Changes in plasma ghrelin and leptin levels in patients with peptic ulcer and gastritis following eradication of Helicobacter pylori infection

Abstract

Background Helicobacter pylori (H. pylori) infection and eradication therapy have been known to influence gastric ghrelin and leptin secretion, which may lead to weight gain. However, the exact relationship between plasma ghrelin/leptin levels and H. pylori infection has remained controversial. The aim of this study was to investigate plasma ghrelin and leptin levels in H. pylori-positive and -negative patients, to compare the two levels of the hormones before and after H. pylori eradication, and to examine the correlation between body mass index (BMI) and active ghrelin or leptin levels, as well as that between atrophic pattern and active ghrelin or leptin levels.MethodsSeventy-two H. pylori-positive patients who underwent upper gastrointestinal endoscopy, 46 diagnosed as having peptic ulcer and 26 as atrophic gastritis, were enrolled. Control samples were obtained from 15 healthy H. pylori-negative volunteers. The extent of atrophic change of the gastric mucosa was assessed endoscopically. Body weight was measured and blood was collected before and 12 weeks after H. pylori eradication therapy. Blood samples were taken between 8 and 10 AM after an overnight fast.ResultsPlasma ghrelin levels were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. In particular, plasma active ghrelin levels were significantly lower in patients with gastritis compared with patients with peptic ulcer. Plasma ghrelin levels decreased after H. pylori eradication in both peptic ulcer and gastritis patients, while plasma leptin levels increased only in peptic ulcer patients. Plasma leptin levels and BMI were positively correlated, and active ghrelin levels and atrophic pattern were weakly negatively correlated in peptic ulcer patients.Conclusion H. pylori infection and eradication therapy may affect circulating ghrelin/leptin levels. This finding suggests a relationship between gastric mucosal injury induced by H. pylori infection and changes in plasma ghrelin and leptin levels.

Helicobacter pyloriand corpus gastric pathology are associated with lower serum ghrelin

“…We conducted this study to evaluate the presence of an association, in dyspeptic patients, between persistent H. pylori infection, the genotype of infecting strain, the type of gastric pathology, and the serum ghrelin and leptin levels in patients with a measured anthropometric nutritional status. Our study demonstrated that H. pylori infected patients had lower serum ghrelin concentrations than the uninfected ones, independently of their BMI or gender, supporting the findings from several groups[ 12 - 14 , 17 , 35 ]. It has been demonstrated that ghrelin exhibits gastroprotective antioxidant and anti-inflammatory effects[ 36 - 38 ], modulating gastric mucosal inflammation induced by H. pylori lipopolysacaccharide (LPS) through several mechanisms which were recently reviewed[ 39 ].…”

Gut microbiota-derived metabolites in obesity: a systematic review

“…It has the ability to ferment a large variety of organic substrates, enabling flexible growth in the colon. Different bacterial species in the Blautia genus have been associated with obesity [74]. There is an association between Blautia and human genetic variants in a genomic region that has been associated with obesity and BMI [75].…”

Plasma desacyl ghrelin‑to‑acyl ghrelin ratio is a predictor of postoperative complications and prognosis after pancreaticoduodenectomy

“…study, H. pylori infection and the brevity of the period from gastrectomy to PD may have affected the delayed recovery of plasma ghrelin. Suppression of plasma ghrelin has been reported in patients with H. pylori (28). Takachi et al (10) indicated the possibility of compensatory ghrelin production in the remnant stomach and duodenum.…”

“…Another limitation is the insufficient extraction of factors that affect ghrelin production and feedback. In addition to nutrition and inflammation, H. pylori infection and cachexia status affect ghrelin production (28,39,40). These factors cannot be ignored because the rate of H. pylori infection is higher in Japanese people, and the progression of pancreatic and biliary carcinoma is strongly related to cachexia (41,42).…”