Ghrelin is primarily secreted from the stomach and has been implicated in the 
coordination of eating behavior and weight regulation. Ghrelin also plays an 
essential role in the mechanism of gastric mucosal defense. Thus, it is 
important to clarify which diseases primarily influence changes in plasma 
ghrelin concentrations. Helicobacter pylori (H pylori) infection is involved in 
the pathogenesis of gastritis, gastric and duodenal ulcer, gastric carcinoma, 
and mucosa-associated lymphoid tissue lymphoma. H pylori eradication is related 
to body weight change. Compared, H pylori infected and negative subjects with 
normal body mass index, plasma ghrelin concentration, gastric ghrelin mRNA, and 
the number of ghrelin producing cells in gastric mucosa are significantly lower 
in H pylori infected subjects than in H pylori-negative controls. Plasma ghrelin 
concentration decreases with the progression of gastric atrophy. Impaired 
gastric ghrelin production in association with atrophic gastritis induced by H 
pylori infection accounts for the decrease in plasma ghrelin concentration. 
However, the ratio of plasma acylated ghrelin to total ghrelin levels is higher 
in patients with chronic atrophic gastritis than in healthy subjects. This may 
result from the compensatory increase in plasma active ghrelin concentration in 
response to gastric atrophy. After H pylori eradication, gastric preproghrelin 
mRNA expression is increased nearly 4-fold in most cases. However, changes in 
plasma ghrelin concentrations before and after H pylori cure are not associated 
with the gastric ghrelin production. Plasma ghrelin changes are inversely 
correlated with both body weight change and initial plasma ghrelin levels.