A brain structure that seems to influence food consumption could one day be targeted to enhance interventions for weight loss or gain.

Studies have shown that activating neurons in this structure, called the bed nucleus of the stria terminalis (BNST) – located around the centre of the brain and about in people – . But it was unknown whether taste influences its activity.

To learn more about its function, at Columbia University in New York and his colleagues first imaged the brains of mice while they drank water flavoured with one of the five basic tastes – sweet, bitter, sour, salty and umami. The researchers previously linked in a region called the amygdala, and have now pinpointed neurons there that only became activated in response to sweet water.

These neurons then activated others in the BNST, “extended amygdala”. This is the first evidence that this structure receives taste signals, says at the University of Arizona, who wasn’t involved in the study.

The researchers then wanted to understand whether these activated BNST neurons influence dietary consumption, so they genetically engineered the cells so that they didn’t activate when mice tasted sweet water. Over 10 minutes, these mice drank substantially less than normal ones, suggesting that activation of BNST neurons enhances consumption of sweet tastes.

But the researchers also found that this artificial activation prompted mice to consume more water of any taste, including whether it was unflavoured, salty or bitter, despite them usually avoiding the latter taste.

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In further experiments, the team found that substantially more BNST neurons were activated by sweet and salty signals in hungry or salt-depleted mice, respectively, compared with those that were fed until they were full or had normal salt levels. This suggests that the BNST integrates signals for hunger and nutrient depletion, in addition to taste, to determine food intake, says Cai.

The findings are highly relevant to people, as our BNST is very similar to that of mice, says Cai. They suggest that developing drugs that activate BNST neurons could potentially help to encourage eating in people with a severe loss of appetite, such as those undergoing cancer treatment, he says.

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However, more than a dozen brain pathways have been linked to food intake, says Cai, and some of these may compensate for any prolonged drug-related changes in BNST activity, so targeting multiple feeding circuits simultaneously will probably be needed, he says.

The study could also help us achieve better results with weight-loss treatments, such as the GLP-1 drug semaglutide. These , so a better understanding of how it alters food consumption could help us gain a clearer picture of how such drugs work and how to make them more effective in people , says at the Max Planck Florida Institute for Neuroscience.

Semaglutide really does seem to help people who are addicted to alcohol reduce their intake, according to the first randomised clinical trial of the drug for this purpose.

Sold under brand names including Wegovy and Ozempic, semaglutide works by mimicking a gut hormone called glucagon-like peptide-1 (GLP-1), hence the technical term for it is a GLP-1 receptor agonist. The drug was first used to treat type 2 diabetes, but because it reduces appetite, Wegovy has now also been licensed for weight loss . Semaglutide has also shown hints of helping an extraordinary number of medical conditions.

When it comes to alcohol use, a 2024 study of 84,000 people linked injecting Ozempic or Wegovy with a lower risk of alcoholism. Promising as that result was, it showed correlation rather than causation.

But now, at the University of Southern California and his colleagues have completed the first randomised clinical trial of semaglutide’s effect on alcohol use disorder, a type of study that can tease out causation.

Their trial involved 48 people in the US who had been diagnosed with the condition, of whom 34 were women and 14 were men. Half received weekly low-dose injections of semaglutide for nine weeks and the rest had placebo injections.

Those on semaglutide consumed fewer drinks per drinking session and had reduced weekly alcohol cravings compared with those on placebo.

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“We didn’t have any evidence of significant adverse effects or safety concerns with the medication in this population and we found overall that across several different drinking outcomes it reduced the quantity of alcohol that people consumed,” says Hendershot.

“The results are promising,” says at Case Western Reserve University School of Medicine in Ohio. “Despite the small sample size, this randomised clinical trial highlights the therapeutic potential of semaglutide in treating alcohol use disorder.”

at Washington University in St Louis, Missouri, says the study adds “yet another piece of evidence that GLP-1RAs [GLP-1 receptor agonists] may be helpful in addiction disorders”.

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Larger studies are needed to corroborate the work, he says, and to answer questions about whether people increase their drinking if they come off semaglutide and what its longer-term effects might be, especially given concerns around loss of .

The study should be treated as promising initial evidence, says Hendershot, but more research is needed. People shouldn’t start taking semaglutide for alcohol problems, he says.

“This is the first study like this and people are excited about it, but we do have approved and effective medication for alcohol use disorder, so until more research has been done, people are advised to pursue existing medications that are out there and approved right now,” says Hendershot.