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Background/aims: Disruptions in tight junction (TJ) protein expression leading to duodenal epithelial barrier impairment may contribute to increased intestinal permeability, potentially playing a role in functional dyspepsia (FD) pathophysiology. Currently published studies evaluated the role of several TJ proteins in FD patients with inconsistent results. Therefore, we conducted this systematic review and metaanalysis to evaluate the duodenal mucosal expression of several TJ proteins in FD., Methods: We performed a systematic electronic search on PubMed, EMBASE, and Scopus using predefined keywords. Diagnosis of FD by Rome III or Rome IV criteria was considered acceptable. Full articles satisfying our inclusion and exclusion criteria were included. The principal summary outcome was the mean difference of several TJ proteins in FD patients and control subjects., Results: A total of 8 and 5 studies were included in our qualitative and quantitative synthesis, respectively, with a total population of 666 participants, out of which 420 were FD patients. No significant differences were observed between FD patients and controls in the expression of claudin-1 (-0.102 [95% CI, -0.303, 0.099]), claudin-2 (0.161 [95% CI, -0.134, 0.456)], claudin-3 (0.278 [95% CI, -0.280, 0.837]), claudin-4 (0.045 [95% CI, -0.264, 0.354]), ZO-1 (-0.221 [95% CI, -0.683, 0.241]), ZO-2 (-0.070 [95% CI, -0.147, 0.007]), ZO-3 (-0.129 [95% CI, -0.376, 0.118]), β-catenin (-0.135 [95% CI, -0.484, 0.214]), E-cadherin (-0.083 [95% CI, -0.229, 0.063]), and occludin (-0.158 [95% CI, -0.409, 0.093])., Conclusions: The expressions of all evaluated proteins including claudin-1, claudin-2, claudin-3, claudin-4, ZO-1, ZO-2, ZO-3, β-catenin, E-cadherin, and occludin did not significantly differ between FD patients and controls. However, due to the limited number of included studies, results should be interpreted with caution.

Functional dyspepsia (FD), a widespread and debilitating digestive disease, is thought to originate from disrupted gut-brain communication. The cause of FD is not completely understood, but recent evidence suggests it could be due to multiple factors and can vary among different patient groups. Factors like gut motility changes, increased sensitivity to pain in the gut, ongoing low-level inflammation, and increased gut permeability have all been linked to the development of FD. Additionally, changes in the gut microbiome have been suggested to play a significant role in the disease. The gut microbiota in the duodenum could either be a cause or a result of the immune and nervous system issues seen in FD, but the ways in which the gut flora in the small intestine affects gut function, digestive metabolites and symptoms are not yet clear, more studies being needed in order to completely assess the relationship between gastrointestinal microbiota and development and progression of FD. This review summarizes the available research on the relationship between FD and the microbiota and examines the various treatments, including probiotics, that have been shown to relieve symptoms. Finally, suggestions for improving diagnosis and treatment for those with FD are presented.