Prof. Surbek is currently Full Professor (Ordinarius) for Gynecology and Obstetrics at the University of Bern and Acting Chair of the Department of Obstetrics and Gynecology. He is Head of the Division of Obstetrics and Feto-Maternal Medicine at the University Hospital, and Head of the Research Laboratory for Prenatal Medicine at the Department of Clinical Research at University of Bern. He graduated from Medical School in Basel, Switzerland, where he specialized in Obstetrics and Gynecology and Fetal-Maternal Medicine. After research fellowships in USA and UK, he obtained a Faculty position at University of Basel, before he was elected as Professor at Univerity of Bern in 2005.

In recent years, it became evident that intrauterine fetal life before birth is of great importance for the later development of cardiovascular and metabolic disorders in adulthood. Professor Surbek’s research group of feto-maternal medicine investigates pregnancy specific diseases such as pre-eclampsia, diabetes in pregnancy and intrauterine growth restriction (IUGR). These abnormalities contribute substantially to increased perinatal morbidity and mortality of both the mother and its child. Even more importantly, it is now recognized that intrauterine fetal exposure to these pathologic conditions of pregnancy lead to cardiovascular and metabolic diseases later in life in adulthood. This phenomenon called “fetal programming” has an important impact on the development of a range of diseases in adults.

Prof. Surbek’s group has established a large tissue and data bank of pregnancies compromised by pre-eclampsia and IUGR. He has a profound expertise and reported recently of altered serum protein patterns in such pregnancies. Another focus of the group’s interest are placental transport proteins, e.g. glucose transporter-1 and –3 (GLUT-1, GLUT-3), transferrin receptor (TfR) and amino acid transporters.

Since the nutrient supply of the fetus takes place exclusively across the placenta, the placental transport proteins and their regulations will affect fetal well-being including fetal growth, and they are the key factors in fetal programming. Future intervention strategies to prevent irreversible abnormal cardiovascular and metabolic programming and later disease in adulthood will depend on elucidation of these mechanisms.

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