Primary tabs

Biography
Sander Kersten, Ph.D. is the director of the Division of Nutritional Sciences and the Schleifer Family Professor at Cornell University. Dr. Kersten received his MSc degree in Human Nutrition from Wageningen University in 1993, and his Ph.D. degree in Nutritional Biochemistry from Cornell University in 1997. After a postdoctoral stay in the laboratory of Dr. Walter Wahli at the University of Lausanne, Switzerland, he moved back to Wageningen University in 2000 with a career development grant from the Royal Netherlands Academy of Arts and Sciences. He was appointed to Associate Professor in 2006 and Full Professor in 2011. In 2014 he became Chair of the Nutrition, Metabolism and Genomics group and in 2019 Chairman of the Division of Human Nutrition and Health at Wageningen University. In January 2024, he moved back to Ithaca as the director of the Division of Nutritional Sciences.
Research in his group aims to elucidate the molecular mechanism that underlies the regulation of lipid metabolism in the liver and adipose tissue during fasting and feeding. In the past, his group demonstrated the importance of the transcription factor PPARα in the metabolic response to fasting in the liver. Using various human liver model systems in combination with transcriptomics, his work also revealed the importance of PPARα in gene regulation and nutrient metabolism in the human liver. In addition, his team elucidated the mechanism responsible for the regulation of fat uptake into adipose tissue during fasting. Specifically, his group discovered the protein ANGPTL4 and elucidated its role as a crucial regulator of lipid uptake into adipose tissue by interfering with the function of lipoprotein lipase. His current research is concentrated on identifying the role of several novel fasting-regulated genes in lipid metabolism in adipose tissue and the liver.
Research interests
Throughout human evolution, starvation was a major threat to our survival. Accordingly, starvation was the key selective pressure shaping the foundational principles of nutrient and energy metabolism. Fasting elicits a multi-organ response that aims to maintain physiological homeostasis and meet the energy requirements of various tissues in the absence of an external energy source. An intricate network of evolutionarily conserved transcriptional, translational, and post-translational regulatory mechanisms underlie the adaptive response to fasting and ensure maximal survival during periods of undernutrition.
As overnutrition is surpassing undernutrition as the most common health threat globally, the thrifty metabolic system that once enabled humans to survive starvation now contributes to the unprecedented rise in obesity and related diseases. My research is driven by the notion that the consequence of overnutrition can only be fully understood by having detailed insight into the foundational mechanisms regulating lipid and energy metabolism during undernutrition and fasting. Further mechanistic understanding of how humans respond to fasting could be key to designing effective preventive and therapeutic strategies for overnutrition and its pathological sequelae, including obesity, insulin resistance, non-alcoholic fatty liver disease, and atherosclerosis. Aligning with this notion, many popular drug targets for cardiometabolic diseases represent fasting-responsive messengers and sensors.
The common thread throughout my professional career has been the study of the mechanisms and functional impact of gene regulation by lipids during feeding and fasting. The main aim of my research is to understand better how lipid metabolism is regulated during feeding and fasting and how lipids govern specific functional outcomes and orchestrate their own metabolism. The primary focus is on the key organs relevant to lipid metabolism represented by the liver and adipose tissue, the transport of lipids to these organs, and the interplay between these organs and other relevant systems such as the immune system. In my research, a multi-pronged approach is used that ranges from dietary intervention studies in human subjects to physiological experiments in transgenic animals and detailed mechanistic studies in vitro.
Keywords: fasting, fatty acids, lipid/lipoprotein metabolism, liver, adipose tissue, macrophages, NAFLD, atherosclerosis, diabetes, obesity, Peroxisome Proliferator-Activated Receptors, lipoprotein lipase, Angiopoietin-like proteins