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

Alonso, Núria; Granada, María Luisa; Salinas, Isabel; Reverter, Jordi L.; Flores, Lílliam; Ojanguren, Isabel; Martínez-Cáceres, Eva; Sanmartı́, Anna

doi:10.1530/eje-07-0300

Cited by 19 publications

(9 citation statements)

References 31 publications

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“…Ghrelin has been reported to be abnormal in other gastrointestinal diseases such as inflammatory bowel diseases (29), coeliac disease (30)(31)(32)(33) and atrophic gastritis (34)(35)(36). Thus, ghrelin seems to be involved in the pathophysiology of gastrointestinal diseases/disorders.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin in patients with irritable bowel syndrome

El‐Salhy

Lillebø²,

Reinemo³

et al. 2009

Int J Mol Med

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Abstract. General gastrointestinal dysmotility occurs in patients with irritable bowel syndrome (IBS). Ghrelin seems to play an important role in regulating gastrointestinal motility. The present study was undertaken, therefore, to establish the possible role of ghrelin in the pathophysiology of IBS. Thirty-seven patients with IBS (19 had IBS-constipation and 18 IBS-diarrhoea) were included in this study. Ten healthy volunteers served as controls. After overnight fast, blood samples were drawn from patients and controls, and a gastroduodenal endoscopy was performed. Biopsies were taken from oxyntic mucosa and duodenum. Ghrelin cell density was determined by computer image analysis after immunohistochemical staining of the tissues. Total and active ghrelin were detected in tissue extracts and plasma by commercially available RIA and ELISA Kits. The density of ghrelinimmunoreactive cells in the oxyntic mucosa was significantly lower in IBS-constipation and significantly higher in IBSdiarrhoea patients than healthy controls (P<0.0001 and <0.0001, respectively). There was no statistical difference in total or active ghrelin between IBS patients and controls, regarding tissue extracts or plasma. In order to compensate for the increase and decrease in the ghrelin cell density, the synthesis and release of ghrelin may be decreased and increased in IBS-diarrhoea and IBS-constipation patients, respectively. It has been speculated that this compensatory mechanism may be subjected from time to time to fatigue with the subsequent increased and decreased synthesis and release of ghrelin in IBS-diarrhoea and IBS-constipation with a subsequent intermittent diarrhoea or constipation seen in these patients, respectively.

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Section: Discussionmentioning

confidence: 99%

Ghrelin in patients with irritable bowel syndrome

El‐Salhy

Lillebø²,

Reinemo³

et al. 2009

Int J Mol Med

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“…Whereas ghrelin serum levels were reported to be low, and to be the most sensitive and specific non-invasive marker for gastric body gastritis (30), ghrelin concentration decreased in patients with autoimmune atrophic gastritis and diabetes type 1 (31). In patients with chronic atrophic gastritis acetylated ghrelin levels increased in the gastric body and fundus.…”

Section: Inflammatory and Infectious Gastrointestinal Diseasesmentioning

confidence: 97%

Ghrelin in gastrointestinal diseases and disorders: A possible role in the pathophysiology and clinical implications (Review)

El‐Salhy

2009

Int J Mol Med

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Abstract. Ghrelin is a peptide hormone, which has been isolated from the stomach. It is localized mostly in endocrine cells in the oxyntic mucosa of the stomach. Ghrelin receptors are expressed equally in all parts of the gastrointestinal tract, with a similar level of expression in the mucosal and muscle layers. This peptide hormone has several functions, the most widely known is its growth hormone (GH)-releasing effect. Ghrelin plays an important role in regulating appetite, feeding and energy metabolism. It also plays a role in mediating immune response and inflammatory processes. Ghrelin stimulates gastric motility and emptying as well as motility in the small and large intestine. Ghrelin has been reported to be affected in several gastrointestinal diseases/disorders such as inflammatory bowel disease, coeliac disease, infectious diseases, functional disorders and diabetes gastroenteropathy. This indicates that ghrelin is involved in the pathophysiology of gastrointestinal diseases/disorders. Several studies have shown that ghrelin and its antagonist are a promising tool for treatment of several gastrointestinal diseases/disorders.

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“…Patients positive for nuclear antibodies (ANA), thyroperoxidase antibodies (TPOa), tyroglobulin antibodies (TGa), and transglutaminase antibodies or with autoimmune disease-related clinical symptoms were excluded. These patients were recruited from the Department of Endocrinology-Diabetology outpatient clinic of the University Hospital Germans Trias i Pujol (Badalona, Spain) [38,39]. The diagnosis of CAG was based on the presence of low-serum pepsinogen I concentration, hypergastrinemia, pepsinogen I/II ratio under 3, positive PCA, and histologic confirmation as previously described [39].…”

Section: Patientsmentioning

confidence: 99%

“…These patients were recruited from the Department of Endocrinology-Diabetology outpatient clinic of the University Hospital Germans Trias i Pujol (Badalona, Spain) [38,39]. The diagnosis of CAG was based on the presence of low-serum pepsinogen I concentration, hypergastrinemia, pepsinogen I/II ratio under 3, positive PCA, and histologic confirmation as previously described [39]. Peripheral blood samples were also obtained from 15 DM1 patients (DM1) and 15 age-and sex-matched controls in whom the previously mentioned organ-specific autoantibodies as well as PCA were also negative.…”

Section: Patientsmentioning

confidence: 99%

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Regulatory T cells in type 1 diabetic patients with autoimmune chronic atrophic gastritis

Alonso

Martínez-Arconada

Granada

et al. 2009

Endocr

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Type A chronic atrophic gastritis (CAG) is increased in type 1 diabetic patients (DM1). To address this issue, we determined and analyzed the number of peripheral blood regulatory T cells (Tregs) in 15 DM1-CAG patients, 15 DM1 patients without associated autoantibodies (DM1) and 15 healthy controls by flow cytometry and compared gastric Tregs expression (CD4+Foxp3+/CD4+) in DM1-CAG patients with that observed in 10 control Helicobacter pylori CAG-infected biopsies. The percentage of peripheral Tregs was higher in DM1-CAG patients compared to DM1 and controls (CD4+Foxp3+: 7.67 +/- 1.91% vs. 5.38 +/- 1.57% and 5.65 +/- 1.76%, P < 0.001, respectively), with no differences between DM1 and controls. Gastric mucosal Tregs were higher in H. pylori CAG than in DM1-CAG patients (31.31 +/- 5.52% vs. 7.68 +/- 3.70%; P < 0.001). Data suggest that Tregs are stimulated in patients with more than one autoimmune disease (DM1 + CAG) in an ineffectual attempt to control autoimmune response and that the number of Tregs in gastric mucosa implicated in the chronification of gastritis differs according to the etiology.

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

Cited by 19 publications

References 31 publications

Ghrelin in patients with irritable bowel syndrome

Ghrelin in patients with irritable bowel syndrome

Ghrelin in gastrointestinal diseases and disorders: A possible role in the pathophysiology and clinical implications (Review)

Regulatory T cells in type 1 diabetic patients with autoimmune chronic atrophic gastritis

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