PIPages
Labs

Seung K Kim

Stanford University, CA·Medicine & Clinical Research

The pancreas does two very different jobs: it makes digestive enzymes, and it houses islets, small clusters of hormone-producing cells that keep blood sugar in a narrow range. When the enzyme-making side of the organ becomes inflamed or cancerous, blood sugar control often fails too, and patients develop a form of diabetes that is neither type 1 nor type 2.

Fields

Medicine & Clinical Research

Physiology

Genetics

Topics

type 3c diabetes

pancreatogenic diabetes

chronic pancreatitis

Grants
4 known grants, through Jun 2029

What they work on

  1. Map gene regulation and measure electrical activity in individual islet cells from living subjects with chronic pancreatitis, with and without prediabetes, to find the earliest changes preceding type 3c diabetes.
  2. Test whether incretin hormones, gut signals released after eating, drive excessive glucagon secretion from alpha cells in chronic pancreatitis patients who have prediabetes.
  3. Use CODEX multiplexed tissue imaging and cultured human islets to test whether specific inflammatory signaling pathways in chronic pancreatitis rewire alpha cell gene expression and function.
  4. Identify the cell of origin and the genetic pathways that initiate pancreatic ductal adenocarcinoma, distinguishing acinar cells that convert to duct-like cells from duct-derived precancerous lesions, in mouse models and human tissue.
  5. Discover immune signals that cross-talk with pancreatic epithelial cells and cancer-associated fibroblasts to promote tumor development and stem-cell-like properties in the tumor microenvironment.
  6. Determine how a pancreatic tumor's genetic makeup shapes its immune environment and its response to immunotherapy directed at macrophages.
  7. Provide and advance islet research services — isolation of high-quality rodent and human islets, insulin and glucagon ELISA, perifusion and static secretion assays, immunohistology and transplantation models — and train investigators in these methods.
  8. Run pilot and feasibility awards and research cores that support diabetes investigators at Stanford and, through a regional program, at UC Berkeley and UC Davis.

More about the research

Research here asks how disease in one part of the pancreas derails the other, how pancreatic cancer starts and uses surrounding cells to hide from the immune system, and it builds shared laboratory resources that let many groups study human and rodent islets.

Why it matters

Diabetes that follows chronic pancreatitis or pancreatic cancer is more common than once thought and poorly understood, so patients are often treated as if they had ordinary type 2 diabetes. Identifying the earliest signaling and gene-regulation failures in islet alpha cells could point to better ways to manage or delay it, and because this diabetes often appears before pancreatic cancer is diagnosed, the same changes may serve as early warning markers at a stage when surgery can still be curative. The cancer program could reveal how pancreatic tumors begin and evade immunotherapy, and the shared islet and diabetes cores give many research groups access to human islets and standardized assays.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Investigating mechanisms underlying diabetes associated with exocrine pancreas diseases

NIH · Aug 2024 – Jun 2029

Pancreatic Cancer Development: Genetic and Immune Regulation

NIH · Aug 2021 – Jul 2027

Stanford Islet Research Core

NIH · Sep 2017 – Jun 2027

Closest labs

Alejandro Caicedo

University of Miami, FL·Physiology

Uncover how nutrients sensed in the gut activate entero-pancreatic neurons, using live-animal calcium imaging of pancreatic cells while different contents are perfused through the duodenum in mice.

Bethany Cummings

University of California-Davis, CA·Physiology

Compare liver and islet responses to injected glucagon in obese mice and after dietary or bariatric-surgery weight loss, to test whether α-cell signaling shifts from the liver to insulin secretion.

Andrew Lowy

University of California-San Diego, CA·Medicine & Clinical Research

Test whether deleting MICAL2, an actin-dismantling enzyme, blocks or delays KRAS-driven pancreatic tumor formation and progression, using whole-body and conditional deletion in genetically engineered mice.

The school

Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.

More about Stanford University

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