We eat when we are hungry and stop when we are full without every really giving a second thought to what controls these sensations. In a recent study, researchers from Korea uncovered the mechanism behind the enzyme that controls our appetite, and believe the findings could lead to a more effective way to control weight gain in humans.

The study found that when the body is low on glucose, a state which occurs when blood sugar levels are low, an enzyme known as AMPK is activated. This enzyme then changes the properties of small protein-like molecules, called neuropeptides, that our brain uses to communicate. According to a recent statement on the research, it does so by taking advantage of a natural "self-destruct" mechanism called autophagy, which allows our body to recycle and degrade cellular materials. The team discovered that two main compounds play a role in regulating hunger, and together they help to dictate when we start and stop eating.

The researchers used mice with “knock out” genes to help them better understand how hunger enzymes worked. By preventing AMPK from functioning correctly, they were able to observe how important of a role it played in hunger. For example, mice without a functional AMPK ate considerably less and showed signs of reduced body weight.

Researchers said the finding, though still preliminary, could help them eventually develop new drugs to combat obesity. Currently, there are a handful of medical approaches to weight loss, and many do actually produce real results. For example, one study conducted by researchers from the University of California, San Diego, tested five pharmacological options for managing obesity in the U.S. and found that they all worked more or less to some degree.

Results suggested that Qsymia and Victoza gave patients the highest chance of shedding at least 5 percent of their body weight. Xenical was the least successful. However, according to study lead author Dr. Siddarth Singh, each drug works different for different patients, and obesity treatment should be personalized, not “one size fits all.”

Source: Oh TS, Cho H, Cho JH, Yu SW, Kim EK. Hypothalamic AMPK-induced autophagy increases food intake by regulating NPY and POMC expression. Autophagy. 2016.

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