NEW research in mice has highlighted the role of a small set of brain cells in appetite regulation, which goes toward explaining how specific anti-obesity drugs work.

The cells studied produce small compounds known as POMC (pro-opiomelanocortin peptides), which play a role in regulating food intake and appetite.

The team, based at the University of Aberdeen Rowett Institute, used advanced genetic techniques to switch on and off key functions of the cells, before observing the effect on how much mice ate in controlled experiments.

The scientists found that the new set of POMC-producing cells, located in the brainstem (a part of the brain near the spinal cord), complements the action of similar cells from the hypothalamus, another region at the base of the brain.

Specifically, the brainstem POMC-producing cells have a role in the short-term action of Lorcaserin, a type of anti-obesity medication.

The findings, published in the journal Cell Metabolism, may be useful to develop new drugs or improve existing ones.

Professor Lora Heisler, who led the team, said: “Our discovery opens the door to new medications that could be developed to control appetite and improve health.”

Drugs targeting serotonin where introduced both in America and Europe in the 1980s and 1990s as obesity treatments, but later withdrawn due to their side effects.

Lorcaserin, which stimulates serotonin receptors, is approved by the Federal Drugs Administration in the United States since 2012 but does not have a UK marketing authorisation.

The only anti-obesity medicine tested and recognised to be safe and effective in the UK is orlistat, which has a different mode of action.

Professor Mike Lean, consultant physician and chair of Human Nutrition at the University of Glasgow, said: “We need better understanding about control of appetite and eating, and there is a place for new medications, but no drug trial for obesity or type 2 diabetes should be conducted without providing patients with optimal evidence-based programmes for diet and lifestyle”.