Circulating ghrelin levels in patients with inflammatory bowel disease

Peracchi, M.; Bardella, Maria Teresa; Caprioli, Flavio; Massironi, Sara; Conte, Dario; Valenti, Luca; Ronchi, Cristina L.; Beck‐Peccoz, Paolo; Arosio, Maura; Piodi, L.

doi:10.1136/gut.2005.079483

Cited by 47 publications

(46 citation statements)

References 9 publications

(12 reference statements)

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“…In fact, ghrelin concentrations have been reported to be high in some inflammatory diseases and to correlate positively with inflammatory cytokines such as TNF-a (20,21). In our study, TNF-a levels and CRP did not differ between DM1 patients with or without type A CAG; thus, differences in ghrelin concentrations between these groups could hardly be explained by the inflammatory process.…”

Section: Discussionmentioning

confidence: 50%

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: Discussionmentioning

confidence: 50%

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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“…We showed that serum ghrelin levels are elevated in IBD patients irrespective of the disease being active or quiescent and these levels were higher in male than female patients, higher in ileal compared to colonic CD and were correlated with lower leptin levels in IBD patients compared to HC [33]. On the other hand, Peracchi et al [93] showed that cir- culating ghrelin was higher in patients with active IBD compared to HC and patients in remission.…”

Section: Ghrelinmentioning

confidence: 85%

Leptin, adiponectin, resistin, and ghrelin – Implications for inflammatory bowel disease

Karmiris

Koutroubakis²,

Kouroumalis

2008

Molecular Nutrition Food Res

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Inflammatory bowel disease (IBD) is characterized by anorexia, malnutrition, altered body composition, and development of mesenteric white adipose tissue (WAT) hypertrophy. Increasing evidence suggests that adipokines synthesized either in WAT or in immune cells, are involved in these manifestations of IBD. Among adipokines leptin, adiponectin and resistin hold a fundamental role while the role of ghrelin in inflammation is not well established. Preliminary studies have shown overexpression of leptin, adiponectin, and resistin in mesenteric WAT of patients with Crohn's disease (CD) and significant alterations of circulating serum levels of these adipokines in IBD. It has also been demonstrated that intestinal inflammation causes an increase in endogenous ghrelin production. In animal models of intestinal inflammation, existing data suggest that leptin, adiponectin, and resistin are pivotal mediators of inflammation. Interesting therapeutic interventions based on these data have been suggested. A specific role for hypertrophic WAT has also been implicated in CD. Further efforts with experimental and clinical studies are needed to better understand the role of adipokines in IBD.

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“…13,[32][33][34] Noteworthy, high serum ghrelin levels have been reported in patients suffering from chronic intestinal inflammatory disorders such as ulcerative colitis and Crohn's disease. In these patients increased ghrelin levels correlates with an increase in systemic TNF-a and C-reactive protein.…”

Section: Discussionmentioning

confidence: 98%