Diabetes – epigenetics
Charlotte Ling’s group
The goal of our research is to dissect the role of epigenetics in the pathogenesis of type 2 diabetes and develop epigenetic-based therapies and biomarkers for precision medicine.
Type 2 diabetes is a multifactorial disease, and combinations of genetic and non-genetic factors such as age, obesity, and physical inactivity increase disease risk. Data from our group and others also show that epigenetic modifications contribute to type 2 diabetes. The epigenome includes DNA methylation, histone modifications, and non-coding RNA.
We have identified epigenetic modifications in pancreatic islets, skeletal muscle, adipose tissue, and the liver from individuals with type 2 diabetes compared with controls. We have shown that genetic and non-genetic factors, such as single nucleotide polymorphisms (SNPs), exercise, diet, obesity, and age alter the epigenetic pattern in human tissues affecting type 2 diabetes. Our group has also identified blood-based epigenetic biomarkers that may be used for precision medicine.
- To discover novel epigenetic modifications and mechanisms responsible for pancreatic islet dysfunction and insulin resistance in individuals with type 2 diabetes, which can be targeted for future type 2 diabetes therapies.
- To develop epigenetic biomarkers of clinical relevance that can be used for precision medicine in type 2 diabetes.
Our pioneering research has improved our understanding of how epigenetic modifications and mechanisms contribute to the development of type 2 diabetes and metabolic disease. Our projects are also developing epigenetic tools that may be used for better prediction, prevention, and treatment of type 2 diabetes and its complications.
Current major grants
- Distinguished professor grant from Swedish Research Council 2022-2031
- Novo Nordisk Distinguished Investigator Grant 2022-2026
- European Research Council (ERC) consolidator grant 2017-2022
Professor of diabetes and epigenetics
+46 706 14 51 46
charlotte [dot] ling [at] med [dot] lu [dot] se