Ghrelin and functional dyspepsia

Abstract

Food consumption is supposed to affect the onset of functional gastrointestinal disorder (FGID), particularly functional dyspepsia (FD). Many secretory fluids and digestive enzymes are secreted from digestive organs in response to food consumption and are then combined with the crushed and mixed food and transported, thereby inducing gastrointestinal motility. Gastrointestinal hormones are active substances that promote these digestive and absorptive functions. Furthermore, in recent years, many gastrointestinal hormones were found to have appetite-­ regulatory activity, and the abnormal secretion of gastrointestinal hormones and changes in their physiological activity have been suggested to contribute to FD onset. Although some gastrointestinal hormones have anorexic effects, only ghrelin have an orexigenic action and it also stimulates gastric motility. This short review presents the physiological activity of ghrelin as well as the regulatory mechanisms underlying appetite, acid secretion, and gastric motility via the brain-gut axis. In this review, we present the action of ghrelin on the secretion of gastric acid and its mechanism. We found that histamine mediates the stimulatory action of ghrelin on acid secretion through the mechanism based on brain-gut axis. Furthermore, we discussed the relationship between FD and ghrelin, and pathophysiology for FD in the state of stress that was simulated through animal experiments with intracerebroventricular (icv) injection of stress-related peptide urocortin 1 (UCN1). Our study has elucidated that UCN1 decreases plasma ghrelin level through CRF receptor 2. The inhibition of ghrelin secretion is mediated by sympathetic nerve through α2-adrenergic receptor in periphery. The mechanism may explain pathophysiology for FD inducing dyspepsia symptoms such as abdominal distension, fullness, and anorexia.