Bethany Cummings
University of California-Davis, CA·Physiology
Blood sugar is controlled by two hormones from the pancreas. Beta (β) cells release insulin, which lowers glucose.
- Fields
Physiology
Medicine & Clinical Research
Biology
- Topics
type 2 diabetes
obesity
pancreatic islets
- Grants
- 2 known grants, through May 2031
What they work on
- 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.
- Determine the α-cell's contribution to insulin secretion in obesity and weight loss using genetic and pharmacological approaches in mice.
- Identify the regulatory factors driving higher glucagon in obesity and after weight loss, using in vivo and ex vivo tools with single-cell resolution.
- Test whether α-cell GLP-1 is required for the rise in insulin secretion when β-cell 14-3-3ζ is inhibited, using islets from mice whose α-cells cannot make GLP-1.
- Define how loss of β-cell 14-3-3ζ induces GLP-1-producing α-cells and identify the receptor class that activates α-cell GLP-1 production.
More about the research
Alpha (α) cells release glucagon, which tells the liver to make more glucose. In obesity, α-cells make too much glucagon, and this helps drive type 2 diabetes (T2DM). However, α-cells also signal locally to neighboring β-cells and boost glucose-stimulated insulin secretion (GSIS), the insulin release triggered when blood sugar rises. The lab's two projects ask how α-cells balance raising blood sugar against helping insulin release. They also ask how β-cells and α-cells talk to each other inside the islets, the small hormone-making clusters of the pancreas.
Why it matters
Several obesity drugs in development target GLP-1 or glucagon receptors. Glucagon-based drugs promote weight loss but only work well when paired with glucose-lowering drugs. Knowing when α-cells raise blood sugar and when they support insulin release could guide the design of combined glucagon therapies for obesity. It could also reveal new islet targets for preventing or treating type 2 diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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
University of California-Davis: 49 labs on PI Pages, $1.0B a year on research, 647 research doctorates a year.
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