Shortened telomeres and gut health: absorption, barrier leaks, and microbiome shifts
Mechanisms of telomere-induced disease: Role of intestinal malabsorption, barrier dysfunction and dsybiosis.
This work looks at whether shortened chromosome ends (telomeres) in gut cells cause poor nutrient absorption, a weakened gut barrier, and changes in gut bacteria for people with aging-related or inflammatory bowel problems.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Baylor College of Medicine NIH-funded |
| Lab location | 1 site (Houston, United States) |
| Project ID | NIH-11326764 on NIH RePORTER |
What this research studies
Researchers will examine how shortened telomeres affect the final stage of gut cell development (enterocytes) that are responsible for absorbing nutrients and keeping the gut lining sealed. They will use laboratory models that mimic telomere shortening and analyze gut tissue, absorption measures, barrier integrity, and the composition of gut bacteria. The team will compare those findings to patterns seen in patients with ulcerative colitis, Crohn’s disease, or inherited telomerase defects to make the results relevant to human disease. The goal is to identify specific ways telomere loss leads to malabsorption, inflammation, or microbiome imbalance and test possible molecular fixes.
Who could benefit from this research
Good fit: People with ulcerative colitis, Crohn’s disease, unexplained malabsorption, inherited telomerase mutations, or suspected age-related intestinal decline would be most relevant for follow-up or future clinical work stemming from this research.
Not a fit: Patients whose conditions are unrelated to intestinal barrier function or telomere biology (for example, isolated cardiac disease or non-gastrointestinal genetic disorders) are unlikely to receive direct benefit from this work.
Why it matters
Potential benefit: If successful, this could uncover targets for new treatments or tests to prevent or reverse malabsorption, leaky gut, and inflammation in people with age-related or telomere-linked intestinal disease.
How similar studies have performed: Prior studies in telomerase-deficient mice have shown telomere shortening can cause intestinal atrophy, inflammation, and cancer progression, but directly connecting telomere loss to enterocyte maturation, barrier defects, and dysbiosis is a newer direction.
Where this research is happening
Houston, United States
- Baylor College of Medicine — Houston, United States (Active)
Researchers
- Principal investigator: Sahin, Ergun — Baylor College of Medicine
- Study coordinator: Sahin, Ergun
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 below.