Thurl E. Harris
University of Virginia, VA·Physiology
Body fat is more than storage: white adipose tissue (WAT) helps control the whole body's energy balance. After a meal, insulin signals fat to store incoming fatty acids as triglycerides.
- Fields
Physiology
Pharmacology
Biochemistry
- Topics
adenosine receptors
A2B adenosine receptor
A1 adenosine receptor
- Grants
- 1 known grant, through Feb 2028
What they work on
- Characterize how signaling through the A2B adenosine receptor (A2BR) in white fat changes between fasted and post-meal states, as receptor expression switches from A1R to A2BR.
- Test the effects of genetic deletion or drug-based manipulation of A2BR on post-meal fat breakdown (lipolysis) and fatty acid storage in adipose tissue.
- Determine how food intake promotes adenosine signaling through A2BR in fat during the post-meal period, and how obesity shifts this receptor balance.
More about the research
During fasting, stress hormones called catecholamines signal fat to release them. In obesity and prediabetes, this system breaks down, especially in the one to four hours after eating. Too much free fatty acid spills into the blood and other organs. This drives insulin resistance and excess glucose production by the liver.
Why it matters
Poor storage of fatty acids and glucose after meals is implicated in the harmful effects of obesity, including insulin resistance and prediabetes. Clarifying how adenosine receptors in fat control fat breakdown after eating, and how this goes wrong in obesity, could point to A2B receptor signaling as a target for improving metabolic health.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sona Kang
University of California-Berkeley, CA·Physiology
Define how FAM3D, a protein genetically linked to type 2 diabetes, suppresses heat production and mitochondrial function in mouse and human brown fat cells.
Jeffrey Schelling
Case Western Reserve University, OH·Medicine & Clinical Research
Determine whether FATP2, a fatty acid transporter in the kidney's proximal tubule, drives fat-induced cell death and progression of diabetic kidney disease, using mouse models.
Philipp Scherer
University of Texas Southwestern Medical Center, TX·Physiology
Adjust insulin signaling only in mouse fat cells, by lowering insulin receptor levels on demand, switching on an artificial insulin receptor, or manipulating the signaling brake PTEN. Measure the effects on whole-body metabolism.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.