The Role of Gastrointestinal Microbiota in Functional Dyspepsia: A Review

Abstract

Functional dyspepsia is a clinically common functional gastrointestinal disorder with a high prevalence, high impact and high consumption of medical resources. The microbiota in the gastrointestinal tract is a large number of families and is one of the most complex microbial reservoirs in the human body. An increasing number of studies have confirmed the close association between dysbiosis of the gastrointestinal microbiota and the occurrence and progression of functional dyspepsia. Therefore, we reviewed the role of dysbiosis of the gastrointestinal microbiota, H. pylori infection and gastrointestinal microbiota metabolites in functional dyspepsia, focusing on the possible mechanisms by which dysbiosis of the gastrointestinal microbiota contributes to the pathogenesis of functional dyspepsia. Several studies have confirmed that dysbiosis of the gastrointestinal microbiota may cause the occurrence and progression of functional dyspepsia by disrupting the biological barrier of the intestinal mucosa, by disturbing the immune function of the intestinal mucosa, or by causing dysregulation of the microbial-gut-brain axis. Probiotics and antibiotics have also been chosen to treat functional dyspepsia in clinical studies and have shown some improvement in the clinical symptoms. However, more studies are needed to explore and confirm the relationship between dysbiosis of the gastrointestinal microbiota and the occurrence and progression of functional dyspepsia, and more clinical studies are needed to confirm the therapeutic efficacy of microbiota modulation for functional dyspepsia.

The regulatory effects of fucoidan and laminarin on functional dyspepsia mice induced by loperamide

“…However, a number of studies have revealed a strong association between FD with gastrointestinal motility and the intestinal microbiota. 49 Just as previous studies have demonstrated, the administration of LOP significantly reduced gut microbial richness and diversity compared to the CK group, 50 which was similar to the condition of FD patients. As a common drug used for the treatment of gastrointestinal dysmotility, although mosapride performed well in the relief of this symptom, it was not able to normalize microbiota richness and diversity in LOP-induced FD mice.…”

Gut Microbiome–Brain Alliance: A Landscape View into Mental and Gastrointestinal Health and Disorders

“…361 FD pathogenesis is linked to GI dysmotility, visceral hypersensitivity, impaired gastric tolerance, disrupted gastrointestinal mucosal integrity, abnormal function of the gut microbiome−brain axis, increased eosinophils in duodenum, dysbiosis, Helicobacter-pylori infection, postgastrointestinal infection, diet, genetics, and mental and psychological factors. 278 An increasing number of studies have confirmed the close association between disturbance in the relative abundance and composition of the gastrointestinal microbiota and the occurrence and progression of FD. Actinomyces, Atopobium, Leptotrichia, Prevotella, and Veilonella counts differ between FD and control patients.…”

“…Furthermore, SCFAs, especially butyrate, provide more than 70% of the energy for the intestinal epithelial cells on top of their abilities to inhibit the multiplication and growth of pathogenic bacteria and the activity of intestinal inflammatory mediators, thus playing an anti-inflammatory role in the intestinal tract. 278 Lipid metabolites can affect intestinal permeability and intestinal immunity. The gut microbiota can produce lipopolysaccharides that could stimulate proinflammatory mediators, thereby disrupting the body's immune system and inducing local and systemic inflammatory responses.…”

“…The main clinical symptoms of patients are early satiety, postprandial discomfort, epigastric pain, epigastric distension, epigastric burning, loss of appetite, belching, nausea, and vomiting, which are often accompanied by anxiety and depression . FD pathogenesis is linked to GI dysmotility, visceral hypersensitivity, impaired gastric tolerance, disrupted gastrointestinal mucosal integrity, abnormal function of the gut microbiome–brain axis, increased eosinophils in duodenum, dysbiosis, Helicobacter -pylori infection, postgastrointestinal infection, diet, genetics, and mental and psychological factors …”

“…SCFAs can regulate the pH value in the intestine and regulate the absorption of water, sodium, calcium, and magnesium. Furthermore, SCFAs, especially butyrate, provide more than 70% of the energy for the intestinal epithelial cells on top of their abilities to inhibit the multiplication and growth of pathogenic bacteria and the activity of intestinal inflammatory mediators, thus playing an anti-inflammatory role in the intestinal tract …”