Circulating acylated ghrelin level decreases in accordance with the extent of atrophic gastritis.
OBJECTIVE
We attempted to clarify the significance of atrophic change of gastric mucosa for reduction of plasma ghrelin concentration irrespective of Helicobacter pylori (Hp) infection.


METHODS
Plasma acylated (acyl-)ghrelin concentration in 220 subjects, both with and without atrophic gastritis, was measured with an enzyme immunoassay kit. The extent of atrophic change of gastric mucosa was assessed and graded endoscopically. Hp infection was determined by assay of the anti-Hp antibody with an ELISA assay kit.


RESULTS
Plasma acyl-ghrelin concentration was significantly lower in the Hp positive than the Hp negative group, and Hp eradication significantly increased plasma acyl-ghrelin concentrations in Hp positive subjects. Plasma acyl-ghrelin was significantly lower in subjects with severely atrophic gastritis than in those with mild or moderate atrophic gastritis, irrespective of Hp infection or age group (<60 years old or > or = 60 years old). In male subjects with a normal body mass index, plasma acyl-ghrelin concentrations in subjects with severely atrophic gastritis were significantly lower than those in subjects with mildly or moderately atrophic gastritis, suggesting that the results of the study are independent of emaciation or obesity. Logistic regression analysis showed that gastric atrophy is the key factor that modulates plasma acyl-ghrelin levels.


CONCLUSIONS
The results suggest that plasma acyl-ghrelin concentration decreases in accordance with the extent of atrophic change in gastric mucosa irrespective of Hp infection, indicating that the low plasma acyl-ghrelin level of subjects with Hp infection is mainly caused by the progress of atrophic changes in gastric mucosa.
Kawashima
Junichi
J
Department of Gastroenterology and Hepatology, Saitama Medical Center, Saitama Medical University, 1981 Kamoda Tsujido-Machi, Kawagoe, Saitama 350-8550, Japan. jun-kawashima@umin.ac.jp
Ohno
Shino
S
Sakurada
Tomoya
T
Takabayashi
Hidehiko
H
Kudo
Mitsuko
M
Ro
Shoki
S
Kato
Shingo
S
Yakabi
Koji
K
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000907:Antibodies, Bacterial / Q000097:blood; D015992:Body Mass Index; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology / Q000473:pathology*; D005757:Gastritis, Atrophic / Q000097:blood* / Q000382:microbiology / Q000473:pathology; D005773:Gastroscopy; D054439:Ghrelin / Q000097:blood*; D016481:Helicobacter Infections / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012720:Severity of Illness Index
D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D054439:Ghrelin
Nature. 1999 Dec 9;402(6762):656-60
10604470
Am J Med. 2004 Sep 15;117(6):429-32
15380500
J Clin Endocrinol Metab. 2005 Jan;90(1):10-6
15483107
Am J Gastroenterol. 2004 Nov;99(11):2121-7
15554990
Biochem Biophys Res Commun. 2001 Jan 26;280(3):904-7
11162609
Diabetes. 2001 Aug;50(8):1714-9
11473029
Gut. 2003 May;52(5):637-40
12692045
Biochem Biophys Res Commun. 2000 Oct 5;276(3):905-8
11027567
Dig Dis Sci. 2006 Aug;51(8):1313-21
16838121