Research Interests

Pancreatic β-cells within islets are functionally heterogeneous, comprising distinct subtypes that respond differently to their environment. We investigate how diverse upstream cues—hormones, nutrients, metabolites, cytokines, neurotransmitters, the extracellular matrix, and signals from neighboring islet cells—are integrated to shape this heterogeneity. By linking receptor, transporter, and enzyme expression to downstream transcription factor activity, chromatin accessibility, and effector gene programs, we aim to define the signaling pathways that govern β-cell identity. Ultimately, we seek to understand how these pathways control functional outcomes such as glucose-stimulated insulin secretion, proliferation, senescence, and subtype transitions across different metabolic states.

Pancreatic stellate cells are emerging as key components of the islet microenvironment, yet the origin, identity, and fate of islet-resident stellate cells remain poorly defined. We study how these cells transition between quiescent and activated states and search for islet-specific markers that distinguish them from their exocrine counterparts. Combining Cre-dependent lineage tracing in mouse models, in vitro β-cell co-culture systems, and single-cell and spatial multiomics of human pancreas and plasma, we explore their roles in ECM production, secretory signaling, vitamin A storage, blood flow regulation, immune modulation, and potential β-cell neogenesis. Our goal is to clarify how islet stellate cells contribute to β-cell function and dysfunction across development, aging, obesity, diabetes, and pancreatic cancer.

Metabolic homeostasis depends on continuous communication between the pancreatic islet and distant organs. We investigate the bidirectional crosstalk through which insulin and organ-derived signals—myokines, hepatokines, adipokines, gut-derived GLP-1 and metabolites, and neural inputs—coordinate whole-body metabolism. By examining how these circuits become dysregulated, we aim to connect pancreatic biology to a broad spectrum of conditions including sarcopenia, MASLD, obesity, lipodystrophy, Alzheimer's disease, IBD, and dysbiosis, as well as pancreatic cancer. This integrative perspective seeks to uncover shared mechanisms that link diabetes to broader metabolic and age-related diseases.