PIPages
Labs

Michelle Kimple

University of Wisconsin-Madison, WI·Pharmacology

Type 2 diabetes develops when beta cells in the pancreas can no longer release enough insulin to control blood sugar. It is increasingly common, and today's children face a lifetime risk of nearly 50%.

Fields

Pharmacology

Physiology

Biochemistry

Topics

type 2 diabetes

pancreatic beta cells

insulin secretion

Grants
1 known grant, through Mar 2028

What they work on

  1. 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.
  2. Quantify how the G protein Gαz drives movement and phosphorylation of Rap1GAP, a signaling protein, and how these changes affect beta-cell function and mass, using proteomics.
  3. Measure changes in the arachidonic acid metabolome of human pancreatic islets during progression to type 2 diabetes, and test how these changes affect beta-cell responses to glucose and GLP-1.

More about the research

Few diabetes drugs target beta cells directly, and those that do help only some patients. This project studies one signaling route that changes in failing beta cells. It asks how the route may first help beta cells cope with obesity and later contribute to their failure.

Why it matters

People with type 2 diabetes have few drugs that directly protect or restore insulin-producing beta cells. Defining how EP3 and Gαz signaling shifts from helpful to harmful could identify targets for increasing the number of working beta cells. It could also explain why GLP-1-based drugs work in some patients but not others, which may improve treatment of type 2 diabetes.

Known grants

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

The role of G protein-dependent and -independent EP3 signaling in beta-cell compensation and diabetes

NIH · Apr 2024 – Mar 2028

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.

Jonathan Campbell

Duke University, NC·Physiology

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.

Dongmin Liu

Virginia Polytechnic Institute and State University, VA·Pharmacology

Characterize the anti-diabetic and anti-obesity effects of daily oral elenolic acid in diet-induced obese and db/db diabetic mice, using metabolic profiling and euglycemic-hyperinsulinemic clamps to measure insulin sensitivity.

The school

University of Wisconsin-Madison: 91 labs on PI Pages, $1.9B a year on research, 854 research doctorates a year.

More about University of Wisconsin-Madison

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