Increased levels of plasma ghrelin in peptic ulcer disease

Suzuki, Hidekazu; Masaoka, Tatsuhiro; Nomoto, Y.; Hosoda, Hiroshi; Mori, Masaki; Nishizawa, Toshihiro; Minegishi, Yuriko; Kangawa, Kenji; Hibi, Toshifumi

doi:10.1111/j.1365-2036.2006.00034.x

Cited by 11 publications

(11 citation statements)

References 29 publications

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“…In contrast to our findings, Suzuki et al (2006) reported that plasma ghrelin levels were significantly higher in patients with peptic ulcer than in those with gastritis without ulcer, which suggests a possible relationship between mucosal injury susceptibility and the elevated plasma ghrelin.…”

Section: Discussioncontrasting

confidence: 99%

Gastroprotective effect of ghrelin against indomethacin-induced gastric injury in rats: possible role of heme oxygenase-1 pathway

Allam

El-Gohary²

2017

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Ghrelin has been shown to ameliorate gastric injury by several mechanisms in experimental animal models. The present study aimed to investigate the effect of pretreatment with ghrelin on indomethacin-induced gastric injury in rats and the role of heme oxygenase-1(HO-1) pathway as a novel mechanism underlying the gastroprotective effect of ghrelin. In all groups studied, ulcer score (U.S), ulcer index (U.I) and preventive index (P.I) were evaluated and the gastric inflammatory biomarkers including levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and myeloperoxidase (MPO) activity as well as prostaglandin E2 (PGE2), malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), HO-1 and bilirubin as an indicator of heme oxygenase activity were measured. Indomethacin induced significant elevation in U.S and U.I as well as the inflammatory and the oxidative markers and reduced the PGE2 in addition to HO-1 level and activity. Pretreatment with ghrelin reversed these results. In order to elucidate the possible role of HO-1 in mediating the protective effects of ghrelin, tin protoporphyrin (SnPP) HO-1 blocker was administrated; it significantly attenuated the gastroprotective effect of ghrelin. In conclusion HO-1 activity significantly contributes toward ghrelin-mediated gastroprotection.

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Section: Discussioncontrasting

confidence: 99%

Gastroprotective effect of ghrelin against indomethacin-induced gastric injury in rats: possible role of heme oxygenase-1 pathway

Allam

El-Gohary²

2017

gpb

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“…These functions are mediated, at least in part, via vagal nerve pathways 29,30. In gastroduodenal mucosal injury, the levels of plasma ghrelin increased in response to the physiological demand for the purpose of gastroduodenal cytoprotection 31,32. However, in the presence of H. pylori -induced severe gastric mucosal atrophy, the plasma ghrelin concentrations shifted to lower levels 33-36.…”

Section: Pathophysiological Link Between Helicobacter Pylori Infectiomentioning

confidence: 99%

What Is the Difference Between -Associated Dyspepsia and Functional Dyspepsia?

Suzuki

Matsuzaki²,

Hibi³

2011

J Neurogastroenterol Motil

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Advances in basic and clinical research have revealed that Helicobacter pylori (H. pylori) infection plays an important role in the development of gastroduodenal dysmotility and hypersensitivity, as also in dyspepsia symptoms. In addition, recent studies have proposed an inflammation-immunological model for the pathogenesis of functional dyspepsia. Since H. pylori is the major microbe that provokes a gastroduodenal inflammatory response, it should not be overlooked when considering the pathophysiology of dyspepsia symptoms. In fact, population-based studies have demonstrated that H. pylori is detected more frequently in dyspepsia patients. However, although many clinical studies tried to reveal the association of H. pylori infection with gastric motility dysfunction or hypersensitivity, the results have been conflicting. On the other hand, many etiological features were revealed for the development of H. pylori-associated dyspepsia, such as abnormal ghrelin or leptic secretion, altered expression of muscle-specific microRNAs, and duodenal inflammatory cell infiltration. In addition, therapeutic strategy for H. pylori-associated dyspepsia would be different from H. pylori-negative functional dyspepsia. This review focuses the issue of whether H. pylori-associated dyspepsia should be considered as a different disease entity from functional dyspepsia.

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“…[7] Ghrelin regulates appetite, glucose metabolism, adipogenic effects, and energy balance. [19,20] The plasma ghrelin level is elevated in patients with peptic ulcer, [21] including both acylated ghrelin and unacylated ghrelin. [7] Both vagal stimulation and fat ingestion may influence the release of ghrelin through vagus nerve.…”

Section: Discussionmentioning

confidence: 99%

Association of vagus nerve severance and decreased risk of subsequent type 2 diabetes in peptic ulcer patients

Chen²,

Fang

et al. 2016

Medicine

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Vagus nerve may play a role in serum glucose modulation. The complicated peptic ulcer patients (with perforation or/and bleeding) who received surgical procedures with or without vagotomy provided 2 patient populations for studying the impact of vagus nerve integrity. We assessed the risk of developing type 2 diabetes in peptic ulcer patients without and with complications by surgical treatment received in a retrospective population study using the National Health Insurance database in Taiwan.A cohort of 163,385 patients with peptic ulcer and without Helicobacter pylori infection in 2000 to 2003 was established. A randomly selected cohort of 163,385 persons without peptic ulcer matched by age, sex, hypertension, hyperlipidemia, Charlson comorbidity index score, and index year was utilized for comparison. The risks of developing diabetes in both cohorts and in the complicated peptic ulcer patients who received truncal vagotomy or simple suture/hemostasis (SSH) were assessed at the end of 2011.The overall diabetes incidence was higher in patients with peptic ulcer than those without peptic ulcer (15.87 vs 12.60 per 1000 person-years) by an adjusted hazard ratio (aHR) of 1.43 (95% confidence interval [CI] = 1.40–1.47) based on the multivariable Cox proportional hazards regression analysis (competing risk). Comparing ulcer patients with truncal vagotomy and SSH or those without surgical treatment, the aHR was the lowest in the vagotomy group (0.48, 95% CI = 0.41–0.56).Peptic ulcer patients have an elevated risk of developing type 2 diabetes. Moreover, there were associations of vagus nerve severance and decreased risk of subsequent type 2 diabetes in complicated peptic ulcer patients.

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Increased levels of plasma ghrelin in peptic ulcer disease

Cited by 11 publications

References 29 publications

Gastroprotective effect of ghrelin against indomethacin-induced gastric injury in rats: possible role of heme oxygenase-1 pathway

Gastroprotective effect of ghrelin against indomethacin-induced gastric injury in rats: possible role of heme oxygenase-1 pathway

What Is the Difference Between -Associated Dyspepsia and Functional Dyspepsia?

Association of vagus nerve severance and decreased risk of subsequent type 2 diabetes in peptic ulcer patients

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