Four chapters, one small organ
The pancreatic islet is the smallest organ in the body and one of the most consequential. When it works, you don't notice. When it stops working, you have diabetes. Most of my career has been an attempt to understand what makes islets work, what makes them fail, and how to catch the failure early enough to do something about it.
2010–2016 · Harvard / JoslinThe many origins of a β-cell
When I started graduate school, a stem-cell biologist named Shinya Yamanaka had just shown that an adult cell — a piece of skin, even — could be reprogrammed back to an embryonic-like state. He'd win the Nobel Prize for it in 2012, my second year, and a generation of regenerative medicine was forming around that single result. The implication was electric: if you could turn skin into stem cells, you could turn stem cells into β-cells, and you could grow a patient their own β-cells back. My PhD work in Rohit Kulkarni's lab sat at the intersection of that promise and the underlying biology — building β-cells from iPSCs, reprogramming the pancreas's own ductal cells into an endocrine fate, and asking what holds β-cell identity together when stress pulls at it. The lab taught me what an islet is. The work taught me how flexible — and how fragile — that identity can be.
2019–2022 · UT Health San AntonioDoes glucose control rescue a failing β-cell?
For decades, the field had taken high blood sugar as the prime mover of β-cell dysfunction in type 2 diabetes — and lowering glucose as the way to restore function. The UKPDS, the landmark trial of glucose control in type 2 diabetes, had been quietly disagreeing for thirty years: glucose control reduces complications, but it does not stop the β-cell from failing. The 2024 Banting Lecture made that point its centerpiece. If not glucose, then what? In Ralph DeFronzo's group, we offered one answer: lipid-driven inflammation persists even after glucose returns to normal, and that persistent lipotoxicity is what keeps β-cells from recovering. Glucose is one pressure among several, not the cause.
2022–2026 · UT Southwesternβ-cells don't fail alone
At UT Southwestern, the question shifted from the cell to the unit — and the institution had been pointing that way for decades. Roger Unger, working in the same center where I would later join Phil Scherer's group, had run the experiment that quietly redefined the field: destroy every β-cell in a mouse, eliminating insulin entirely, then silence the α-cells. Glucose stayed normal. The implication was almost heretical at the time — diabetes is not, fundamentally, an insulin-deficiency disease. It's a disorder of the islet as a coordinated whole. By the time I arrived at the Touchstone Diabetes Center, that framing had become foundational in research — but not in the clinic. My own training spanned both, and the gap was hard to miss. Diabetes care still revolves around lowering glucose, preserving β-cells, and restoring insulin secretion: the islet's parts, treated one at a time. β-cells don't sit alone; they live inside an islet, alongside α-cells, δ-cells, and the vasculature that knits them into a single small organ. The lesson I took from those years: when β-cells stop working, what fails first is rarely the cell — it's the communication between them that does.
2026–present · San DiegoThe struggling organ
If the islet fails as a unit, and the unit fails before the cell, then diabetes is an organ-failure disease — and there are many ways to get there. That reframing matters most for the patients who don't fit the conventional account — lean people who develop diabetes, people with obesity who never do. The glucose-and-BMI model has no clean explanation for either. The organ-failure model does: the islet behaves like a small networked organ that can fail silently, years before any standard test detects it. Making that failure detectable early — while reversal is still on the table — is my current work.
And if glucose control alone doesn't prevent that failure — as we've known for decades — then the right question for a patient shifts. Not just "how do I fix my sugar?" but "how do I protect my organ?" I look forward to the day patients walk into clinic and ask their doctors both.
The thread across all four chapters is the same: a small tissue, big stakes, and a long window of time during which something can still be done. The current work is what makes that window usable.
For published papers, see Publications. For the full academic record, see my CV.