The vitamin D receptor (VDR), a nuclear transcription factor, mediates the genomic vitamin D effects. Through this mechanism, vitamin D controls the active intestinal calcium absorption and thus regulates the systemic calcium homeostasis and bone mineralization. Recently, new vitamin D functions have been discovered, that were not related to calcium regulation. Therefore, the aim of this work was to identify new non-calcium related vitamin D functions in the intestine by comparing a VDR-deficient mouse model with wildtype mice. The lack of VDR led to an increased microvilli length of duodenal enterocytes which was accompanied by an increased abundance of the essential microvilli-morphogenesis regulator ezrin. Furthermore, the VDR-deficit led to adaptations in proteins associated to cell adhesion, e.g. claudin-2 and the 67kDa-lamininreceptor as well as proteins related to the cellstress response system.