Published online Feb 7, 2019. doi: 10.3748/wjg.v25.i5.539
Peer-review started: November 22, 2018
First decision: December 12, 2018
Revised: December 20, 2018
Accepted: January 14, 2019
Article in press: January 14, 2019
Published online: February 7, 2019
Functional gastrointestinal disorders (FGID) are heterogeneous disorders with a variety of clinical manifestations, primarily defined by signs and symptoms rather than a definite underlying cause. Their pathophysiology remains obscure and, although it is expected to differ according to the specific FGID, disruptions in the brain-gut axis are now thought to be a common denominator in their pathogenesis. The hormone ghrelin is an important component of this axis, exerting a wide repertoire of physiological actions, including regulation of gastrointestinal motility and protection of mucosal tissue. Ghrelin’s gene shows genetic polymorphism, while its protein product undergoes complex regulation and metabolism in the human body. Numerous studies have studied ghrelin’s relation to the emergence of FGIDs, its potential value as an index of disease severity and as a predictive marker for symptom relief during attempted treatment. Despite the mixed results currently available in scientific literature, the plethora of statistically significant findings shows that disruptions in ghrelin genetics and expression are plausibly related to FGID pathogenesis. The aim of this paper is to review current literature studying these associations, in an effort to uncover certain patterns of alterations in both genetics and expression, which could delineate its true contribution to FGID emergence, either as a causative agent or as a pathogenetic intermediate.
Core tip: Functional gastrointestinal disorders are diverse clinical entities whose pathogenesis and phenotype are thought to stem from both genetic and environmental factors. Many reviews have attempted to summarize general pathogenetic mechanisms related to functional gastrointestinal disorders (FGIDs), but more specific knowledge is currently limited. Studies on the brain-gut axis peptide ghrelin have chiefly concentrated on its association with obesity and eating disorders. This review focuses on the possible role of ghrelin in FGID pathogenesis, in an attempt to elucidate the contribution of certain genetic alterations to the emergence of disease.