Scientists found that a protein called SLC13A3 plays a major role in causing fatty liver disease, a condition where fat builds up in the liver. Using mice, researchers discovered that when this protein is turned up, it makes the liver store more fat and become unhealthy. When they turned down this protein, the liver improved. The protein works by affecting something called NAD+, which helps control how the body handles fat. This discovery could lead to new treatments for millions of people with fatty liver disease who currently have few options to help them.

The Quick Take

  • What they studied: How a liver protein called SLC13A3 causes fatty liver disease and whether controlling this protein could help treat the condition
  • Who participated: Laboratory mice were fed unhealthy diets high in fat, cholesterol, and sugar to develop fatty liver disease similar to what happens in humans
  • Key finding: When researchers reduced SLC13A3 levels in the livers of sick mice, the fatty liver disease improved significantly. The protein controls a chemical called NAD+ that tells the liver how much fat to store
  • What it means for you: This research suggests that drugs targeting SLC13A3 might help treat fatty liver disease in humans, but this is still early-stage research. More studies are needed before any new treatments could be available

The Research Details

Researchers used laboratory mice to study how a specific liver protein affects fatty liver disease. They created two groups of mice: one group had extra copies of the SLC13A3 gene (making more of the protein), and another group had the gene turned off (making less of the protein). All mice were fed an unhealthy diet similar to what many people eat—high in fat, cholesterol, and sugar.

The scientists then measured how much fat accumulated in the livers and checked which genes were turned on or off. They also measured levels of NAD+, a chemical that acts like an energy messenger in cells, helping control whether the body stores fat or burns it.

This type of study is called a ‘mechanistic study’ because it focuses on understanding the exact biological mechanisms—the step-by-step processes—that cause disease.

This research approach is important because it identifies a specific target that could be used to develop new medicines. Rather than just describing what happens in fatty liver disease, the researchers showed that controlling one specific protein can improve the condition. This gives doctors a clear direction for developing new treatments

This is laboratory research using mice, which is an important first step in drug development but doesn’t directly prove the same results will work in humans. The study appears to be well-designed with clear comparisons between different groups. However, because the sample size isn’t specified and this is mouse research, the findings need to be confirmed in human studies before people should expect new treatments

What the Results Show

When researchers increased SLC13A3 in mouse livers, the disease got worse—the livers stored more fat and showed more signs of damage. This proved that the protein is important for causing the disease.

When they decreased SLC13A3 levels, the opposite happened: the livers stored less fat, and the signs of disease improved. This showed that reducing this protein could be a way to treat the condition.

The researchers discovered that SLC13A3 works by controlling NAD+ levels in the liver. NAD+ is like a master switch that tells cells whether to store fat or burn it for energy. When SLC13A3 is high, NAD+ levels change in ways that make the liver store more fat.

The protein also controls several other genes that are involved in fat storage and metabolism, including genes called SREBF1, CD36, PPARγ, and SCD1. These genes are like the ‘instructions’ that tell the liver how much fat to make and store.

The study showed that SLC13A3 levels were higher in mice with worse fatty liver disease, suggesting the protein’s activity matches disease severity. The research also revealed that this protein affects multiple pathways involved in fat metabolism, not just one single mechanism, which explains why it’s such an important control point for the disease

Fatty liver disease is a major health problem affecting millions of people worldwide, but current treatments are limited. Most existing research has focused on other causes like inflammation or insulin resistance. This study is novel because it identifies SLC13A3 as a previously unknown key player in the disease. This adds a new piece to the puzzle of how fatty liver disease develops and opens up a completely new direction for treatment research

This research was conducted in mice, not humans, so we don’t yet know if the same results will occur in people. The study doesn’t tell us how quickly changes would happen in humans or what dose of a potential medicine would be needed. Additionally, the study focused on one specific type of diet-induced fatty liver disease, so results might differ in people with other causes of the condition. More research is needed to understand if this protein is equally important in all types of fatty liver disease

The Bottom Line

This research is too early-stage to make specific recommendations for patients. It’s a promising discovery that suggests future treatments might target SLC13A3, but no such treatments exist yet. People with fatty liver disease should continue following their doctor’s current advice: maintain a healthy weight, eat a balanced diet low in processed foods and added sugars, exercise regularly, and limit alcohol. (Confidence level: This is preliminary research; recommendations are based on current standard care, not this study)

This research is most relevant to people with metabolic dysfunction-associated steatotic liver disease (MASLD), formerly called non-alcoholic fatty liver disease. It’s also important for researchers developing new treatments and for doctors who treat liver disease. People without fatty liver disease don’t need to change their behavior based on this single study, though the findings support the general importance of maintaining a healthy lifestyle to prevent the disease

Since this is mouse research, it will likely take several years before human trials could begin. If a drug targeting SLC13A3 is eventually developed and approved, it would probably take 5-10 years or more from now. In the meantime, people with fatty liver disease should focus on proven lifestyle changes that can improve their condition

Want to Apply This Research?

  • Track weekly diet quality scores (rating meals 1-10 for healthiness) and weekly exercise minutes, as these are proven ways to improve fatty liver disease while researchers develop new treatments based on discoveries like this one
  • Users with fatty liver disease could use the app to set and monitor goals for reducing processed foods and added sugars, increasing physical activity to 150 minutes per week, and maintaining a healthy weight—all evidence-based approaches that may help until new treatments become available
  • Establish a monthly check-in system where users log lifestyle changes and any health improvements reported by their doctor (such as improved liver enzyme levels from blood tests), creating a long-term record of what works for their individual situation

This research is preliminary laboratory work in mice and does not yet provide guidance for human treatment. Fatty liver disease is a serious medical condition that requires professional medical evaluation and management. If you have been diagnosed with fatty liver disease or metabolic dysfunction-associated steatotic liver disease (MASLD), please consult with your healthcare provider about appropriate treatment options. Do not make changes to your medical care based solely on this research summary. This article is for educational purposes only and should not be considered medical advice.