Changes in composition and functions of different subcellular compartments of the enterocytes caused by vitamin D administration to vitamin D deficient chicks will be reviewed in this article. Special emphasis will be focused on alterations in lipid composition, fluidity and calcium transport properties of brush border, mitochondria and basolateral membranes. The possible mechanisms by which cholecalciferol provokes an increase in the Krebs cycle NAD⁺ -Iinked oxidoreductase activities will be also described. Finally, a detailed analysis of the effects of vitamin D on the two mechanisms of calcium exit through the basolateral membranes, the plasma membrane Ca²⁺-ATPase and Na⁺/Ca²⁺ exchanger, will be discussed. Vitamin D is a secosteroid produced by a wide range of live organisms. Fungi, phytoplankton, zooplankton, plants, insects, fish, reptiles, amphibians, birds and mammals can synthesize vitamin D [1]. Cholecalciferol (vitamin D₃) is the natural form of the vitamin while ergocalciferol (vitamin D₂) is a synthetic compound originally produced by irradiation of ergosterol from plants. Both vitamin D₂ and D₃ are metabolized by the same pathways to produce active metabolites with identical effects. Thus, the term vitamin D refers to either form of the vitamin.