Serge Ferrari

Prof. Serge Ferrari

Génétique et métabolisme de l’ostéoporose


Serge Ferrari (MD) graduated from the Geneva Faculty of medicine in 1989 and has been research and clinical fellow, instructor in medicine at Harvard Medical School in 1997-2001. He has been recipient of Professorship grant from the Swiss National Science Foundation and is currently Full Professor of Medicine at the Geneva Faculty of Medicine. He is Head of the Service of Bone Diseases of the Geneva University Hospital. He is Vice-chair of the council of scientific advisors of the International Osteoporosis Foundation and Vice-President of the Swiss Association against Osteoporosis. He is editor-in-chief of BoneKey and BoneKey Reports (Nature publishing group) from the International Bone and Mineral Society. He has published over 200 articles and book chapters in the field of osteoporosis, bone and mineral metabolism.

Research aims

Regulatory mechanism of bone remodeling and controls of glucose metabolism
Main interests of Prof. Ferrari's lab are the molecular mechanism of bone formation in the context of osteoporosis. Osteocytes orchestrate bone modeling and remodeling in response to mechanical loading and parathyroid hormone. They discovered that the matricellular protein periostin is an essential mediator of these two anabolic stimuli particularly for the cortical surface. They are translating it into clinical output with the development of an ELISA assay and the validation of periostin as a biomarker for cortical microarchitecture. Dr. Nicolas Bonnet is now developing new promising independent projects on the molecular mechanisms governing the fat-bone unit in chronic disease such as osteoporosis and type 2 diabetes. Their recent data clearly demonstrated the ability of bone to regulate whole body glucose homeostasis through regulation of thermogenesis and insulin secretion. Their goal is now to better characterize the role of bone remodeling and osteokine secretion in the crosstalk between the bone and the other organs directly involved in glucose homeostasis (skeletal muscle, WAT, BAT, liver, pancreas, brain...) in the context of diabetoporosis.