Diabetes mellitus is the most common metabolic disorder, affecting hundreds of millions of people worldwide. This multifactorial disease is influenced by genetic background, age, and lifestyle. Despite extensive research and significant advances that have improved treatments for both type 1 (T1D) and type 2 diabetes (T2D), critical knowledge gaps remain, particularly in understanding the molecular processes underlying the disease.
Our research focuses on uncovering the molecular mechanisms linking these risk factors to metabolic dysfunction. Specifically, we study pancreatic alpha and beta cells, which play central roles in glucose regulation by secreting glucagon and insulin, respectively, to maintain stable blood sugar levels throughout the day.
A major area of interest in our lab is exploring how aging increases susceptibility to metabolic decline, insulin resistance, and the development of T2D. We investigate the effects of aging on pancreatic alpha and beta cells through multiple approaches, including the analysis of DNA methylation patterns and cellular senescence. Additionally, we study the role of telomere shortening, a hallmark of aging, on metabolic decline using a novel mouse model with human-length telomeres. As part of this work, we employ advanced technologies such as nanopore sequencing in collaboration with the lab of Yehuda (Dudy) Tzfati (Hebrew University, Life Sciences).
In addition, our lab works together with Ben Glaser (Hadassah Medical Center, Endocrinology) and closely collaborates with Yuval Dor (our department). We also have ongoing partnerships with Prof. Klaus Kaestner's group at the University of Pennsylvania, focusing on age-related changes in alpha and beta cells, which incorporate genomic analysis of a large pool of human samples from the PANC-DB data repository.
Through these partnerships and collaborative efforts, we aim to address critical knowledge gaps and provide new insights into therapeutic strategies for diabetes and age-related metabolic diseases.
