Zonulin is a human protein that regulates intestinal permeability by modulating tight junctions between epithelial cells in the digestive tract. It is a functional analogue to the zonula occludens toxin from Vibrio cholerae. Zonulin binds to receptors on the surface of intestinal epithelial cells and triggers a signaling cascade that leads to the disassembly of tight junctions, thereby increasing intestinal permeability. This process allows antigens, pathogens, and other molecules to cross the intestinal barrier, potentially triggering immune responses and contributing to systemic inflammation.
Clinically, elevated levels of zonulin have been linked to a range of gastrointestinal and autoimmune disorders. Research by Fasano and colleagues demonstrated that the zonulin pathway is significantly activated in patients with celiac disease and type 1 diabetes. In celiac patients, higher concentrations of zonulin and anti-zonulin antibodies are observed during active disease phases, with levels dropping in remission following a gluten-free diet. This makes zonulin a useful biomarker for monitoring intestinal barrier function and disease activity in these conditions.
Beyond celiac disease, increased zonulin expression is associated with what is commonly referred to as “leaky gut,” a condition implicated in a variety of chronic health issues, including metabolic syndrome, obesity, multiple sclerosis, rheumatoid arthritis, asthma, and inflammatory bowel diseases. As such, zonulin serves as an emerging biomarker in both research and clinical settings for evaluating gut barrier integrity, investigating disease mechanisms, and potentially guiding therapeutic interventions aimed at restoring epithelial barrier function.
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