2 Cannabis Compounds May Be the Secret to Help Millions With Fatty Liver Disease, Scientists Say

Researchers studying liver disease typically focus on diet, exercise, or drug compounds modeled on hormones and enzymes. A March 2026 study took a different direction: it looked at two compounds from cannabis – ones that don’t cause any kind of high – and found they produced improvements in fatty liver disease in obese mice during preclinical testing. The cellular pathways those compounds activated had never been connected to CBD or CBG before.

The disease they were targeting, known as MASLD (metabolic dysfunction-associated steatotic liver disease), is currently the most widespread chronic liver condition in the world, affecting roughly one-third of adults and strongly associated with obesity, high blood pressure, and insulin resistance. Doctors typically recommend lifestyle changes such as improved diet and increased physical activity to manage the disease, but maintaining these habits long-term can be challenging, and there are very few approved medications available.

CBD and CBG, in this mouse study, appear to reduce liver fat through cellular mechanisms that operate largely outside the pathways most cannabinoid research has examined. The study didn’t confirm a treatment, and it wasn’t conducted in humans. The preclinical pathways it uncovered are specific and plausible, and they change how scientists are thinking about what cannabis compounds can actually do inside the liver.

How CBD and CBG Tackle Cannabis Fatty Liver Disease

The research was led by Prof. Joseph (Yossi) Tam, Dr. Liad Hinden, and PhD student Radka Kočvarová at the School of Pharmacy at the Faculty of Medicine of the Hebrew University of Jerusalem. Published in the British Journal of Pharmacology, the study suggests that CBD and CBG, which are non-psychoactive and do not cause a high, can improve liver health by changing how the organ manages energy and cleans itself.

Most studies on cannabinoids and the liver focus on two receptors called CB1 and CB2, which are part of the body’s endocannabinoid system – an internal signaling network that regulates metabolism, inflammation, and appetite. This March 2026 study found something different. CBD and CBG alleviate hepatic steatosis in obese mice by shifting energy buffering toward phosphocreatine and enhancing lysosomal lipid degradation and trafficking. These findings reveal that the two phytocannabinoids promote a metabolic shift in liver cells toward phosphocreatine utilization as an alternative energy source, and enhance lysosomal function under obesogenic conditions – positioning them as promising candidates for the treatment of MASLD via previously unrecognized pathways.

That means researchers are no longer limited to thinking about cannabis compounds purely through the lens of the endocannabinoid system – a meaningful shift in the pharmacology of CBD and CBG.

A Cellular Backup Battery for the Liver

One of the two main mechanisms identified in the preclinical study involves energy storage at the cellular level. In this study, researchers assessed the metabolomic and lipidomic impact of CBD and CBG in a mouse model of diet-induced obesity and MASLD. Male mice fed a high-fat diet for 14 weeks were treated for 4 weeks with daily intraperitoneal CBD, CBG, or vehicle. Both compounds enhanced the production of phosphocreatine, a form of stored energy that helps liver cells replenish their fuel supply under stress.

Phosphocreatine works like a cellular backup battery. When a cell runs low on ATP (adenosine triphosphate – the molecule that powers virtually every biological process), phosphocreatine donates its stored energy to rapidly regenerate it. In a liver under chronic stress from excess fat, this kind of energy reserve can make the difference between a cell that functions and one that deteriorates.

CBD and CBG alleviate hepatic steatosis in obese mice by shifting energy buffering toward phosphocreatine and enhancing lysosomal lipid degradation and trafficking. These effects are associated with increased creatine kinase activity and lysobisphosphatidic acid (LBPA) levels, highlighting a previously unrecognized hepatoprotective mechanism of phytocannabinoids under lipotoxic conditions. In plain terms: the cannabinoids appear to rewire how liver cells store and spend energy, giving stressed liver tissue more resilience under preclinical conditions.

Restoring the Liver’s Cellular Cleanup Crews

The second mechanism involves a part of the cell most people have never heard of: the lysosome. Lysosomes are tiny compartments inside cells that act as recycling centers – they break down and dispose of damaged proteins, worn-out organelles, and toxic material. When lysosomes stop working properly, waste accumulates inside the cell. In the liver, that accumulation accelerates fat buildup and cellular damage.

CBD or CBG treatment improved glycemic control, reduced hepatic triglycerides, and normalized serum lipids, without affecting energy expenditure. That last point matters because it suggests the liver improvements weren’t simply a result of the animals burning more calories. The effect was targeted.

