How obesity harms blood vessels in belly fat
Official title: Obesity-Induced Endothelial Dysfunction in Arteries of Visceral Adipose
Funded at University of Delaware · NIH-11191484 · Data updated 2026-11-12
This project looks at whether a fat-uptake protein called CD36 and a blood-flow channel named Kir2.1 explain why obesity weakens the lining of blood vessels in belly fat in adults.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Delaware NIH-funded |
| Lab location | 1 site (Newark, UNITED STATES) |
| Project start | May 15, 2016 |
| Project end | May 31, 2027 |
| Funding year | 2025 |
| Award (this year) | $324,948 |
| NIH project number | 5P20GM113125-10 |
| Project ID | NIH-11191484 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal participants are adults with obesity who can donate visceral fat during abdominal or bariatric surgery, or adults willing to provide subcutaneous fat samples for comparison.
✕Less likely to help
People without excess visceral (belly) fat or those who cannot provide tissue samples are unlikely to participate or directly benefit from this project.
What this research studies
The team will compare small arteries from visceral (belly) fat and subcutaneous (under-skin) fat to learn why vessels in belly fat stop widening with increased blood flow in obesity. They will study the activity of Kir2.1 channels and the role of the fatty-acid receptor CD36 using experiments in mice and analyses of adult human tissue samples. The researchers will test whether blocking CD36 or restoring Kir2.1 function can rescue blood vessel responses in obese visceral fat. Results are intended to reveal specific mechanisms that could be targeted to protect blood vessels in people with obesity.
Why it matters
Potential benefit: If successful, this work could point to new ways to protect or restore blood-vessel function in people with obesity, lowering cardiovascular risk.
How similar studies have gone: Previous lab work links Kir2.1 to flow-induced dilation and implicates CD36 and fatty acids in vascular harm, but applying these findings to visceral arteries in obesity is a new and not-yet-tested approach.
Where this research is happening
-
University of Delaware
Newark, United States Active
Researchers
- Principal investigator: Fancher, Ibra — University of Delaware
- Study coordinator: Fancher, Ibra
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.