Jonathan Campbell
Duke University, NC·Physiology
After a meal, the gut and pancreas release hormones that tell the body's tissues how to handle the incoming sugar and fat. Getting these signals right keeps blood sugar steady.
- Fields
Physiology
Medicine & Clinical Research
Pharmacology
- Topics
glucose-dependent insulinotropic polypeptide
incretins
glucagon
- Grants
- 3 known grants, through Jun 2030
What they work on
- Test whether pericytes, cells lining blood vessels, are the main GIP receptor (GIPR)-expressing cells in fat tissue, using mouse models that mark and lineage-trace GIPR-positive cells over time.
- Determine whether GIPR signaling in pericytes supports healthy formation of new fat cells during overnutrition, using mice lacking GIPR only in pericytes and drugs that activate GIPR.
- Test whether liver glucagon receptors use G-protein signaling to raise glucose output but β-arrestin signaling to increase insulin sensitivity, using physiological and drug studies in new mouse models.
- Validate the dual roles of liver glucagon signaling in human volunteers, in parallel experiments to the mouse studies, to judge their relevance to glucagon-based therapies.
- Measure how alpha cells process proglucagon into glucagon via the enzyme PC2 or into GLP-1 via the enzyme PC1, and how this shapes insulin release from beta cells, using donated human islets.
- Test whether alpha-to-beta-cell communication becomes a larger driver of insulin secretion as metabolic stress and insulin resistance rise, through clinical studies of people across the metabolic spectrum.
More about the research
Getting them wrong contributes to type 2 diabetes and obesity. Several widely used diabetes and obesity drugs mimic these hormones, yet how they work is still not fully understood. This research asks how three related hormones act on fat tissue, the liver and the insulin-making cells of the pancreas. The three hormones are GIP (glucose-dependent insulinotropic polypeptide), glucagon, and GLP-1 (glucagon-like peptide 1). The goal is a clearer picture of normal metabolism and of how current and future drugs exert their effects.
Why it matters
Drugs that target the GIP, GLP-1 and glucagon systems are used worldwide to treat type 2 diabetes and obesity. This work could explain how these drugs act on fat tissue, the liver and the pancreas. It could support new glucagon-based drugs that activate only helpful signaling routes, for better blood sugar control in people with type 1 or type 2 diabetes, obesity or liver disease. It could also clarify how type 2 diabetes develops.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
Barak Blum
University of Wisconsin-Madison, WI·Physiology
Test the hypothesis that reducing Robo2 receptors in beta cells, the pancreas's insulin-making cells, is essential for islets of Langerhans to expand successfully when insulin demand rises.
Michelle Kimple
University of Wisconsin-Madison, WI·Pharmacology
Determine how the EP3 receptor affects separate cellular pools of calcium and cAMP in mouse and human beta cells, and how these changes alter insulin secretion and beta-cell mass, using cellular imaging.
The school
Duke University: 61 labs on PI Pages, $1.6B a year on research, 417 research doctorates a year.
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