OBJECTIVES: 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.
OBJECTIVES: There are contradictory reports on the relationship between Helicobacter pylori and circulating ghrelin. We sought to clarify the influence of H. pyloriinfection on gastric and plasma ghrelin dynamics in humans. METHODS: Using endoscopic biopsies from the corpus of 56 H. pylori-infectedpatients 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. pyloriinfection 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-infectedpatients (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. pyloriinfection 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.
Authors: Joel H Rubenstein; Hal Morgenstern; Daniel McConell; James M Scheiman; Philip Schoenfeld; Henry Appelman; Laurence F McMahon; John Y Kao; Val Metko; Min Zhang; John M Inadomi Journal: Gastroenterology Date: 2013-08-30 Impact factor: 22.682
Authors: Lucia Pacifico; John F Osborn; Valeria Tromba; Sara Romaggioli; Stefano Bascetta; Claudio Chiesa Journal: World J Gastroenterol Date: 2014-02-14 Impact factor: 5.742
Authors: Omero Alessandro Paoluzi; Del Vecchio Giovanna Blanco; Roberta Caruso; Ivan Monteleone; Giovanni Monteleone; Francesco Pallone Journal: World J Gastroenterol Date: 2014-01-21 Impact factor: 5.742