Prof Torsten Plösch
University Medical Center Groningen, The Netherlands
Torsten Plösch studied biology at the University of Oldenburg, Germany, with the focus on cell biology, microbiology, and zoology. He then moved to the University of Groningen, Netherlands, to work on the metabolism and transport of hydrophobic compounds in mouse models. There, he received his Ph.D. in 2004 (thesis “The ABC of cholesterol transport”; supervisor: Prof. F. Kuipers). He then switched his focus to the epigenetic regulation of metabolic processes and established Epigenetic Programming as a new research area at the University Medical Center Groningen. Currently, Dr. Plösch is University Lecturer and head of the research laboratory at the Department of Obstetrics and Gynecology of the UMCG.
Until now, he has authored more than 60 scientific papers, most of them on molecular aspects of metabolism and its epigenetic regulation. Dr. Plösch is a board member of the UMCG research program ROAHD (http:/www.roahd.nl), of the International Society for Developmental Origins of Health and Disease (DOHaD, https://dohadsoc.org/), and of the International Science Committee of the American Physiological Society. Moreover, he serves on the editorial board of the Journal of Developmental Origins of Health and Disease.
Dr. Plösch’s research is focused on the influence of the early fetal and neonatal environment on the health of the offspring at adult age (BARKER hypothesis, DOHaD hypothesis). Specifically, his lab studies how disturbances in maternal-fetal nutrient supply during pregnancy and early postnatal nutrition influence later metabolic regulation, namely with regards to lipid metabolism and cardiovascular diseases. The key idea is that nutrients or other biologically active molecules induce epigenetic changes in the placenta, embryo, fetus or newborn which persist into adulthood and hence change the susceptibility to develop chronic disease (metabolic programming, epigenetic programming). A new research focus is the influence of the microbiome via its metabolites on the host epigenome.