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Hungry neurons

Obesity has fast become one of the world's most serious health problems, and a study of the brain's involvement in feeding may help in the quest for effective treatments.

Feelings of hunger and satiety are regulated by cells of the arcuate nucleus in response to hormones such as insulin, ghrelin and leptin. Two types of neuron seem to be involved in this process — pro-opiomelanocortin (POMC) neurons, which reduce appetite, and neurons that release neuropeptide Y and agouti-related protein (NPY/AgRP), which have been thought to have the opposite effect.

Researchers led by Richard Palmiter (Howard Hughes Medical Institute, Maryland, USA) and Serge Luquet (University of Washington, Seattle, USA) questioned whether NPY/AgRP neurons are vital for feeding in mice.

Their results indicated that NPY/AgRP neurons are essential in adult animals, in which elimination of their activity led to starvation. However, ablation of NPY/AgRP neurons in neonates appeared to have no effect.

Palmiter suggests that “Killing these neurons before they're functionally engaged gives the developing mouse brain a way to compensate. But it's still a tall challenge. You're asking some other neuron, presumably, to either increase what it normally does, or to do something that it never did before” (The Guardian, 28 October 2005).

But how do these results relate to humans? “Everybody in the field believes that NPY/AgRP neurons and POMC neurons are undoubtedly doing the same in humans as they do in rodents” says Palmiter, “So I would predict that if you could do the experiment in humans, the results would be the same” (BBC News Online, 28 October 2005).

If this is the case, the next step will be to find a way to modulate the activity of these neurons to reduce obesity.


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Archibald, S. Hungry neurons. Nat Rev Neurosci 6, 916 (2005).

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