Dyspepsia and Appetite Regulation

Abstract

Dyspepsia includes symptoms of postprandial fullness, early satiety, and epigastric burning/pain, and most patients with dyspepsia have no identifiable cause of their disease, leading to a diagnosis of functional dyspepsia (FD). There are a number of different factors that affect gut activity, but components of the nervous and endocrine systems are essential for normal gut function. Communications between the brain and gut occur via direct neural connections such as the vagus nerve or through endocrine signaling events requiring hormone delivery to the circulation. Disturbance in any part of the process of feeding results in a decline in food intake. With our increasing knowledge of the interactions between the gut and the brain, there is an expanding list of pharmacologic compounds targeting different stage of this pathway. Currently available therapeutic management of dyspepsia, particularly FD, is based on putative underlying pathophysiologic mechanisms, including gastric acid sensitivity, slow gastric emptying, and Helicobacter pylori infection. Additionally, as knowledge is gained about the reaction of patients with functional gastrointestinal (GI) disorders, therapies in development now may become incorporated into the clinical armamentarium. Serotonergic modulators, cholecystokinin (CCK)-1 antagonists, opioid agonists, N-methyl-d-aspartate (NMDA) receptor antagonists, neurokinin (NK) antagonists, capsaicin-like agents, ghrelin or motilin receptor agonists, and antidepressants are among the agents currently under investigation.