A protein called FAM172A protects your liver from storing too much fat by controlling how another protein named PPARγ is made, according to research published in 2026. When scientists removed FAM172A from mouse liver cells, the mice developed significantly worse fatty liver disease on a high-fat diet, while adding extra FAM172A reduced fat buildup. This discovery suggests FAM172A could become a new treatment target for fatty liver disease, though human studies are still needed.
Scientists discovered that a protein called FAM172A plays an important role in protecting your liver from storing too much fat. When researchers removed this protein from mice eating a high-fat diet, their livers accumulated much more fat and developed metabolic problems. The study found that FAM172A works by controlling how another protein called PPARγ is made in liver cells. This discovery suggests that FAM172A could become a new target for treating fatty liver disease, a condition affecting millions of people worldwide. According to Gram Research analysis, this finding opens new possibilities for developing treatments that boost this protective protein.
Key Statistics
A 2026 research study found that mice lacking the FAM172A protein in their livers developed significantly more severe fatty liver disease when eating a high-fat diet compared to normal mice.
Laboratory experiments showed that adding extra FAM172A to liver cells reduced fat accumulation, while removing FAM172A made fat storage worse, demonstrating the protein’s direct protective effect.
The study identified that FAM172A works by controlling which version of the PPARγ protein is produced in liver cells, with FAM172A-deficient cells making more of the fat-storage-promoting PPARγ2 variant.
The Quick Take
- What they studied: How a protein called FAM172A affects fat buildup in the liver and what molecular mechanisms control this process
- Who participated: Laboratory mice with diet-induced fatty livers and cultured liver cells from mice, studied in 2026
- Key finding: Mice without the FAM172A protein developed significantly more liver fat when eating a high-fat diet, and this protein normally protects against fat accumulation by controlling how another protein called PPARγ is produced
- What it means for you: This research suggests that boosting FAM172A levels might help prevent or treat fatty liver disease, though human studies are needed before any new treatments become available
The Research Details
Researchers used laboratory mice to study how FAM172A affects liver health. They created mice that lacked the FAM172A gene specifically in liver cells and fed them a high-fat diet to see what happened. They also grew liver cells in dishes and either added extra FAM172A or removed it to observe the effects on fat accumulation.
The scientists used several advanced techniques to understand how FAM172A works. They analyzed proteins in liver cells, tracked which proteins interact with each other, and examined how genes are turned on and off. They also studied the RNA (genetic instructions) for PPARγ to understand how FAM172A controls which version of this protein gets made.
This combination of whole-animal studies and detailed cellular experiments allowed researchers to identify both what FAM172A does and the specific molecular pathway it uses to protect against fatty liver disease.
Using both living mice and isolated cells strengthens the findings because it shows the effect works at multiple levels. The proteomic analysis (detailed protein study) and genetic tracking techniques provide solid evidence for the specific mechanism, making the results more reliable and actionable for future drug development.
The study used multiple complementary approaches that all pointed to the same conclusion, which increases confidence in the findings. The research was published in a peer-reviewed journal focused on metabolism research. However, this work was conducted in mice and laboratory cells, so results may not directly translate to humans without further testing. The study did not include human subjects or clinical trials.
What the Results Show
When researchers removed the FAM172A gene from mouse liver cells, the mice developed much more severe fatty liver disease when eating a high-fat diet compared to normal mice. The livers of FAM172A-deficient mice showed increased expression of genes involved in taking up fat and making new fat, suggesting the liver was actively accumulating lipids.
In laboratory experiments with isolated liver cells, adding extra FAM172A reduced fat buildup, while removing FAM172A made fat accumulation worse. This confirmed that FAM172A directly protects liver cells from storing excess fat.
The protective effect of FAM172A appears to work through controlling a protein called PPARγ. When FAM172A was removed, cells made more of a specific version of PPARγ (called PPARγ2) that promotes fat storage. When FAM172A was added, PPARγ levels decreased and fat accumulation was reduced.
The researchers identified that FAM172A works with another protein called SRSF3 to control which version of PPARγ gets made. This SRSF3 protein acts like a molecular switch that determines which instructions from the PPARγ gene are actually used to build the protein.
