This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Katznelson, L. Articles by Klibanski, A. Search for Related Content PubMed PubMed Citation Articles by Katznelson, L. Articles by Klibanski, A.

Effects of Growth Hormone Secretion on Body Composition in Patients with Crohn’s Disease

Neuroendocrine Unit and General Clinical Research Center (L.K., W.P.F., N.Z., A.K.), Gastrointestinal Unit (B.E.S.), and Department of Radiology (D.I.R.), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114; and Gastroenterology Department, Beth Israel Deaconess Medical Center (M.A.P.), Boston, Massachusetts 02215

Address all correspondence and requests for reprints to: Laurence Katznelson, M.D., Neuroendocrine Unit Massachusetts General Hospital, 55 Fruit Street, Bulfinch 457, Boston, Massachusetts 02114. E-mail: lkatznelson1{at}partners.org.

Crohn’s disease is a multisystem disorder characterized by chronic intestinal inflammation. Accumulation of mesenteric fat occurs in patients with Crohn’s disease, although the mechanisms underlying site-specific changes in adipose deposition are unclear. To investigate whether there are alterations in site-specific adipose deposition in patients with Crohn’s disease and to determine hormonal influences that may underlie such changes, we investigated body composition and serum hormone levels in 20 men with Crohn’s disease (mean age, 45 ± 2 yr) and 20 age-, gender-, and body mass index-matched normal controls (mean age, 43 ± 3 yr). None of the Crohn’s patients was receiving glucocorticoid therapy. Subjects underwent hourly GH sampling for 12 h beginning at 2000 h and fasting serum IGF-I and testosterone measurements. Body composition was assessed by quantitative computed tomography of the abdomen and bioelectrical impedance analysis. In the Crohn’s disease and control subjects, mean serum GH levels were 1.07 ± 0.2 and 1.7 ± 0.2 ng/ml (P = 0.06), serum IGF-I levels were 162.7 ± 10.5 and 194.8 ± 15.7 ng/ml (P = 0.1), and serum testosterone levels were 489 ± 33 and 514 ± 38 ng/ml (P = NS), respectively. Percentage body fat was significantly higher in the Crohn’s patients (21 ± 0.8% vs. 17.7 ± 0.9%, respectively; P = 0.013). Intraabdominal fat (IAF) was significantly higher in the Crohn’s subjects vs. controls (115 ± 11 vs. 69 ± 7 cm², respectively; P = 0.001). The ratio of intraabdominal to total body fat was higher in the Crohn’s subjects than in the controls (0.4 ± 0.1 vs. 0.3 ± 0.1, respectively; P = 0.025). Subcutaneous fat area was similar in the two groups. IAF was higher in Crohn’s patients even when controlling for testosterone and mean serum GH. Mean serum GH contributed independently to the differences in IAF (P = 0.001). The ratio of IAF to total body fat remained higher in the Crohn’s subjects when controlling for serum testosterone, but was no longer significant in a model that also included IGF-I and mean serum GH. GH levels contributed independently to the differences in the intraabdominal to total body fat ratio (P = 0.02). In the Crohn’s patients, serum GH correlated negatively with intraabdominal and total body fat and the ratio of intraabdominal to total body fat. Crohn’s disease is associated with an increase in central fat accumulation, with more IAF and a higher ratio of intraabdominal to total body fat compared with controls. Although serum GH levels were similar in the two groups, GH contributed significantly to the abdominal fat measurements. These data show that GH has an important role in modulating visceral fat distribution in patients with Crohn’s disease.

This work was supported in part by a research grant from Pharmacia Corp. and NIH Grant M01-RR-01066.

Abbreviations: AUC, Area under the curve; BMI, body mass index; CDAI, Crohn’s disease activity index; CT, computed tomography; DHEAS, dehydroepiandrosterone sulfate; HOMA, homeostasis model assessment; IAF, intraabdominal fat; SCF, sc fat; TF, total fat.

This article has been cited by other articles:

				L. Peyrin-Biroulet, M. Chamaillard, F. Gonzalez, E. Beclin, C. Decourcelle, L. Antunes, J. Gay, C. Neut, J.-F. Colombel, and P. Desreumaux Mesenteric fat in Crohn's disease: a pathogenetic hallmark or an innocent bystander? Gut, April 1, 2007; 56(4): 577 - 583. [Full Text] [PDF]

				W J Sandborn and W A Faubion Biologics in inflammatory bowel disease: how much progress have we made? Gut, September 1, 2004; 53(9): 1366 - 1373. [Full Text] [PDF]