Researchers found that a protein called LACTB is overactive in people with fatty liver disease, a condition where fat builds up in the liver and causes problems. In studies with mice, when scientists reduced LACTB levels, the mice’s livers got healthier, their bodies handled sugar better, and inflammation decreased. The protein works by breaking down another important protein (CPT2) that helps the liver burn fat. This discovery suggests that blocking LACTB could be a new way to treat fatty liver disease, which affects millions of people worldwide and is becoming more common.

The Quick Take

  • What they studied: Whether a protein called LACTB causes fatty liver disease and how it damages the liver
  • Who participated: Liver tissue samples from patients with fatty liver disease and laboratory mice fed a high-fat diet to mimic the disease
  • Key finding: When LACTB was reduced, the mice showed significant improvements in liver fat content, blood sugar control, and inflammation markers. When LACTB was increased, the disease got worse.
  • What it means for you: This research suggests a potential new treatment target for fatty liver disease, but it’s still in early stages. More research in humans is needed before any new treatments become available. If you have fatty liver disease, continue following your doctor’s current recommendations while scientists work on new options.

The Research Details

Scientists used two main approaches to understand LACTB’s role in fatty liver disease. First, they examined liver tissue from actual patients with the disease and compared it to healthy tissue. They also studied mice fed a high-fat diet, which develops the same liver problems as humans. In the lab, they tested what happened when they increased LACTB levels (making more of the protein) and when they decreased it (making less of the protein). They used genetic techniques to turn the LACTB gene on and off to see how this affected the liver’s health and function.

The researchers also studied the molecular mechanisms—essentially how LACTB works at the cellular level. They discovered that LACTB interacts with another protein called CPT2, which is responsible for helping the liver burn fat for energy. By understanding this interaction, they could explain why reducing LACTB helps the liver work better.

This combination of human tissue analysis, animal studies, and laboratory experiments allowed the researchers to build a complete picture of how LACTB contributes to fatty liver disease.

This research approach is important because it moves from observation to understanding cause and effect. By studying both human tissue and animal models, the researchers could confirm that LACTB isn’t just present in fatty liver disease—it actually causes or worsens the condition. The laboratory work explaining the molecular mechanism is crucial because it shows exactly how LACTB damages the liver, which is necessary for developing effective treatments.

The study used multiple complementary approaches (human tissue, animal models, and laboratory experiments), which strengthens the findings. The research was published in a respected peer-reviewed journal focused on metabolic diseases. However, the study was conducted primarily in mice, so results may not translate exactly to humans. The specific sample size of human participants wasn’t provided, which limits our ability to assess how representative the human findings are. Additional human studies would be needed to confirm these results before any new treatment could be used in patients.

What the Results Show

The researchers discovered that LACTB protein levels are significantly higher in the livers of both fatty liver disease patients and mice fed a high-fat diet compared to healthy controls. This was the first clue that LACTB plays a role in the disease.

When scientists reduced LACTB in mice with fatty liver disease, multiple improvements occurred: the amount of fat stored in the liver decreased substantially, the mice’s bodies became better at controlling blood sugar (insulin resistance improved), and markers of liver inflammation went down. These improvements suggest that blocking LACTB could address multiple aspects of the disease at once.

Conversely, when researchers artificially increased LACTB levels in mice, the disease got worse—more fat accumulated in the liver, insulin resistance increased, and inflammation worsened. This proved that LACTB directly causes or worsens the disease rather than just being a side effect.

The mechanism behind these effects involves a protein called CPT2, which normally helps the liver burn fat. LACTB attaches to CPT2 and causes it to be broken down and removed from cells. With less CPT2 available, the liver can’t burn fat efficiently, leading to fat accumulation and the cascade of problems that follow.

The research showed that the beneficial effects of reducing LACTB depend entirely on CPT2 being present. When scientists removed CPT2, reducing LACTB no longer helped, confirming that CPT2 is essential for LACTB’s effects on the liver. This finding is important because it shows the specific pathway involved and could help researchers design more targeted treatments. The study also demonstrated that LACTB affects multiple aspects of liver disease simultaneously—fat accumulation, sugar metabolism, and inflammation—suggesting it’s a central control point in the disease process.

Previous research had identified LACTB as important in cancer and general lipid (fat) metabolism, but its specific role in fatty liver disease was unknown. This study fills that gap by showing LACTB is a key player in this common disease. The findings align with what scientists know about how proteins are broken down in cells and how this process affects metabolism. The discovery that LACTB controls CPT2 levels adds a new mechanism to our understanding of how fatty liver disease develops, complementing previous research on other factors involved in the disease.

The study was primarily conducted in mice, and animal models don’t always behave exactly like human bodies. The human tissue samples were examined but not studied as extensively as the mouse experiments, so we can’t be certain the same mechanisms work identically in people. The research doesn’t tell us whether blocking LACTB would be safe or effective as a long-term treatment in humans. Additionally, the study focused on one specific pathway; fatty liver disease is complex and involves many other factors not addressed here. Finally, the study doesn’t explain why LACTB levels become elevated in the first place, which would be important for prevention strategies.

The Bottom Line

This research is promising but preliminary. Current evidence suggests that LACTB could be a therapeutic target, but human clinical trials are needed before any new treatment becomes available. For now, the most reliable approaches to managing fatty liver disease remain: maintaining a healthy weight, eating a balanced diet low in processed foods and added sugars, exercising regularly, and limiting alcohol. If you have fatty liver disease, work with your healthcare provider on these proven strategies while monitoring for new treatment options. Confidence level: This is early-stage research with moderate confidence in the basic findings, but low confidence in real-world human applications at this time.

This research is most relevant to people with metabolic dysfunction-associated fatty liver disease (MASLD), particularly those who haven’t responded well to lifestyle changes. It’s also important for researchers and pharmaceutical companies developing new treatments. People at risk for fatty liver disease—those who are overweight, have type 2 diabetes, or have metabolic syndrome—should be aware of this emerging research. However, this research shouldn’t change anyone’s current treatment plan; it’s too early for that. People without liver disease don’t need to take action based on this study.

If LACTB-blocking treatments are developed, it would likely take 5-10 years or more before they become available to patients. This includes laboratory development, animal safety testing, and human clinical trials. In the meantime, proven lifestyle modifications can help manage fatty liver disease and may prevent progression.

Want to Apply This Research?

  • Users with fatty liver disease could track liver health markers: weekly weight, daily exercise minutes, dietary fat intake, and alcohol consumption. They could also monitor energy levels and any symptoms their doctor has identified as related to their liver condition.
  • The app could help users implement the lifestyle changes that currently work best for fatty liver disease: setting daily step goals (aiming for 150 minutes of moderate activity weekly), logging meals to reduce processed foods and added sugars, and tracking alcohol intake. Users could set reminders for regular doctor visits to monitor liver function tests.
  • Long-term tracking should include monthly weight trends, quarterly liver function test results (when available from healthcare providers), and ongoing lifestyle habit adherence. Users should be prompted to discuss any new research developments with their doctor at regular appointments, and the app could send notifications when new treatments become available for discussion.

This research describes early-stage laboratory and animal studies that have not yet been tested in humans. The findings are promising but preliminary and should not be used to make changes to your current treatment plan. If you have fatty liver disease or are concerned about your liver health, consult with your healthcare provider about appropriate management strategies. This article is for informational purposes only and does not constitute medical advice. Do not start, stop, or change any medications or treatments based on this research without discussing it with your doctor first.