How a liver immune protein (SMPDL3B) affects fatty liver in people with obesity
Official title: Role of SMPDL3B in obesity-associated non-alcoholic fatty liver disease
Funded at University of Kentucky · NIH-11325730 · Data updated 2026-11-12
This project looks at whether restoring a liver immune protein called SMPDL3B can reduce inflammation and slow fatty liver disease in people with obesity.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Kentucky NIH-funded |
| Lab location | 1 site (Lexington, United States) |
| Project start | July 1, 2022 |
| Project end | April 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $478,167 |
| NIH project number | 5R01DK131786-05 |
| Project ID | NIH-11325730 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for future clinical work would be adults with obesity who have non-alcoholic fatty liver disease (NAFLD) or early non-alcoholic steatohepatitis (NASH).
✕Less likely to help
People whose liver disease is caused primarily by alcohol or who already have advanced cirrhosis are unlikely to benefit from these specific findings.
What this research studies
Researchers will study how SMPDL3B in liver immune cells controls a fatty-acid receptor called CD36 and how that signaling drives inflammation in obesity-related fatty liver disease. They will use mouse models and human liver organoids made from patient tissue to see how changing SMPDL3B levels affects liver inflammation and disease features. The team will also test whether blocking the interaction between the protein TSP1 and CD36 raises SMPDL3B and lowers inflammatory signaling in macrophages. Together these approaches aim to link basic molecular changes to disease progression and point to possible treatment targets.
Why it matters
Potential benefit: If successful, this work could point to new ways to reduce liver inflammation and prevent progression from NAFLD to NASH in people with obesity.
How similar studies have gone: Laboratory and animal studies support the importance of this pathway, but using SMPDL3B restoration or blocking TSP1/CD36 as a treatment is still largely experimental.
Where this research is happening
-
University of Kentucky
Lexington, United States Active
Researchers
- Principal investigator: Wang, Shuxia — University of Kentucky
- Study coordinator: Wang, Shuxia
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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.