If your a filthy fagger, you’ve no doubt said to yourself ‘fluff it — quitting puts on 2 dress sizes!’ Just for a change, your right.
Researchers have discovered that nicotine decreases the want of food via the activation of Pro-opiomelanocortin – POMC – neurons. (Mutations in the POMC gene have been associated with early onset obesity, adrenal insufficiency, and red hair-pigmentation)
Importantly, the researchers have shown that nicotine causes a dip in appetite via a different pathway to the one that it triggers addiction through.
This means that it’s possible to make a drug that isn’t addictive, but still has nicotine’s goodly appetite-suppressing powers. We don’t usually cut and paste posts, we have to make an exception here, the abstract for this study is overtly clever.
ABSTRACT: Smoking decreases appetite, and smokers often report that they smoke to control their weight. Understanding the neurobiological mechanisms underlying the anorexic effects of smoking would facilitate the development of novel treatments to help with smoking cessation and to prevent or treat obesity. By using a combination of pharmacological, molecular genetic, electrophysiological, and feeding studies, we found that activation of hypothalamic α3β4 nicotinic acetylcholine receptors leads to activation of pro-opiomelanocortin (POMC) neurons. POMC neurons and subsequent activation of melanocortin 4 receptors were critical for nicotinic-induced decreases in food intake in mice. This study demonstrates that nicotine decreases food intake and body weight by influencing the hypothalamic melanocortin system and identifies critical molecular and synaptic mechanisms involved in nicotine-induced decreases in appetite.
The research, led by Professor Marina Picciotto of Yale University, may eventually lead to drugs that help smokers to give up without putting on weight and could help combat obesity in non-smokers too. Picciotto says nicotine seems to lower their ‘set weight’, and once they give up the weight returns to normal. Scientists have long known that nicotine is an appetite suppressant, but just how it kept hunger at bay remained unclear.
“On average smokers are 2.5 kilograms lighter than non-smokers,” says Picciotto.
In the study, researchers gave nicotine to mice daily for 30 days and found that the mice reduced their food intake by nearly 50 per cent and lost 15 to 20 per cent of their body fat.
The activation of receptors by nicotine modifies the state of neurons through two main mechanisms. On one hand, the movement of cations (+) causes a depolarization – a change in a cell’s membrane potential, making it more positive (+) or less negative (-) of the plasma membrane, which results in an excitatory postsynaptic potential in neurons, but also by the activation of voltage-gated ion channels. On the other hand, the entry of calcium acts, either directly or indirectly, on different intracellular cascades leading, for example, to the regulation of the activity of some genes or the release of neurotransmitters.
Picciotto and her team discovered that a rare receptor – beta 4 (α3β4) receptor – was involved, significantly, they found beta 4 receptors were present on nerve cells in particular parts of a brain – the hypothalamus – known to be linked with feeding behavior. Picciotto says these receptors actually aren’t intended for nicotine, but for acetyl choline, a natural neurotransmitter involved in a host of processes including muscle activation The researchers believe this will open up the possibility of designing drugs to produce appetite suppression, without the addictive side-effects of nicotine.
- The researchers first observed that mice given nicotine via the drug cytisine /sophorine, which binds to α3β4 nicotinic receptors in the brain, ate less and had less body fat than mice not given either drug. When the researchers gave mice a chemical compound that blocked nicotine receptors, the appetite-suppressing effects of these drugs went away.
- Since cytisine binds particularly well to a type of nicotinic receptor called α3β4, the researchers figured that receptor might be the major player in decreasing appetite. Sure enough, when the researchers genetically knocked out that receptor in some mice, those mice were immune to the drugs’ appetite-reducing effects.
- The researchers then looked at what parts of the brain had α3β4 receptors, since different nicotinic receptors are present in different groups of neurons. These particular receptors show up in POMC cells, they found. This makes sense, given POMC cells are clustered in the hypothalamus—an area of the brain that plays a role in controlling lots of basic functions, including appetite.
- Since smoking tamps down appetite, many smokers gain weight when they stop—a common reason people hesitate to quit.
- Importantly, these results show that nicotine causes a dip in appetite by a different pathwaythan it triggers addiction. This means that it’s possible to make a drug that isn’t addictive, but still has nicotine’s appetite-suppressing powers.
- Drugs that work on this POMC pathway could help smokers keep the weight off when they give up cigarettes, encouraging them to quit, and also be used to help non-smokers struggling with their weight.
reference: Yann S. Mineur et al.
'Nicotine Decreases Food Intake Through Activation of POMC Neurons'
Science, June 10, 2011. DOI:10.1126/science.1201889