Overall, these results suggest that expression Kaempferide levels of disaccharidases and transporters are associated with the abundance of Bacteroidetes, Firmicutes, and Betaproteobacteria in the mucoepithelium. Although the major deficits in ASD are social and cognitive, many affected individuals with ASD also have substantial GI morbidity. Major findings in this study that may shed light on GI morbidity in ASD include the observations that: levels of transcripts for disaccharidases and hexose transporters are reduced in AUT-GI children; AUT-GI children have microbial dysbiosis in the mucoepithelium; and dysbiosis is associated with deficiencies in host disacharidase and hexose transporter mRNA expression. Based on these findings, we propose a model whereby deficiencies in disaccharidases and hexose transporters alter the milieu of carbohydrates in the distal small intestine and proximal large intestine, resulting in the supply of additional growth substrates for bacteria. These changes manifest in significant and specific compositional changes in the microbiota of AUT-GI children. A previous report on GI disturbances in ASD found low activities of at least one disaccharidase or glucoamylase in duodenum in 58% of children. In our study, 93.3% of AUT-GI children had decreased mRNA levels for at least one of the three disaccharidases. In addition, we found decreased levels of mRNA for two important hexose transporters, SGLT1 and GLUT2. Congenital defects in these enzymes and transporters are extremely rare, and even the common variant for adult-type hypolactasia was not responsible for reduced LCT expression in AUT-GI children in this cohort. Therefore, it is unlikely that the combined deficiency of disaccharidases and transporters are indicative of a primary malabsorption resulting from multiple congenital or acquired defects in each of these genes. Transcripts for the Diatrizoic acid enterocyte marker, villin, were not reduced in AUT-GI ilea and did not predict the expression levels of any of the disaccharidases or transporters in multiple regression models. This suggests that a general loss of enterocytes is unlikely. However, we cannot exclude the possibility that defects in the maturational status of enterocytes or enterocyte migration along the crypt-villus axis contribute to deficits in disaccharidase and transporter expression. The ileal expression of CDX2, a master transcriptional regulator in the intestine, was a significant predictor of mRNA expression of all five disaccharidases and transporters in AUT-GI and Control-GI children, based on linear regression models.