A steamy slab of steak lies on a plate soaked in steak sauce accompanied by garlic-mashed potatoes and cheese-covered broccoli. You reach for your fork and take a bite. Little by little the massive helping of food is soon demolished. Already feeling full and a bit lethargic, you stare at a luscious piece of strawberry cheesecake. You think to yourself, “I don’t need this… I definitely shouldn’t eat it… But wait, it looks so good. I’ll just have a bite.” Before you know it, you’ve eaten the whole thing and moved onto another piece. Feeling bloated and almost sick, you sit back and relax as the lump of food sitting in your stomach begins to travel through your digestive system.
To many, this may seem like an exquisite meal. However, those that eat this excessively on a regular basis, usually combined with other unhealthy choices, commonly experience obesity. Fact is, eating like this has a huge impact on not only the digestive system but adiposity signaling as well. Adiposity signaling is communication between the brain and body fat stores in the body via the bloodstream. The way in which adiposity signaling functions has become an area of scientific interest.
For a molecule to be considered for adiposity signaling it must meet certain conditions. It must be able to secrete into the plasma relative to the fat stores, move from the brain into the bloodstream, show expression in the brain of signaling molecules that are involved with energy homeostasis, and decrease food intake. As of now, only two molecules are known to be directly associated with adiposity signaling, leptin and insulin. The effects of the molecules’ actions on neurons occur in the hypothalamus of the brain. More specifically, the region most concerned with these effects is called the hypothalamic arcuate nucleus. This area contains two neurons, proopiomelanocortin (POMC) and neuropeptide Y (NPY) with agouti related protein (AgRP), that express insulin and leptin receptors. However, POMC and NPY/AgRP have different effects depending on the levels of leptin and insulin. POMC is activated by insulin and leptin and reduces food intake and increases energy usage. NPY/AgRP also reduces food intake but is inhibited by leptin and insulin. In other words, if NPY/AgRP is secreted, food intake is stimulated.
Although the mechanism in which fat stores and the brain are connected is much more complicated than what has been explained, POMC and NPY/AgRP play an integral role. It is their existence that tells the body to eat more food or not. Even though regular exercise combined with a healthy diet should deter obesity, not everyone is able to maintain such a lifestyle. If scientists are able to engineer a drug capable of inhibiting NPY/AgRP and promoting POMC, weight loss could become more efficient.
Brain to Fat Communication
