2007Clinical EndocrinologyOpen access

Plasma acylated ghrelin levels are higher in patients with chronic atrophic gastritis

Davide Campana, Francesca Nori, Uberto Pagotto, Rosaria De Iasio, Antonio Maria Morselli‐Labate, Renato Pasquali, Roberto Corinaldesi, Paola Tomassetti

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Abstract

OBJECTIVES: Ghrelin is mainly produced by the endocrine cells of the gastric oxyntic mucosa. For this reason we decided to investigate the modification of the circulating levels not only of total but also of acylated ghrelin in a series of patients with chronic atrophic gastritis. DESIGN: Twenty-five patients with chronic atrophic gastritis and 25 healthy subjects were studied. In all 50 subjects gastrin and total and acylated ghrelin levels were evaluated. All patients underwent endoscopy with multiple biopsies, and the possibility of Helicobacter pylori infection was investigated. RESULTS: Significantly higher acylated ghrelin levels (82.8 +/- 61.3 vs. 35.1 +/- 17.1 pmol/l), acylated/total ghrelin ratio (0.422 +/- 0.202 vs. 0.152 +/- 0.085) and gastrin levels (1071 +/- 816 vs. 66 +/- 22 ng/l) were observed in the 25 patients with chronic atrophy than in the healthy subjects. Otherwise, no significant relationships were found when total ghrelin was correlated with the presence of atrophy, or with gastrin levels. In the healthy subjects, but not in the patients, acylated and total ghrelin levels were significantly higher in female than in male patients. CONCLUSIONS: The increase in acylated ghrelin levels and in the acylated/total ghrelin ratio in patients with atrophy of the body and fundus can be explained by hypothesizing an increase in the acylating process in the presence of gastric atrophy. It suggests that there may be a compensatory increase in plasma active ghrelin concentration in response to gastric atrophy, a condition which causes a loss of ghrelin-producing cells and an increase in gastric pH.

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OBJECTIVES: Ghrelin is mainly produced by the endocrine cells of the gastric oxyntic mucosa. For this reason we decided to investigate the modification of the circulating levels not only of total but also of acylated ghrelin in a series of patients with chronic atrophic gastritis. DESIGN: Twenty-five patients with chronic atrophic gastritis and 25 healthy subjects were studied. In all 50 subjects gastrin and total and acylated ghrelin levels were evaluated. All patients underwent endoscopy with multiple biopsies, and the possibility of Helicobacter pylori infection was investigated. RESULTS: Significantly higher acylated ghrelin levels (82.8 +/- 61.3 vs. 35.1 +/- 17.1 pmol/l), acylated/total ghrelin ratio (0.422 +/- 0.202 vs. 0.152 +/- 0.085) and gastrin levels (1071 +/- 816 vs. 66 +/- 22 ng/l) were observed in the 25 patients with chronic atrophy than in the healthy subjects. Otherwise, no significant relationships were found when total ghrelin was correlated with the presence of atrophy, or with gastrin levels. In the healthy subjects, but not in the patients, acylated and total ghrelin levels were significantly higher in female than in male patients. CONCLUSIONS: The increase in acylated ghrelin levels and in the acylated/total ghrelin ratio in patients with atrophy of the body and fundus can be explained by hypothesizing an increase in the acylating process in the presence of gastric atrophy. It suggests that there may be a compensatory increase in plasma active ghrelin concentration in response to gastric atrophy, a condition which causes a loss of ghrelin-producing cells and an increase in gastric pH.

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Available abstract

OBJECTIVES: Ghrelin is mainly produced by the endocrine cells of the gastric oxyntic mucosa. For this reason we decided to investigate the modification of the circulating levels not only of total but also of acylated ghrelin in a series of patients with chronic atrophic gastritis. DESIGN: Twenty-five patients with chronic atrophic gastritis and 25 healthy subjects were studied. In all 50 subjects gastrin and total and acylated ghrelin levels were evaluated. All patients underwent endoscopy with multiple biopsies, and the possibility of Helicobacter pylori infection was investigated. RESULTS: Significantly higher acylated ghrelin levels (82.8 +/- 61.3 vs. 35.1 +/- 17.1 pmol/l), acylated/total ghrelin ratio (0.422 +/- 0.202 vs. 0.152 +/- 0.085) and gastrin levels (1071 +/- 816 vs. 66 +/- 22 ng/l) were observed in the 25 patients with chronic atrophy than in the healthy subjects. Otherwise, no significant relationships were found when total ghrelin was correlated with the presence of atrophy, or with gastrin levels. In the healthy subjects, but not in the patients, acylated and total ghrelin levels were significantly higher in female than in male patients. CONCLUSIONS: The increase in acylated ghrelin levels and in the acylated/total ghrelin ratio in patients with atrophy of the body and fundus can be explained by hypothesizing an increase in the acylating process in the presence of gastric atrophy. It suggests that there may be a compensatory increase in plasma active ghrelin concentration in response to gastric atrophy, a condition which causes a loss of ghrelin-producing cells and an increase in gastric pH.

Key concepts: Ghrelin, Internal medicine, Atrophic gastritis, Atrophy, Gastrin, Endocrinology, Medicine, Gastritis

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