Hormone removes the pleasure of smoking

October 19, 2013 - 05:00

A peptide prevents the brain of a smoker from registering satisfaction from a cigarette.

“Can’t get no satisfaction?” (Photo: Colourbox)

The hormone GLP-1 is released when we eat and makes us feel full or sated toward the end of the meal.

 GLP-1 receptors are also activated in parts of the brain that are linked to satisfaction or a sense of reward. This indicates the hormone is directly involved in our experience of gratification.

Scientists reason that by blocking these receptors they can prevent smokers from feeling satisfied after a cigarette.

“Without this kind of reward, a smoker will not keep smoking. It can reduce addiction and the risk of a relapse,” says Elisabet Jerlhag, a researcher at the Sahlgrenska Academy of the University of Gothenburg.

Jerlhag and colleagues have investigated this new potential weapon in the battle against smoking.

Smokers require treatment

The ranks of daily, habitual smokers are on the decline but tobacco smoke remains a substantial public health challenge. One in four Norwegians smoke on occasion and the numbers of such “party smokers” are fairly stable. 

Even those who are not heavy, daily smokers can find it hard to stub their cigs for good.

“Nicotine is remarkably habit-forming, and many people find it terribly hard to quit smoking. We need to start accepting dependency as a disorder that requires treatment,” says Jerlhag.

Tested on nicotine mice

To test whether GLP-1 regulates gratification, the researchers experimented with another chemical substance, Exendin-4 (Ex4), which imitates GLP-1’s effect on receptors. The substance was administered to a group of lab mice who had been given doses of nicotine.

The researchers then observed the mice’s movement patterns as well as the dopamine releases in their brains.

They found that nicotine made the mice more active, but the addition of Ex4 reduced that activity. However, mice that had not been given nicotine to start with did not experience the mitigating effect of Ex4. Nicotine increased the release of dopamine in their brains, but this was reduced when Ex4 had been given earlier.

The researchers concluded that GLP-1 receptors regulated the effect of nicotine on the reward functions in the brains of mice, and that Ex4 diminished the effect of nicotine.

Same effect on alcohol, amphetamines and cocaine

The researchers point out that other experiments have shown the same mitigating effect of Ex4 with other habit-forming substances such as alcohol, amphetamines and cocaine.

“Because Ex4 also reduced the motivation for consuming sucrose, this could indicate that GLP-1 receptors play a key role in the gratification created by addictive substances and the rewards of natural activities,” they add.

The researchers believe that substances that mimic the GLP-1 hormone should be considered for new prospective treatment regimens to help battle smoking and nicotine addiction.

Developing new medications

This method, which prevents smoking from soothing the nicotine cravings, is different from existing methods for treating habitual tobacco use, such as nicotine patches, or drugs such as bupropion or varenicline.

The hope is that the findings can lead to the development of new medications that mimic GLP-1. These kind of drugs have already been approved for diabetes, so that it should be relatively easy to get the green light to use them to help smokers kick their habit.

“Rewards are a prime reason why we become addicts. So we think medications that work in the same way as GLP-1 can have a positive impact on nicotine dependency. This is a whole new approach,”  Jerlhag says.

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Read the Norwegian version of this article at forskning.no

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Translated by
Glenn Ostling

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