What’s the News: Trouble sticking to your diet? It may not be entirely your fault. Scientists, reporting in the journal Cell Metabolism, have now learned that when you starve yourself of calories, your brain cells also starve, causing your neurons to begin eating parts of themselves for energy. The self-cannibalism, in turn, cranks up hunger signals. This mouse study may lead to better treatments for human obesity and diabetes.
What’s the Context:
- Autophagy, which literally means “self-eating,” is a common process in the body where cells form internal sacs of digestive enzymes to break down and recycle used parts. Cells will ramp up the process when they are starved of nutrients and need a boost of energy. In 2008, researchers found that a certain protein can induce autophagy in ovarian cancer cells, essentially causing the cancer to cannibalize itself.
- While the self-eating process occurs throughout the body, scientists previously believed that autophagy in brain cells remains relatively constant, even in times of starvation (via LiveScience).
- But there is a part of your brain—the hypothalamus—that monitors the nutritional status of your cells. Previous research has suggested that the levels of small fat molecules, called free fatty acids, in your hypothalamus may play a part in regulating hunger.
How the Heck:
- Scientists at the Albert Einstein College of Medicine decided to investigate agouti-related peptide (AgRP) neurons, a type of hypothalamic neuron involved in food intake and energy balance. The researchers found that when they starved neurons in vitro, autophagy spiked. Researchers then withheld food from mice and saw the same effect in their AgRP neurons. Moreover, as the cells began to munch on stored fat, they released free fatty acids, which in turn boosted the levels of AgRP, triggering hunger.
- The researchers then repeated the experiment in mice lacking the autophagy protein atg7 in their hypothalamus. The mice had lower levels of AgRP and free fatty acids, and higher levels of certain hypothalamic neurons and hormones that suppress hunger and stimulate exercise. The mutant mice ate less after fasting, were able to burn more energy, and were more active, leaving them about 10 percent leaner than the normal mice.
The Future Holds: The researchers think that the work could help humans suffering from obesity and diabetes, if scientists are able to develop treatments that selectively control autophagy in AgRP neurons.
Not So Fast: Not everyone is convinced that the research can be translated into treatments. “Perhaps the biggest [challenge] is that autophagy is a cellular process that happens in dang near every cell,” neuroscientist Randy Seeley told The Scientist. “There is no way to control the process in only AgRP neurons.”
Image courtesy of malias / flickr