The researchers also found that CBD and CBG restored the activity of “cellular cleaning crews” known as cathepsins – enzymes that work within the cell’s recycling centers to break down harmful fats and waste. With this process, the liver was better able to clear out dangerous lipids, including triglycerides and ceramides, which are known to trigger inflammation. Cathepsin activity tends to decline in fatty liver disease; CBD and CBG appear to switch it back on, at least in the preclinical mouse model.

Both compounds produced improvements in the mouse study, but they weren’t equal. CBG significantly reduced body fat mass and improved insulin sensitivity more robustly than CBD. It was also particularly effective at lowering total cholesterol and LDL cholesterol levels.

CBG, which is sometimes called the “parent” or “mother” of cannabinoids because it’s the chemical precursor from which THC and CBD are both derived, is far less studied than CBD – and far less commercially available. For a compound that’s barely on most consumers’ radar, these preclinical findings represent a meaningful expansion of what researchers now know about its metabolic potential.

The practical gap between a mouse study and a human treatment is wide. The researchers did not establish what dose would translate to humans, how it would be delivered, or what safety profile might emerge at therapeutic doses. No clinician currently recommends cannabis or cannabis-derived compounds as a treatment for fatty liver disease on the basis of this study.

The Treatment Gap for MASLD

Doctors managing MASLD have very few pharmaceutical tools. Lifestyle changes – better diet, more exercise – remain the primary recommendation, but they’re hard to sustain long-term. The one notable recent exception is resmetirom, a thyroid hormone receptor-beta agonist. Resmetirom, sold under the brand name Rezdiffra, received FDA approval on March 14, 2024. It is the first medication approved for treating metabolic dysfunction-associated steatohepatitis (MASH) – a more advanced stage of MASLD characterized by liver inflammation and scarring known as fibrosis.

Its approval applies specifically to MASH, not to MASLD broadly. Researchers estimate that at least 25 million people in the United States could benefit from this drug, but only a small percentage of those have been identified in the clinic. For the millions with earlier-stage fatty liver disease, there remains no approved drug at all.

A patent application related to the therapeutic effects of phytocannabinoids in metabolic disorders has been submitted by Yissum, the Technology Transfer Company of the Hebrew University of Jerusalem, with Prof. Joseph Tam listed as an inventor. The application covering the use of CBD and CBG for metabolic conditions has been filed and licensed through Yissum to Carmen’s Biopharma, a U.S.-based biotechnology firm working to advance the research toward clinical use. Human trials to establish dosing, safety, bioavailability (how much of the compound reaches the liver and in what form), and long-term outcomes have not yet begun.

Read More: The Link Between Vitamin D Deficiency and Fatty Liver

What This Means for You

MASLD is the most common chronic liver disorder in the world, affecting approximately one-third of the adult population and closely linked to obesity, high blood pressure, and insulin resistance. If you or someone close to you has been diagnosed with it, or lives with type 2 diabetes, obesity, or metabolic syndrome – conditions that substantially raise the risk – the direction of this research is relevant to watch.

For now, neither CBD products from a health food store nor cannabis in any form constitutes a medical treatment for fatty liver disease. The 2026 Hebrew University study was conducted in obese mice over four weeks, and the researchers themselves have not proposed a human dosing protocol. No health authority has approved cannabis-derived compounds for MASLD. The compounds used in the study were pharmaceutical-grade isolates, not the variable formulations found in retail CBD products.

Scientists now have a more specific cellular target – energy buffering via phosphocreatine and lysosomal restoration – and two plant-derived molecules that interact with those targets in measurable ways in preclinical testing. If human trials confirm even a portion of what the mouse data showed, it would represent the first plant-based pharmacological pathway for a disease that currently has almost no drug options for its earlier stages. Talk to your doctor if you have concerns about liver health, and watch for phase 1 human trial announcements from the Hebrew University team in the coming years.

Disclaimer: This information is not intended to be a substitute for professional medical advice, diagnosis, or treatment and is for information only. Always seek the advice of your physician or another qualified health provider with any questions about your medical condition and/or current medication. Do not disregard professional medical advice or delay seeking advice or treatment because of something you have read here.

AI Disclaimer: This article was created with the assistance of AI tools and reviewed by a human editor.