Vitamin D is regulator of calcium homeostasis. When dietary calcium intake is low, the hormonal form of vitamin D, 1,25 dihydroxyvitamin D, regulates gene expression in the intestine, kidney, and bone to ensure that serum calcium levels are maintained. While the regulation of intestinal calcium absorption is the most important physiologic role for vitamin D during growth, it isn't the only role for vitamin D in the intestine. Our gene expression profiling studies of the mouse intestine and of human intestinal organoids have revealed the full breadth of vitamin D action in intestine. We find that in addition to regulating genes that mediate calcium absorption, vitamin D regulates many different genes, most of which are unique to different compartments of the small intestine (i.e. crypt vs villus) or intestinal segments (i.e. small intestine vs colon). These genes control a diverse array of functions, e.g. cell growth and migration, xenobiotic metabolism, lipid metabolism. Some of these explain why vitamin D may prevent cancer and strengthen intestinal barrier function. In addition, other research shows that vitamin D can modulate the function of gut associated immune cells to reduce intestinal inflammation during inflammatory bowel disease. The translational implications of these molecular changes will be discussed.
Dr. Fleet is the Margaret McKean Love Endowed Professor in Nutrition, Cellular, and Molecular Sciences at the University of Texas at Austin. Dr. Fleet's research is focused on the molecular and physiological functions of vitamin D in the control of calcium metabolism and the prevention of cancer. His research employs the tools of molecular biology, genomics, and genetics to address questions relevant to human health and disease prevention.