral responsiveness to GH has been investigated and reported to be increased in obese men and premenopausal women; however, the use of weight-based GH doses in these studies made data interpretation difficult. GH binding protein (GHBP) measurement constitutes an indirect estimate of GH receptor number. GHBP has been reported to be elevated in obesity; however, results from a recent study implied that this was only in men and premenopausal but not postmenopausal women. Therefore, we pursued this question further by challenging a cohort of healthy normal-weight and obese subjects with a non-weight-based dose of GH and examined the relationship of GHBP with the IGF-I response in the context of their body composition.

Ninety-eight (40 male) healthy subjects with a wide range of ages and body mass index (BMI) were studied. Ninety-one (34 male) of these subjects were divided into groups of similar age: men and women with a BMI less than 30 [normal-weight men (NM), BMI 26 (22–29) kg/m2 (n = 19) and women (NW), BMI 24 (19–29) kg/m2 (n = 23) and with a BMI > 30 (obese men (OM), 41 (30–72) kg/m2 (n = 15) and women (OW), 43 (30–68) kg/m2 (n = 34)]. Fat mass and percentage fat were measured by a bioelectrical impedance analyzer. An IGF-I generation test, which involved a sc injection of 21 IU (7 mg) GH, was performed. At baseline serum samples were assayed for GHBP; serum IGF-I and IGFBP3 levels were measured both at baseline and 24 h after GH administration.

There was a higher increment IGF-I in obese men and women, compared with the equivalent normal-weight subjects [NM vs. OM: 245 (33–342) vs. 291 (192–427) ng/ml (P < 0.05); NW vs. OW: 220 (103–435) vs. 315 (144–450) ng/ml (P < 0.0005)]. Increment IGF-I was negatively correlated with baseline IGF-I (F = 12.1) and positively correlated with GHBP (F = 18.2) (R2 = 0.29). GHBP levels were significantly higher in OM and OW (pre- and postmenopausal) than in the equivalent normal-weight groups [NM vs. OM: 2175 (995–4190) vs. 3030 (1540–5470) pmol/liter (P < 0.05); NW vs. OW: 2131 (1010–5040) vs. 3585 (1540–5740) pmol/liter (P < 0.0005)]. GHBP levels correlated highly with BMI, percentage fat, and fat mass (R > 0.6, P < 0.0001). Baseline IGF-I was not affected by body composition.

In conclusion, in obese compared with normal-weight healthy subjects, there is a larger increment IGF-I to a single bolus of GH in men, and irrespective of menopausal status, women. Increment IGF-I is associated positively with GHBP level, which in turn is associated with markers of increasing obesity in men and women. GH responsiveness is increased in obesity.




This article has been cited by other articles:


Home page
J. Clin. Endocrinol. Metab.Home page
N. Bouhours-Nouet, F. Gatelais, F. Boux de Casson, S. Rouleau, and R. Coutant
The Insulin-Like Growth Factor-I Response to Growth Hormone Is Increased in Prepubertal Children with Obesity and Tall Stature
J. Clin. Endocrinol. Metab., February 1, 2007; 92(2): 629 - 635.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
Y. Wei, Z. Rhani, and C. G. Goodyer
Characterization of Growth Hormone Receptor Messenger Ribonucleic Acid Variants in Human Adipocytes
J. Clin. Endocrinol. Metab., May 1, 2006; 91(5): 1901 - 1908.
[Abstract] [Full Text] [PDF]


Home page
J. Clin. Endocrinol. Metab.Home page
V. Popovic, D. Miljic, S. Pekic, P. Pesko, M. Djurovic, M. Doknic, S. Damjanovic, D. Micic, G. Cvijovic, J. Glodic, et al.
Low Plasma Ghrelin Level in Gastrectomized Patients Is Accompanied by Enhanced Sensitivity to the Ghrelin-Induced Growth Hormone Release
J. Clin. Endocrinol. Metab., April 1, 2005; 90(4): 2187 - 2191.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2005 by The Endocrine Society