Ozempic: Weight Loss Medication Helps Treat Liver Damage Caused By Alcohol

The study showed that GLP-1 receptor agonists, such as semaglutide (Ozempic), reduce alcohol consumption and protect the liver against alcohol-related damage in mice. However, by decreasing the activity of enzymes that metabolize alcohol, blood alcohol levels may become higher than expected. Although the drug shows potential as a treatment for alcoholic liver disease, its effects on alcohol metabolism require further research before clinical use.

In recent years, glucagon-like peptide-1 (GLP-1) receptor agonists, such as semaglutide, have become widely used in the treatment of obesity and diabetes mellitus, mainly because they reduce appetite and help decrease food intake.

Furthermore, these medications are being studied to treat metabolic liver diseases, such as steatohepatitis associated with metabolic dysfunction, a more severe form of fatty liver.

At the same time, excessive alcohol consumption remains a significant public health problem and can cause alcoholic liver disease, characterized by fat accumulation in the liver, inflammation, and fibrosis.

Since these diseases share similar mechanisms and there is already evidence that these medications also reduce the desire to consume alcohol, the hypothesis arose that GLP-1 receptor agonists could be useful in the treatment of alcoholic liver disease.

The aim of the study was to analyze how this medication influences liver health when there is high alcohol consumption. To investigate this question, researchers used mice for a period of sixteen days.

Part of the animals received a liquid diet containing alcohol, while the others received a liquid diet without alcohol. Within these two conditions, half of the animals received the medication by subcutaneous injection and the other half did not. During the first week, the doses were progressively increased until reaching the full level.

On the last day, the animals were examined to assess the amount of fat accumulated in the liver, genes involved in lipid production, inflammation markers, indicators of oxidative stress, and blood alcohol levels, to observe if the medication interfered with alcohol metabolism.

The results showed that the animals treated with the medication ate less and also consumed less alcohol, showing a reduction in body weight. In addition, the livers of the animals that received the agonist showed less fat, less inflammation, and less damage caused by oxidative stress, even when they continued to ingest alcohol.

An unexpected finding was that the drug reduced the activity of the cytochrome P450 2E1 enzyme, responsible for metabolizing alcohol in the liver and producing toxic substances. This reduction occurred in both animals exposed to alcohol and those that did not consume alcohol.

Fugated sections stained with fluorescence in blue showing the cell nucleus and in red the marker for the P450 2E enzyme, responsible for metabolizing alcohol in the liver and producing toxic substances. A decrease in staining occurs in livers that received GLP-1.

As a consequence of this metabolic alteration, blood alcohol levels remained higher after a fixed dose of ethanol, even when the alcohol was administered directly into the bloodstream, without passing through the digestive system.

These results indicate that GLP-1 receptor agonists may have a dual benefit in the context of alcohol-related liver disease: they appear to reduce voluntary alcohol consumption and also exert a direct protective effect on the liver, decreasing fat, inflammation, and oxidative damage.

However, the fact that the drug raises blood alcohol levels by slowing its metabolism requires further investigation and caution before applying this type of treatment in humans.

READ MORE:

GLP-1 receptor agonism results in reduction in hepatic ethanol metabolism. 

Frhaan Zahrawi, Arumugam Suyavaran, Bubu A. Banini, and Wajahat Z. Mehal 

npj Metab Health Dis 3, 36 (2025). 

https://doi.org/10.1038/s44324-025-00077-y

Abstract:

Glucagon-like peptide 1 receptor (GLP-1R) agonists are used along with ethanol consumption, but their interactions are not understood. Our aim was to determine the effects of GLP-1R agonism on the liver in mouse models of high ethanol consumption. We identified that GLP-1R agonism reduced ethanol consumption, mitigated ethanol-induced upregulation of several liver metabolizing enzymes, including Cyp2e1 and also reduced Cyp2e1 independent of ethanol intake. As expected from a reduction in Cyp2e1, GLP-1R agonism resulted in increased blood ethanol levels. This occurred after a single dose of ethanol when given by gavage, and by the intraperitoneal route. This suggests that GLP-1R agonism can reduce ethanol-mediated hepatotoxicity despite continued ethanol consumption and elevate blood alcohol levels.