How high-fat diets may reduce calorie burning in brown fat
High Fat Feeding Reduces Energy Expenditure in Brown Adipose Tissue
This project looks at whether eating a high-fat diet changes gut bacteria and brain signals so brown fat burns less energy, which could help explain diet-related weight gain.
Quick facts
| Grant type | R01 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 ID | NIH-11322020 on NIH RePORTER |
What this research studies
From the patient perspective, researchers are studying how a high-fat diet changes the mix of gut bacteria and increases a bacterial molecule called lipoteichoic acid (LTA). They will use animal models, including germ-free mice, to trace how LTA might act on a brain receptor (TLR2) and alter hypothalamic circuits that control sympathetic nerves to brown fat. The team will measure nerve activity, brown fat gene signals like UCP1, and body heat production, and test whether changing microbes or blocking TLR2 restores brown fat activity. These experiments aim to link diet, the gut microbiome, brain signaling, and calorie burning in brown fat.
Who could benefit from this research
Good fit: Adults with overweight or diet-related obesity, especially those consuming high-fat diets, would be the most relevant group for the findings or any future clinical follow-ups.
Not a fit: People whose weight issues are driven primarily by rare genetic syndromes, certain medications, or non-dietary medical conditions may not benefit from mechanisms related to brown fat and gut microbes.
Why it matters
Potential benefit: If this work holds up, it could point to new ways to raise brown fat energy use — for example by changing gut bacteria or blocking specific brain signals — to help prevent or treat obesity.
How similar studies have performed: Previous animal studies have shown high-fat diets alter gut microbes and reduce brown fat activity, but directly linking a bacterial molecule like LTA through hypothalamic TLR2 to nerve firing and UCP1 suppression is a newer, less-tested idea.
Where this research is happening
Ann Arbor, United States
- University of Michigan at Ann Arbor — Ann Arbor, United States (Active)
Researchers
- Principal investigator: Wiley, John W — University of Michigan at Ann Arbor
- Study coordinator: Wiley, John W
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.