“Smokers will soon be able to stub out their habit – without having to worry about piling on the pounds,” reported the Daily Mirror. It said that “scientists have discovered how nicotine suppresses the appetite and could develop drugs to help people quit without putting on weight”.
This research involved a series of complex scientific experiments in mice. The researchers wanted to investigate how nicotine causes the brain to send signals to the body to suppress appetite. They found that nicotine activates a group of nerve cells in an area of the brain called the hypothalamus (the small part of the brain that regulates hormones and automatic processes in the body). These nerve cells activate other receptors in the body that play a role in regulating appetite.
These findings give us a better understand of how nicotine may affect appetite, but it is important to note that this research was in animals. While there may be similar processes in humans and mice, nicotine may not affect human appetite in exactly the same way. Further studies will be needed to understand the effects in humans, and a new treatment to help smokers quit but avoid gaining weight is a long way off.
Where did the story come from?
The scientific research was conducted by researchers at Yale University School of Medicine and other academic institutions in the US. Funding was provided by grants from the National Institutes of Health and other sources. The study was published in the peer-reviewed journal Science .
In general, the news stories accurately represented this research. However, it is too early to say that “the key to helping smokers stay slim” has been found, or that this will pave the way for new drugs to counter the problem of weight gain.
What kind of research was this?
This was laboratory research in mice. Smoking is known to affects appetite, and smoking helps smokers to control their weight while quitting leads to weight gain.
This research aimed to provide a better understanding of the neurological mechanisms by which nicotine suppresses appetite. The researchers hoped that this would help pave the way for new treatments that could help people to quit smoking and avoid weight gain.
What did the research involve?
This complex scientific research involved a combination of molecular, pharmacological, behavioural and genetic experiments on mice.
The researchers used mice which they divided into nine groups. The groups of mice were injected with different doses of either nicotine, inactive saline, or one of three other chemicals that bind to nicotine receptors in the brain These chemicals – hexamethonium, cytosine and mecamylamine – all work in different ways. The researchers looked at the effects of using these chemicals daily on the weight, body fat, water consumption and food intake of the mice.
Some of the mice were genetically engineered to lack certain nicotine receptors in specific brain regions. This enabled the researchers to determine the receptors and nerve cells (neurons) of interest.
What were the basic results?
The researchers found that nicotine and other chemicals that act like nicotine decreased weight gain over time in mice. They found that the mice ate around 50% less food but drank similar amounts of water.
Of particular interest were neurons in the arcuate nucleus, an area of the brain thought to control feeding behaviour. The arcuate nucleus is a part of a larger brain region called the hypothalamus, which is involved in regulating various bodily functions, such as temperature and metabolism. The hypothalamus mainly achieves this through control of the pituitary gland (which controls the release of other hormones in the body) and control of the autonomic nervous system (which controls “automatic” body processes such as heart rate and blood pressure, body temperature, hunger, digestion and sleep).
The researchers used some genetically modified mice which did not have nicotine receptors in the arcuate nucleus (called α3β4 nicotinic acetylcholine receptors). These genetically modified mice no longer showed changes in weight gain when they were given nicotine.
The researchers then focussed on a particular group of neurons in the arcuate nucleus that are known to decrease food intake and increase energy expenditure (called pro-opiomelanocortin neurones or POMC). They found that these neurons contained the α3β4 nicotinic acetylcholine receptors. When normal mice were given nicotine, these neurons were activated, whereas other types of neuron in the arcuate nucleus were not.
The researchers then genetically modified some mice so that they did not have POMC neurons. These genetically modified mice did not decrease their food intake when they were given nicotine.
Finally, the researchers found that the POMC neurons released a chemical called melanocortin. This was demonstrated by using genetically modified mice that lacked the receptor for melanocortin and so could not respond to it. These mice did not reduce their food consumption when given nicotine.
How did the researchers interpret the results?
The researchers say that their study demonstrates that nicotine decreases food intake and body weight by influencing the melanocortin system of the hypothalamus. They say that they have also identified the critical nervous system pathways that are involved in nicotine-induced decreases in appetite.
This scientific research aimed to provide a better understanding of the biological systems in the brain and body that are affected by nicotine and that cause nicotine to suppress appetite. It has demonstrated that certain neurons in the hypothalamus are activated by nicotine. These POMC neurons then activate other receptors in the body that affect appetite.
These findings help us understand how nicotine may have an effect on appetite, but it is important to note that this research was in animals. While similar processes may exist in humans, nicotine may not affect appetite in exactly the same way in humans as in mice. Much more research needs to take place, and any new treatments to help smokers quit but avoid weight gain are a long way off.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
Daily Mirror, 10 June 2011
BBC News, 10 June 2011
Daily Mail, 10 June 2011
Links to the science
Science: 332; 1330-1332