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The effect of H. pylori eradication on meal-associated changes in plasma ghrelin and leptin

DOI: 10.1186/1471-230x-11-37

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Abstract:

Veterans referred for upper GI endoscopy were evaluated at baseline and ≥8 weeks after endoscopy, and H. pylori status and body weight were ascertained. During the first visit in all subjects, and during subsequent visits in the initially H. pylori-positive subjects and controls, blood was collected after an overnight fast and 1 h after a standard high protein meal, and levels of eight hormones determined.Of 92 enrolled subjects, 38 were H. pylori-negative, 44 H. pylori-positive, and 10 were indeterminate. Among 23 H. pylori-positive subjects who completed evaluation after treatment, 21 were eradicated, and 2 failed eradication. After a median of seven months following eradication, six hormones related to energy homeostasis showed no significant differences, but post-prandial acylated ghrelin levels were nearly six-fold higher than pre-eradication (p = 0.005), and median integrated leptin levels also increased (20%) significantly (p < 0.001). BMI significantly increased (5 ± 2%; p = 0.008) over 18 months in the initially H. pylori-positive individuals, but was not significantly changed in those who were H. pylori-negative or indeterminant at baseline.Circulating meal-associated leptin and ghrelin levels and BMI changed significantly after H. pylori eradication, providing direct evidence that H. pylori colonization is involved in ghrelin and leptin regulation, with consequent effects on body morphometry.The healthful regulation of energy homeostasis in humans, depends on centrally-acting hormones such as ghrelin and leptin [1,2]. Serum ghrelin concentrations increase during fasting, and decrease after eating [3]; ghrelin decreases energy expenditure and promotes weight gain [4]. In contrast, leptin produced primarily by adipocytes, reduces appetite and increases energy utilization [5]. The gastric epithelium expresses both ghrelin and leptin (and their receptors) [6,7]; inflammation can modify their production [8,9].Helicobacter pylori, which colonizes the human stom

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