Impaired Production of Gastric Ghrelin in Chronic Gastritis Associated with<i>Helicobacter pylori</i>

Osawa, Hiroyuki; Nakazato, Masamitsu; Date, Yukari; Kita, Hiroto; Ohnishi, Hirohide; Ueno, Hiroaki; Shiiya, Tomomi; Satoh, Kiichi; Ishino, Yumiko; Sugano, Kentaro

doi:10.1210/jc.2004-1330

Cited by 162 publications

(155 citation statements)

References 27 publications

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“…Plasma ghrelin concentrations in these patients are not decreased, in contrast to results reported in DM1 patients and in CAG due to H. pylori infection (4,5). The fact that plasma ghrelin concentrations were not low in our DM1-CAG patients could be explained by the results obtained on histologic studies.…”

Section: Discussioncontrasting

confidence: 80%

“…On the other hand, endocrine hyperplasia of ECL due to an increase in gastrin levels secondary to achlorhydria is a frequent finding in gastric mucosa of CAG patients (17). Although ghrelin is known to be synthesised by X/A-like cells, immunohistochemical studies of ECL hyperplastic lesions in the setting of type A CAG, as well as gastric carcinoids, have shown that these lesions are strongly positive for ghrelin and do express ghrelin mRNA, which demonstrates that this cell population also synthesise the protein (5). For this reason, it has been hypothesised that ECL acquire the capability to synthesise ghrelin during proliferative states or that ghrelin is the product of a peculiar neoplastic cell population, increased by gastrin stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…Most studies on chronic atrophic gastritis (CAG) observed a low plasma ghrelin concentration due to Helicobacter pylori (H. pylori) infection (4-6) with a positive association between this concentration and biochemical markers of gastric mucosa atrophy such as pepsinogen I and pepsinogen I/II ratio (4,5,7). Severity of histologic changes and gastritis topography has been reported to affect circulating ghrelin levels which are markedly decreased in cases of extensive atrophic gastritis involving the corpus (4).…”

Section: Introductionmentioning

confidence: 99%

“…A possible explanation for this low ghrelin concentration is the loss of ghrelinproducing cells. In fact, attenuation of ghrelin mRNA expression and reduction in ghrelin-positive cell number in gastric mucosa have been described in patients with H. pylori infection (5). Atrophic autoimmune gastritis, or type A CAG, is characterised by chronic inflammation of oxyntic mucosa predominantly affecting the gastric corpus which results in achlorhydria and atrophy of oxyntic glands and progressive disappearance of parietal and chief cells.…”

Section: Introductionmentioning

confidence: 99%

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Plasma ghrelin concentrations in type 1 diabetic patients with autoimmune atrophic gastritis

Alonso¹,

Granada²,

Salinas³

et al. 2007

European Journal of Endocrinology

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Objective: Type 1 diabetes mellitus patients (DM1) show increased prevalence of pernicious anaemia, the histological substrate of which is type A chronic atrophic gastritis (CAG) in the stomach corpus, the main source of ghrelin. We aimed to compare plasma ghrelin concentrations in DM1 patients with type A CAG (DM1-CAG), DM1 patients without type A CAG and healthy controls and in DM1-CAG group, to ascertain a possible relationship between ghrelin and biochemical markers of gastric mucosa atrophy and/or neuroendocrine (NE) cell hyperplasia and histological gastric biopsy findings. Design and methods: Fifteen DM1-CAG patients were matched for age, sex and body mass index with 15 DM1 patients without type A CAG and 15 controls. Pepsinogen I, pepsinogen II, gastrin, parietal cell antibodies, chromogranin A (CgA) and ghrelin were determined in all subjects. In DM1-CAG patients, immunohistochemical analysis of gastric biopsies using antibodies to CgA and ghrelin was performed. Results: Ghrelin concentrations differed among groups; however, paired comparisons between groups were not significant. In DM1-CAG, no correlation was found between ghrelin and gastric body atrophy markers, pepsinogen I and the pepsinogen I/II ratio. Immunohistochemical studies of DMI-CAG patients showed CgA staining in 12 and ghrelin staining in 6, which was confined to the foci of NE cell hyperplasia. Those patients who stained positive for ghrelin had higher ghrelin concentrations when compared with the negative patients. Conclusions: Ghrelin concentrations are not decreased in DM1-CAG patients; thus, our data suggest that ghrelin is not a good marker of gastric mucosa atrophy in these patients, given the possible ghrelin synthesis in hyperplastic gastric endocrine/enterochromaffin-like cells.

