EM2C will contribute to understanding how genetic variations contribute to common, complex diseases, such as diabetes and related traits. The Center is led by Stephen Parker, PhD.
One in five Americans are affected by diabetes*, making it one of the most prevalent health conditions in the United States. Studies have shown that the interactions between genes and environmental factors are critical to understand tissue-level cellular state changes that influence health and diseases, including metabolic diseases such as diabetes. The potential impact of this field of research is huge.
Large-scale population research brings invaluable information to comprehend the biological mechanisms that lead to metabolic diseases. At the University of Michigan (U-M) Medical School, the newly-created Epigenomic Metabolic Medicine Center (EM2C) will perform population-scale single-cell multi-omics profiling with the goal of better understanding how genetic variations contribute to common, complex diseases, such as diabetes and related traits. Once new genetic mechanisms are identified, researchers can use this information to develop better strategies to detect, treat, and prevent these diseases.
EM2C’s long-term aim is to generate and integrate single-cell multi-omics datasets from key metabolic tissues (skeletal muscle, adipose tissue, liver, pancreatic islets, hypothalamus, kidney, and small and large Intestines) from at least 1,000 individuals. These datasets will be integrated with genotype and phenotype information to create a comprehensive picture of genetic and environmental factors associated with complex metabolic diseases.
The Center is led by Stephen Parker, PhD, Associate Professor, Computational Medicine and Bioinformatics, Human Genetics, and Biostatistics, and EM2C’s director, who said:
“This is such an exciting and dynamic area of research and I’m looking forward to the collaborative opportunities and team science that will be enabled by the EM2C.”
Brian Athey, PhD, Chair of the U-M Department of Computational Medicine and Bioinformatics (DCMB), said: “I can think of no one better than Professor Steve Parker to establish the U-M Center Epigenomic Metabolic Medicine Center (EM2C) in the Caswell Diabetes Institute (CDI). Steve is a recognized national leader in single cell multi-omics data analytics in metabolic disease, focusing on Type 2 Diabetes (TD2). EM2C will accelerate our ability to personalize treatment and therapeutic discoveries.”
At EM2C, Parker brings together over 25 scientists from three U-M research groups, the Caswell Diabetes Institute (CDI(link is external)), the Taubman Institute(link is external), DCMB, and the Department of Human Genetics, all leaders in their respective research area. EM2C’s research will coordinate and focus this expertise on population-scale single-cell multi-omics and data analytics investigation, with a focus on epigenome profiling. Within CDI and across campus, the Center will catalyze new and cutting-edge research programs that will lead to new diagnostic and therapeutic strategies in diabetes and metabolic disease research.
“The EM2C represents a core component of strategic planning by the CDI. Integrating epigenomic data acquisition and analysis into the diabetes and metabolism focused research will keep U-M at the head of the pack, in addition to providing new knowledge with which to understand and combat diabetes,” said Martin Myers, MD, PhD, Director, Elizabeth Weiser Caswell Diabetes Institute, Director, Michigan Diabetes Research Center, Marilyn H Vincent Professor of Diabetes Research, and Professor of Internal Medicine and of Molecular and Integrative Physiology.
EM2C will also push the technology further by increasing throughput and analysis speed—while decreasing costs. Generating such a foundational resource will position U-M as a world-leader in this new and exciting field, especially as it relates to molecular quantitative trait locus (QLT) scans and will enable expansion of key research initiatives across campus.
* Source: CDC(link is external)
References:
“Genetic risk converges on regulatory networks mediating early type 2 diabetes,” Nature. DOI: 10.1038/s41586-023-06693-2
Original Article - https://medicine.umich.edu/dept/dcmb/news/archive/202402/new-epigenomic-...
