My research focuses on uncovering the mechanisms supporting β-cell compensation, with particular interest in the role of α-cell to β-cell communication during compensation. Preliminary studies from our lab show that β-cells increase their reliance on glucagon signaling to enhance insulin secretion in response to insulin resistance caused by nutrient stress. Using mouse models, my work aims to define modulations to signaling through the glucagon receptor in compensating β-cells. Defining the mechanisms responsible for compensation will allow us to better understand how β-cells defend against insulin resistance in the prediabetic stage and potentially uncover strategies to prevent the transition to overt T2D.

Honors and Award
Genetics T-32 Pre-doctoral Training Grant (2026-2027)