Impact of Helicobacter pylori infection on gastric and plasma ghrelin dynamics in humans.
OBJECTIVE
There are contradictory reports on the relationship between Helicobacter pylori and circulating ghrelin. We sought to clarify the influence of H. pylori infection on gastric and plasma ghrelin dynamics in humans.


METHODS
Using endoscopic biopsies from the corpus of 56 H. pylori-infected patients and 25 uninfected subjects, ghrelin mRNA expression levels and gastric ghrelin peptide contents were measured by real-time polymerase chain reaction and radioimmunoassay, respectively. We also measured plasma ghrelin concentrations and analyzed the numbers of ghrelin immunoreactive cells in the fundic gland area. Fifty-one patients with H. pylori infection were treated with a 7-day triple therapy consisting of lansoprazole, clarithromycin, and amoxicillin.


RESULTS
The gastric ghrelin mRNA expression level of H. pylori-positive patients (1.64 +/- 1.27 in arbitrary units) was significantly lower than in H. pylori-negative subjects (4.87 +/- 4.1, p < 0.0001). A similar trend was noted for ghrelin peptide contents (31.2 +/- 27.5 vs 81.2 +/- 64.1 ng/mg protein, respectively, p < 0.0001). There was no significant difference in the number of ghrelin immunoreactive cells/mm(2) in terms of H. plyori status. Plasma ghrelin concentrations in H. pylori-infected patients (144.6 +/- 7.8.8 fmol/ml) were significantly lower than in uninfected subjects (196.1 +/- 97.2, p < 0.05) and increased following cure of the infection. Plasma ghrelin levels correlated positively with the expression levels of ghrelin mRNA (r = 0.583, p < 0.0001) and peptide products (r = 0.574, p < 0.0001). There was a significant stepwise decrease in gastric ghrelin mRNA expression (p < 0.05), peptide contents (p < 0.01) and density of ghrelin immunoreactive cells (p < 0.05) with progression of histological severity of glandular atrophy in the corpus. The histological severity of chronic inflammation also negatively influenced the ghrelin mRNA expression (p < 0.001) and peptide production (p < 0.005).


CONCLUSIONS
H. pylori infection has a negative impact on gastric and plasma ghrelin dynamics. Chronic inflammatory and atrophic changes associated with the infection may affect gastric ghrelin biosynthesis and contribute to the low circulating levels.
Isomoto
Hajime
H
Second Department of Internal Medicine, Nagasaki University School of Medicine, Sakamoto, Nagasaki, Japan.
Ueno
Hiroaki
H
Saenko
Vladimir A
VA
Mondal
Muhtashan S
MS
Nishi
Yoshito
Y
Kawano
Naoko
N
Ohnita
Ken
K
Mizuta
Yohei
Y
Ohtsuru
Akira
A
Yamashita
Shunichi
S
Nakazato
Masamitsu
M
Kohno
Shigeru
S
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001707:Biopsy, Needle; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D005756:Gastritis / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D054439:Ghrelin; D013006:Growth Hormone / Q000378:metabolism; D016481:Helicobacter Infections / Q000378:metabolism* / Q000473:pathology; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D036361:Peptide Hormones / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D011863:Radioimmunoassay; D013270:Stomach / Q000473:pathology
D054439:Ghrelin; D036361:Peptide Hormones; D012333:RNA, Messenger; D013006:Growth Hormone