Investigating the role of a protein in liver disease and metabolic disorders
Official title: Role of SUN1 in MASLD and metabolic disease
Funded at University of Michigan at Ann Arbor · NIH-11057704 · Data updated 2026-11-12
This study is looking at how a protein called SUN1 might affect liver health in people with metabolic dysfunction-associated steatotic liver disease (MASLD), and we're inviting patients to help by sharing genetic samples to see how different versions of this protein could play a role in this condition.
Quick facts
| Grant type | R03 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Michigan at Ann Arbor NIH-funded |
| Lab location | 1 site (Ann Arbor, United States) |
| Project start | April 1, 2024 |
| Project end | March 31, 2026 |
| Funding year | 2025 |
| Award (this year) | $117,000 |
| NIH project number | 5R03DK137052-02 |
| Project ID | NIH-11057704 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates for participation include adults over 21 years old who are at risk for or diagnosed with metabolic dysfunction-associated steatotic liver disease.
✕Less likely to help
Patients with liver disease caused by factors other than metabolic dysfunction, such as viral hepatitis or alcohol-related liver disease, may not benefit from this research.
What this research studies
This research focuses on metabolic dysfunction-associated steatotic liver disease (MASLD), a common chronic liver condition that can lead to serious health issues. The study examines the role of a specific protein, SUN1, which is believed to influence liver health and metabolic processes. By analyzing genetic variants of SUN1, researchers aim to understand how these variants may contribute to the development of MASLD and related metabolic disorders. Patients may be involved in providing genetic samples to help identify the impact of SUN1 on liver disease.
Why it matters
Potential benefit: If successful, this research could lead to new therapeutic strategies for preventing or treating MASLD and related metabolic diseases.
How similar studies have gone: Previous research has shown promising results in understanding the genetic factors contributing to liver diseases, suggesting that this approach may yield valuable insights.
Where this research is happening
-
University of Michigan at Ann Arbor
Ann Arbor, United States Active
Researchers
- Principal investigator: Brady, Graham F. — University of Michigan at Ann Arbor
- Study coordinator: Brady, Graham F.
Related research
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Dysfunctional fat tissue and its link to fatty liver and diabetes
Researchers are studying how problems in fat tissue contribute to fatty liver disease and type 2 diabetes in adults.
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Them1’s role in fat metabolism and MASLD progression
Aims to understand how a fat-regulating protein (Them1) affects energy use in fat and liver, and how this could contribute to MASLD in people who are overweight.
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A patient-facing overview of a study that looks at why a common liver disease progresses to more serious conditions in Alaska Native and American Indian people.
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This grant studies how the body's endocannabinoid system affects the progression from obesity to diabetes and the associated risk for cardiovascular disease in adults.
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Pediatric MASLD: a blood test to detect liver disease progression in kids
A child-friendly blood test is being developed to spot liver disease progression in kids with MASLD without needing biopsies.
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Growth Hormone and DNA Repair in Children's MASLD outcomes
A small, patient-friendly study will explore how growth hormone and the ATM DNA repair pathway affect liver health in children with MASLD.
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.