Your brain cells might be the culprits behind failed diet resolutions
Neurons responsible for feelings of hunger? Turns out these specialized brain cells release "feed me" signals when they are starved for calories. They will also slow the body’s metabolism, which is why they thwart many a diet attempt. A new study by researchers at the Albert Einstein College of Medicine in the Bronx, New York have pinpointed the biochemical mechanism which overrides our willpower.
The starvation mechanism and feelings of hunger produced by these neurons is signaled through a process called autophagy – a term which means “self-eating” – in which the cell breaks down. It does this to recycle its used parts, but also to harvest energy. Most brain cells keep their autophagy at a steady level and don't respond to starvation. These appetite-sensing neurons, however, are different, the researchers found, and are now the only known brain cells to ramp up autophagy in times of starvation.
The increased breakdown of the neurons increases cellular levels of compounds called free fatty acids. Fatty acids, in turn, are distributed to cells to serve as a fuel for muscular contraction and general metabolism. In other words, the release of fatty acids is a means of harvesting energy. Fatty acids are important sources of fuel because, metabolized, they yield large quantities of ATP. Many cell types can use either glucose or fatty acids for this purpose. In particular, heart and skeletal muscle prefer fatty acids. Brain cells, ironically, cannot use fatty acids as a source of fuel; they rely solely on glucose.
Higher levels of fatty acids circulating in the body signal the special “starvation-sensitive” brain cells to release an appetite-inducing protein called agouti-related peptide (AgRP).
When the researchers created mice whose brain cells couldn't send out the appetite-increasing proteins, these mice were leaner and ate less than normal after being starved. When compared with normal mice, the mutant mice were about 10 percent leaner, were able to burn more energy, were more active and also ate less after food was withheld. Because the AgRP protein is only expressed in appetite-controlling neurons, blocking this process should only affect the appetite signaling, not the cellular breakdown and use of stored energy in other parts of the body.
If the process works in the same way in humans as it does in mice, interrupting this pathway could help curb hunger and obesity. Researchers are continuing to study how disrupting mechanisms in this pathway can changes eating habits.
Research into curbing appetite has tremendous impetus in a world becoming increasingly overweight, and in a country in which two-thirds of the population is overweight or obese.
The study was published Aug. 2 in the journal Cell Metabolism.