Measurement of zonulin in stool is a very important indicator for assessing a leaky gut. Elevated serum levels of zonulin, or more specifically, Zonulin Family Protein (ZFP), have been found in pathological conditions such as metabolic syndrome and obesity, conditions associated with increased intestinal permeability (leaky gut). Elevated serum zonulin levels are in concordance with the results of the reference method for measuring gut permeability, i.e., the Lactulose/Mannitol assay.
The concordance between fecal zonulin levels and lactulose/mannitol test results has not yet been fully confirmed, in contrast to the documented relationship between serum zonulin levels and lactulose/mannitol test results.
Elevated levels of zonulin in the stool have been linked to metabolic syndrome and obesity, and also increased levels have been reported in smokers.
The gastrointestinal tract's primary functions are traditionally considered limited to the digestion and absorption of nutrients and electrolytes and the regulation of water homeostasis. However, a closer look at the anatomical and functional arrangements of the gastrointestinal tract reveals that another vital function of this organ is its ability to regulate the movement of macromolecules between the environment and the host through a barrier mechanism. The intestinal epithelial barrier, with its intercellular tight junctions, intestinal lymphatic tissue, and the neuroendocrine network, controls the balance between tolerance and immunity to non-auto-antigens. Zonulin is the only known physiological modulator of intercellular tight junctions involved in the movement of macromolecules and, therefore, in regulating the balance of immune responses between tolerance and reaction. When the zonulin-regulated transport pathway is deregulated in genetically susceptible individuals, intestinal and extraintestinal autoimmune, inflammatory, and neoplastic disorders may occur.
The zonulin example contradicts the traditional theories governing the development of these diseases and shows that these pathological conditions can be prevented if the interaction between genes (genetic background) and environmental conditions is deterred by restoring the zonulin-dependent intestinal barrier.
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