Abstract
To examine gastrointestinal hormone profiles and functional changes in gastroesophageal reflux disease (GERD), blood levels of the orexigenic hormone ghrelin were measured in rats with experimentally induced GERD. During the experiment, plasma acyl ghrelin levels in GERD rats were higher than those in sham-operated rats, although food intake was reduced in GERD rats. Although plasma levels of the appetite-suppressing hormone leptin were significantly decreased in GERD rats, no changes were observed in cholecystokinin levels. Repeated administration of rat ghrelin to GERD rats had no effect on the reduction in body weight or food intake. Therefore, these results suggest that aberrantly increased secretion of peripheral ghrelin and decreased ghrelin responsiveness may occur in GERD rats. Neuropeptide Y and agouti-related peptide mRNA expression in the hypothalamus of GERD rats was significantly increased, whereas proopiomelanocortin mRNA expression was significantly decreased compared to that in sham-operated rats. However, melanin-concentrating hormone (MCH) and prepro-orexin mRNA expression in the hypothalamus of GERD rats was similar to that in sham-operated rats. These results suggest that although GERD rats have higher plasma ghrelin levels, ghrelin signaling in GERD rats may be suppressed due to reduced MCH and/or orexin synthesis in the hypothalamus.
Highlights
Gastroesophageal reflux disease (GERD) is caused when gastric acid flows back into the esophagus, resulting in erosion of the esophageal mucosal epithelium
There are various peripheral and central appetite-related hormones involved in the control of appetite and satiation; ghrelin is secreted by the stomach and stimulates appetite and gastrointestinal motility [3], whereas cholecystokinin (CCK) and leptin, which are secreted in response to food intake, suppress appetite [4, 5]
Ghrelin is secreted by X/A-like cells found in the gastric mucosa, and it binds to the growth hormone secretagogue receptor (GHSR) present at the end of the vagus nerve to stimulate feeding behavior by suppressing the satiety stimulus transmitted by CCK [6, 7]
Summary
Gastroesophageal reflux disease (GERD) is caused when gastric acid flows back into the esophagus, resulting in erosion of the esophageal mucosal epithelium. Gastric secretion inhibitors, such as proton pump inhibitors, can alleviate GERD symptoms [1]. There are various peripheral and central appetite-related hormones involved in the control of appetite and satiation; ghrelin is secreted by the stomach and stimulates appetite and gastrointestinal motility [3], whereas cholecystokinin (CCK) and leptin, which are secreted in response to food intake, suppress appetite [4, 5]. As a first step in elucidating the involvement of appetiterelated hormones in GERD, we examined the profiles of Gastroenterology Research and Practice peripheral appetite-related peptides, with a focus on changes in ghrelin levels and ghrelin responsiveness
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