Brief Reports
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 21, 2005; 11(11): 1644-1648
Published online Mar 21, 2005. doi: 10.3748/wjg.v11.i11.1644
Impact of Helicobacter pylori infection on ghrelin and various neuroendocrine hormones in plasma
Hajime Isomoto, Hiroaki Ueno, Yoshito Nishi, Chun-Yang Wen, Masamitsu Nakazato, Shigeru Kohno
Hajime Isomoto, Yoshito Nishi, Shigeru Kohno, Second Department of Internal Medicine, Nagasaki University School of Medicine, Sakamoto 1-7-1, Nagasaki, Japan
Chun-Yang Wen, Department of Molecular Pathology, Atomic Bomb Disease Institute, Nagasaki University School of Medicine, Sakamoto 12-4, Nagasaki, Japan
Hiroaki Ueno, Masamitsu Nakazato, Third Department of Internal Medicine, Miyazaki Medical College, Kiyotake, Miyazaki, Japan
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Hajime Isomoto, Second Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki, Japan. hajimei2002@yahoo.co.jp
Telephone: +81-95-849-7567 Fax: +81-95-849-7568
Received: August 19, 2004
Revised: August 20, 2004
Accepted: September 6, 2004
Published online: March 21, 2005
Abstract

AIM: Ghrelin, an endogenous ligand for growth hormone secretagogue receptor, influences appetite, energy balance, gastric motility and acid secretion. The stomach is the main source of circulating ghrelin. There are inconsistent reports on the influence of Helicobacter pylori (H pylori) infection on circulating ghrelin levels. We sought to elucidate the relationship between ghrelin and various peptides in plasma, with special reference to H pylori.

METHODS: Plasma ghrelin levels were measured by radioimmunoassay in 89 subjects who were referred for upper gastrointestinal endoscopy, consisting of 42 H pylori infected and 47 uninfected ones. Plasma gastrin, somatostatin, leptin, insulin-like growth hormone 1 (IGF-1) and chromogranin A concentrations were also measured. Twelve patients were treated with anti- H pylori regimen.

RESULTS: Ghrelin circulating levels were greatly decreased in H pylori-positive than negative individuals (194.2±90.2 fmol/mL and 250.4±84.1 respectively, P<0.05), but did not significantly alter following the cure of infection (176.5±79.5 vs 191.3±120.4). There was a significant negative correlation between circulating ghrelin and leptin levels, as well as body mass index, for the whole and uninfected population, but not in H pylori-infected patients. Plasma ghrelin concentrations correlated positively with IGF-1 in H pylori-negative group and negatively with chromogranin A in the infected group. There were no significant correlations among circulating levels of ghrelin, gastrin and somatostatin irrespective of H pylori status.

CONCLUSION: H pylori infection influences plasma ghrelin dynamics and its interaction with diverse bioactive peptides involved in energy balance, growth and neuroendocrine function.

Keywords: Helicobacter pylori; Ghrelin; Leptin; Gastrin; Insulin-like growth factor