Intestinal calcium absorption is essential for the prevention of bone loss in the aging population and in patients with chronic kidney disease or gastrointestinal pathology. Therefore, calcium and vitamin D supplementation is widely used as an essential part of anti-osteoporotic therapy. However, this therapy is still confronted with issues of safety, compliance, and limited efficacy.

Using several transgenic mouse strains, we observed that vitamin D supplementation without adequate intestinal calcium transport has deleterious effects on bone. To develop novel therapeutic strategies, a comprehensive mechanistic understanding of intestinal calcium absorption is required. In several pathologies including chronic kidney disease, intestinal calcium transport is considered to be altered although the exact mechanisms are not fully elucidated.

The current postdoctoral project focuses on deciphering the molecular mechanisms underlying intestinal calcium transport using global gene expression profiling besides a candidate gene approach. The functional relevance of the identified proteins will be investigated in normal and pathological conditions as well as during anti-osteoporotic treatment using several pre-clinical mouse models. This multimodal approach will lead to novel insights in the mechanisms responsible for calcium transport and will contribute to the optimization of current therapies or to the development of novel treatment modalities. The proposed project will combine cellular, biochemical, physiological and molecular techniques as well as animal experiments. You will work in close collaboration with other members of the lab (Post-doc, PhD students, technicians). This project is also embedded in a broader platform, in which you will collaborate with different researchers experienced in gastroenterology and nephrology.