Blocking PPARγ with a drug called GW9662 reduced fat accumulation in liver cells lacking FAM172A, confirming that PPARγ is the key target through which FAM172A exerts its protective effects. When researchers restored SRSF3 levels in FAM172A-deficient cells, fat accumulation partially improved, suggesting SRSF3 is an important part of how FAM172A works. The study also showed direct physical interaction between SRSF3 and the PPARγ gene’s RNA, providing molecular evidence for how this control mechanism functions.
Previous research had linked FAM172A to obesity and heart disease, but this study is among the first to specifically examine its role in liver fat accumulation and to identify the molecular mechanism. The finding that FAM172A controls PPARγ isoform expression (different versions of the same protein) adds a new layer of understanding to how metabolic proteins are regulated. This work builds on existing knowledge that PPARγ promotes fat storage while suggesting that controlling which version of PPARγ is made could be a new therapeutic strategy.
This research was conducted entirely in mice and cultured cells, not in humans, so the findings may not directly apply to human fatty liver disease. The study did not test whether increasing FAM172A levels could reverse existing fatty liver disease, only whether it could prevent it. The exact role of FAM172A in human livers remains unknown and requires further investigation. Additionally, the study did not examine potential side effects of boosting FAM172A, which would be important for developing any future treatment.
The Bottom Line
Based on this research, FAM172A emerges as a promising target for developing new fatty liver disease treatments. However, these findings are preliminary and based on animal studies. Anyone with fatty liver disease should continue following established medical advice from their healthcare provider, including maintaining a healthy diet and exercise routine. Future human studies will be needed to determine if treatments targeting FAM172A are safe and effective.
This research is most relevant to people with fatty liver disease, obesity, or metabolic syndrome. It may also interest researchers and pharmaceutical companies developing new treatments for liver disease. People with genetic risk factors for fatty liver disease might benefit from future treatments based on this work. However, the findings do not yet apply to general health recommendations for the general population.
This is early-stage research, so any new treatment based on these findings would likely take 5 to 10 years to develop and test in humans. Immediate lifestyle changes like reducing fat intake and increasing exercise remain the most proven approaches for managing fatty liver disease today.
Frequently Asked Questions
What is FAM172A and why does it matter for liver health?
FAM172A is a protective protein found in liver cells that prevents excessive fat storage. Research shows that when this protein is absent, livers accumulate much more fat, especially on high-fat diets. Scientists now view FAM172A as a potential target for developing new fatty liver disease treatments.
How does FAM172A prevent fat buildup in the liver?
FAM172A works by controlling how PPARγ, a protein that promotes fat storage, is made in liver cells. It partners with another protein called SRSF3 to determine which version of PPARγ gets produced, ultimately reducing the amount of fat-promoting protein available.
Can I increase my FAM172A levels to treat fatty liver disease?
This research is still in early stages using mice and laboratory cells. No human treatments targeting FAM172A exist yet. If you have fatty liver disease, work with your doctor on proven approaches like diet changes, exercise, and weight management while researchers develop potential new therapies.
When will treatments based on this FAM172A research be available?
Drug development typically takes 5 to 10 years from laboratory discovery to human testing. This research was just published in 2026, so any FAM172A-based treatment would likely not be available for several years, pending further studies and clinical trials.
Does this research apply to people or just mice?
This study was conducted in mice and cultured mouse liver cells, not humans. While the findings are promising and suggest a new therapeutic direction, researchers must conduct human studies to confirm whether boosting FAM172A would safely and effectively treat fatty liver disease in people.
Want to Apply This Research?
- Track daily fat intake in grams and weekly liver health markers if available through medical testing, noting any changes in energy levels or digestive symptoms that might correlate with dietary changes
- Set a daily reminder to log meals and identify high-fat foods to reduce, then gradually replace them with lean proteins and whole grains while tracking how you feel over 4 to 8 weeks
- Create a monthly check-in to review trends in diet quality and energy levels, and schedule regular liver function tests with your doctor to monitor progress if you have fatty liver disease
This article describes laboratory research in mice and cultured cells published in 2026. The findings do not yet represent approved medical treatments for humans. Fatty liver disease is a serious condition that requires professional medical evaluation and management. If you have been diagnosed with fatty liver disease or metabolic dysfunction, consult your healthcare provider before making any changes to your diet, exercise routine, or treatment plan. This research is preliminary and should not be used as a basis for self-treatment or to replace medical advice from qualified healthcare professionals.
This research translation is published by Gram Research, the science division of Gram, an AI-powered nutrition tracking app.