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.
Highlights
Helicobacter pylori (H. pylori) infection and eradication therapy have been known to influence gastric ghrelin and leptin secretion, which may lead to weight gain
Plasma active ghrelin levels were significantly lower in patients with gastritis than in patients with peptic ulcer. (ii) Plasma active and desacyl ghrelin levels decreased after H. pylori eradication in both peptic ulcer and gastritis patients, while plasma leptin levels increased only in peptic ulcer patients. (iii) Plasma leptin levels and body mass index (BMI) were positively correlated, and the active ghrelin levels and atrophic pattern were weakly negatively correlated in peptic ulcer patients
Consistent with Bocian et al [7], the present results showed that plasma ghrelin levels decreased after H. pylori eradication in both peptic ulcer and gastritis patients, and plasma leptin levels increased in peptic ulcer patients
Summary
Helicobacter pylori (H. pylori) infection and eradication therapy have been known to influence gastric ghrelin and leptin secretion, which may lead to weight gain. While active ghrelin has been implicated in the control of food intake and shown to evoke weight gain by actions in the hypothalamus [14, 15], desacyl-ghrelin is thought to be involved in energy balance in some way, but its exact role is unknown. It has recently been found that leptin is present in gastric mucosa [17,18,19] This hormone plays a role of mediator in the long-term regulation of energy balance, suppressing food intake, and thereby inducing weight loss [8, 20]
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