2025 PRESENTER PROFILES
Genetic Regulation of Beta-Cell Mass and Function in Humans—Lessons from GWAS and Rare Genetics
Sunday, June 22, at 1:30 p.m. CT
Room W194 AB • McCormick Place Convention Center
Integrating Multiomic Data to Understand Complex Gene Regulatory Networks in Islets

Anna Gloyn, DPhil
Professor of Pediatrics & Genetics,
Stanford University
What is your presentation about?
Coordinated efforts to study human islets from hundreds of donors have generated enormous amounts of multi-modal data. There are challenges and opportunities with integrating these data to uncover how genetic variation, which alters risk for diabetes, impacts islet development and function. My presentation will showcase collaborative efforts to catalogue, harmonize, and analyze data from multiple resources to deliver insights into islet pathophysiology in diabetes.
How do you hope your presentation will impact diabetes research or care?
I hope that my presentation will draw attention to multiple islet resources, including the new National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)-funded PanKbase, which are available to support our research community and can be used to both generate and test hypotheses for islet-cell dysfunction in diabetes.
How did you become involved with this area of diabetes research or care?
One of the most enjoyable aspects of research is team science. I have worked with collaborator Patrick MacDonald for over 10 years to contribute genetic and genomic data on human islets to the Alberta Human Islet Core and more recently have generated genetic data for the NIDDK-funded Human Pancreas Analysis Program (HPAP) and the Integrated Islet Distribution Program (IIDP), where I direct the Human Islet Genotyping Initiative (HIGI).
Genetically Modified Pseudoislets to Study Role of Non-Coding elements on Beta-Cell Function

Romina J. Bevacqua, PhD
Assistant Professor,
Icahn School of Medicine at Mount Sinai
What is your presentation about?
Most of our knowledge of beta-cell function stems from mice, which are significantly different from humans. Recent efforts have been able to identify specific regulators of pancreatic human beta-cell function—among these, non-coding presumptive enhancers of beta-cells, enriched for type 2 diabetes risk variants. In my presentation, I will discuss the application of novel genetic systems to primary human islet organoids to study these recently identified human-specific regulatory mechanisms.
How do you hope your presentation will impact diabetes research or care?
Genome-wide association studies (GWAS) show that the vast majority of genetic risk for diabetes (at >400 risk loci) maps to non-coding DNA, largely enhancers. Yet, the target genes of most of these enhancers, their specific tissue of action, and their dynamic regulation remain largely unknown, particularly in humans. Generating human-specific tools for the study of these human-specific mechanisms, we hope to better comprehend how beta-cells become dysregulated in disease.
How did you become involved with this area of diabetes research or care?
I have been interested in genetics, gene regulation, and gene editing since my graduate studies. During my postdoctoral studies, I became interested in adapting and expanding gene editing systems to primary, largely non-dividing, human islet cells. While challenging, this allowed the study of the specific mechanisms behind adult human beta-cell function and dysfunction in disease.