When we don't eat, hunger-inducing neurons in the brain start eating bits of themselves. That act of self-cannibalism turns up a hunger signal to prompt eating, according to Rajat Singh of Albert Einstein College of Medicine.
"A pathway that is really important for every cell to turn over components in a kind of housekeeping process is also required to regulate appetite," said Singh.
The cellular process uncovered in neurons of the brain's hypothalamus is known as autophagy (literally self-eating.)
Singh says the new findings in mice suggest that treatments aimed at blocking autophagy may prove useful as hunger-fighting weapons in the war against obesity.
The new evidence shows that lipids within the so-called agouti-related peptide (AgRP) neurons are mobilized following autophagy, generating free fatty acids. Those fatty acids in turn boost levels of AgRP, itself a hunger signal.
When autophagy is blocked in AgRP neurons, AgRP levels stop rising in response to starvation, the researchers show.
