Type 1 diabetes (T1D) is a multifactorial metabolic disease caused by immune-mediated destruction of the insulin-producing ß-cells in the pancreatic islets of Langerhans. The overall goal of my research is to advance our understanding of fundamental islet biology and the detrimental mechanisms causing ß-cell failure in T1D. A better understanding of the genetic risk factors, the triggering mechanisms, the islet-immune dialogue, and the pathways leading to ß-cell death may pave the way for future therapeutic options to prevent ß-cell destruction in T1D.

Associate Professor of type 1 diabetes pathophysiology, Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen. Born in Gentofte 1974. Married. Two children.

Education
June 2005: PhD in Health Sciences, Faculty of Health and Medical Sciences, University of Copenhagen.
April 2001: MSc in Biology, August Krogh Institute, University of Copenhagen.
January 1998: BSc in Molecular Biology, Roskilde University.

Current positions
Associate Professor (20%), Department of Biomedical Sciences, University of Copenhagen
Senior Researcher and Team Leader (80%), Department of T1D Biology, Steno Diabetes Center Copenhagen.

Previous positions
2018-2020: Senior Researcher and Team Leader, Steno Diabetes Center Copenhagen.
2017-2018: Senior Researcher, Steno Diabetes Center Copenhagen.
2013-2017: Senior Researcher, Herlev University Hospital.
2011-2013: Senior Researcher, Glostrup Research Institute.
2009-2011: Senior Scientist, Hagedorn Research Institute/Novo Nordisk A/S
2006-2008: Post Doctoral Research Fellow, Steno Diabetes Center/Hagedorn Research Institute
2002-2005: PhD Student, Steno Diabetes Center and University of Copenhagen.

Selected academic qualifications and honors

• Reviewer for several scientific journals including The Lancet Diabetes & Endocrinology, Diabetologia, Diabetes Obesity & Metabolism, Gastroenterology, Cell Death & Disease, Scientific Reports, Molecular & Cellular Endocrinology, DNA and Cell Biology, Environmental Toxicology, Science Reports, BMC Molecular Biology, etc.
• Grant reviewer for Juvenile Diabetes Research Foundation (JDRF), Fonds Wetenschappelijk Onderzoek Vlaanderen (FWO), French National Research Agency (ANR), Dutch Diabetes Research Foundation (DDRF), Welcome Trust, and Diabetes UK.
• Steering group member and co-founder of CPH-DIRECT (Copenhagen Diabetes Research Center), University Hospital Herlev/SDCC.
• Obtainment of >13 million DKK in funding as PI or co-PI including two project grants as PI from the Independent Research Fund Denmark (2013 and 2017).
• Leadership courses, Novo Nordisk A/S and the Capital Region (2011 and 2019).
• Talent award: Rising Star, University Hospital Herlev, 2014.
• Postdoc award, Independent Research Fund Denmark, 2006.

We perform hypothesis-driven, multifaceted and cross-disciplinary translational research. In our work, we utilize clinical samples, ß-cell models, human islets, and mouse models. We have three overall focus areas within the T1D pathophysiology field:

Functional genomics: Based on the strong genetic component of T1D with more than 50 known risk loci, a prime target is to identify causal disease genes and to functionally validate these in ß-cells. Our hypothesis is that many risk-conferring genes operate in the ß-cells and are involved in crucial functions such as regulation of apoptotic cell death and the dialogue with the immune system. We apply various integrative systems biology approaches to pinpoint possible candidate genes that we then take further in wet lab experiments.

Inflammatory cytokines: Specific pro-inflammatory cytokines exert cytotoxic effects on ß-cells and play a crucial role in T1D. Hence, another focus area is to decipher pro-apoptotic cytokine signal transduction in islets and ß-cells. Further, the levels of pro- and anti-inflammatory cytokines in the circulation may reflect the detrimental processes going on in the pancreas during development and remission of T1D. Therefore, these factors may constitute biomarkers that can be used prognostically to predict disease course, remission potential, and risk of development of complications.

Incretin islet biology: A more recent arm of our research deals with incretin hormone biology. The incretins GLP-1 and GIP increase insulin secretion in a glucose-dependent manner and exert anti-apoptotic and proliferative effects on ß-cells. Recent research also suggests that GIP under some circumstances can stimulate α-cell glucagon secretion. However, the underlying mechanisms responsible for the effects of incretins in islets remain unclear and need further exploration. Our work is devoted to a better understanding of incretin islet biology and to explore the potential of incretins to rescue ß-cells from immune-mediated destruction. Potentially, incretin therapy constitutes a new option to increase and sustain ß-cell function in newly diagnosed T1D patients which is the long-term aim of this research.