Abstract
It is proposed that gluten- and casein-rich diets (GRD and CRD) can synergistically exacerbate dysbiosis as comorbidity in autism by worsening leaky gut that affects the brain through the gut–brain axis. In this study, 35 young male rats were divided into 7 groups, Group 1 serves as control; Group 2, clindamycin (CL)-treated; and Group 3, propionic acid (PPA)-induced rodent model of autism. These three groups were fed standard diet until the end of the experiment. Groups 4–7 are rats treated similarly with CL and PPA, then fed on CRD or GRD until the end of the experiment. Serum zonulin, glutathione (GSH), lipid peroxides, and gut microbial composition were measured in the seven studied groups. Data demonstrate the significant increase in serum zonulin as marker of leaky gut in the CL-treated groups fed on CRD or GRD. Lipid peroxides were significantly higher in the serum of GRD-fed rats compared to CRD-fed or normal diet-fed rats. GSH was much lower in CL-treated groups fed on CRD or GRD compared to PPA-treated rats fed on both diets. Both diets differentially affected the diversity of the gut microbiota. This study demonstrates that CRD and GRD exacerbates leaky gut, according to serum zonulin, which was used as marker for increased gut permeability.
Highlights
About 20% of children and adolescents demonstrate mental, behavioral, and neurodevelopmental disorders and these are the prominent reasons of disability in young individuals [1,2]
This study demonstrates that casein-rich diet (CRD) and gluten-rich diets (GRD) exacerbates leaky gut, according to serum zonulin, which was used as marker for increased gut permeability
The main findings of the present translational study is a trend of an increase (P = 0.09) in serum zonulin in propionic acid (PPA)-autism model fed on ND, CRD, and GRD compared to control healthy model fed on ND
Summary
About 20% of children and adolescents demonstrate mental, behavioral, and neurodevelopmental disorders and these are the prominent reasons of disability in young individuals [1,2]. CL treatment could be used as indirect strategy to test the neurotoxic effect of PPA through the induction of C. difficile overgrowth [25] This information initiates our interest to measure serum zonulin as marker of impaired gut microbiota together with GSH and lipid peroxides as antioxidant and oxidative stress status markers, respectively, in CLtreated and PPA-induced rodent model of autism fed on standard diet (SD), casein-rich diet (CRD), and GRD. This might help in understanding and ascertain the relationship between casein and gluten sensitivity, oxidative stress, and leaky gut in ASD
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