Ghrelin; Influences on Helicobacter pylori-associated Gastric Diseases.
- Author:
Jeong Young CHOI
1
;
Ki Baik HAHM
Author Information
1. Department of Gastroenterology, Ajou University School of Medicine and Genomic Research Center for Gastroenterology, Suwon, Korea. hahmkb@hotmail.com
- Publication Type:Review ; English Abstract
- Keywords:
Ghrelin;
Helicobacter pylori;
Leptin;
Nuclear factor-KappaB;
Protection
- MeSH:
Amino Acid Sequence;
Appetite Stimulants;
Gastritis/*metabolism/microbiology;
Ghrelin/*blood/chemistry;
Helicobacter Infections/*metabolism;
*Helicobacter pylori;
Humans;
Insulin-Like Growth Factor I/analysis;
Leptin/*blood;
Mitogen-Activated Protein Kinases/metabolism;
Molecular Sequence Data;
NF-kappa B/metabolism;
Neurosecretory Systems/*metabolism;
Peptide Hormones/*blood;
Signal Transduction;
Weight Gain
- From:The Korean Journal of Gastroenterology
2006;48(2):75-81
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-KappaB (NF-KappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.