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Section: Discussioncontrasting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Plasma ghrelin concentrations in type 1 diabetic patients with autoimmune atrophic gastritis

Alonso¹,

Granada²,

Salinas³

et al. 2007

European Journal of Endocrinology

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“…There are data in adults to suggest that H. pylori may modify plasma concentrations and/or gastric mucosal expression of ghrelin (25)(26)(27)(28)(29)(30)(31) as well as gastric mucosal leptin levels (32). However, to our knowledge, only one cross-sectional study has examined, by means of 13C-urea breath test, the influence of H. pylori infection on serum ghrelin and leptin concentrations in children (33), but there are no longitudinal data on the effect of H. pylori eradication on serum ghrelin and leptin in children.…”

Section: Introductionmentioning

confidence: 99%

Long-term effects of Helicobacter pylori eradication on circulating ghrelin and leptin concentrations and body composition in prepubertal children

Pacifico¹,

Anania²,

Osborn³

et al. 2008

European Journal of Endocrinology

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Background: Helicobacter pylori, and the chronic gastric inflammation that it causes, may compromise the function and survival of ghrelin-producing cells, resulting in a decrease of circulating ghrelin levels. This finding raises the possibility that the infection might affect growth in children by reducing the ghrelin production. Aims: To determine baseline circulating levels of ghrelin and leptin in prepubertal children with and without H. pylori infection and to evaluate the long-term effects of H. pylori eradication on circulating levels of ghrelin and leptin as well as on body composition. Patients: Thirty children with H. pylori-associated gastritis, 35 children with H. pylori-negative gastric mucosa, and 20 healthy controls were studied. Results: At baseline, while leptin levels were significantly lower in H. pylori-positive patients, ghrelin concentrations did not differ among the three study groups. However, a significant inverse correlation between ghrelin concentrations and histological severity of gastritis was found. Eradication of the organism was associated with a progressive decrease in ghrelin concentrations over baseline at both 6-and 12-month follow-ups. SDS-body mass index (BMI), lean and fat mass, as well as leptin concentrations, significantly increased over baseline at both follow-ups. Conclusions: In prepubertal children, serum ghrelin concentrations are inversely related to the severity of H. pylori-associated gastritis. In these youngsters, long-term eradication of H. pylori infection is associated with a significant increase in BMI, lean and fat mass along with a significant decrease in circulating ghrelin levels and an increase in leptin levels.

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Infection by CagA-Positive Helicobacter pylori Strains and Bone Fragility: A Prospective Cohort Study

Gennari

Merlotti

Figura

et al. 2020

Journal of Bone and Mineral Research

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Helicobacter pylori (HP) infection is a common and persistent disorder acting as a major cofactor for the development of upper gastrointestinal diseases and several extraintestinal disorders including osteoporosis. However, no prospective study assessed the effects of HP on bone health and fracture risk. We performed a HP screening in a population‐based cohort of 1149 adults followed prospectively for up to 11 years. The presence of HP infection was assessed by serologic testing for serum antibodies to HP and the cytotoxin associated gene‐A (CagA). The prevalence of HP infection did not differ among individuals with normal bone mineral density (BMD), osteoporosis, and osteopenia. However, HP infection by CagA‐positive strains was significantly increased in osteoporotic (30%) and osteopenic (26%) patients respect to subjects with normal BMD (21%). Moreover, anti‐CagA antibody levels were significantly and negatively associated with lumbar and femoral BMD. Consistent with these associations, patients affected by CagA‐positive strains had a more than fivefold increased risk to sustain a clinical vertebral fracture (HR 5.27; 95% CI, 2.23–12.63; p < .0001) and a double risk to sustain a nonvertebral incident fracture (HR 2.09; 95% CI, 1.27–2.46; p < .005). Reduced estrogen and ghrelin levels, together with an impaired bone turnover balance after the meal were also observed in carriers of CagA‐positive HP infection. HP infection by strains expressing CagA may be considered a risk factor for osteoporosis and fractures. Further studies are required to clarify in more detail the underlying pathogenetic mechanisms of this association. © 2020 American Society for Bone and Mineral Research (ASBMR).

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Impaired Production of Gastric Ghrelin in Chronic Gastritis Associated withHelicobacter pylori

Cited by 162 publications

References 27 publications

Plasma ghrelin concentrations in type 1 diabetic patients with autoimmune atrophic gastritis

Plasma ghrelin concentrations in type 1 diabetic patients with autoimmune atrophic gastritis

Long-term effects of Helicobacter pylori eradication on circulating ghrelin and leptin concentrations and body composition in prepubertal children

Infection by CagA-Positive Helicobacter pylori Strains and Bone Fragility: A Prospective Cohort Study

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