The Brain and Obesity

This week in class we talked about how the brain functions in your body’s search for food, specifically how the brain controls your appetite and how if there is a defect in the system, the body can rapidly put on a lot of weight.  What basically happens in your body is this, insulin and leptin are secreted in proportion to the amount of fat cells in your body.  These two molecules, called adiposity signals, will in normal cases be secreted in larger amounts and cause you to feel less hungry when your fat stores are sufficient, that is that you have adequate access to food, and be secreted in smaller amounts making you feel more hungry when your fat stores are deficient, when you aren’t taking in enough food.  These two molecules do this by acting upon the hypothalamus within your brain, specifically on the region of the hypothalamus called the hypothalamic arcuate nucleus.  This nucleus contains two kinds of receptors for leptin and insulin that have opposite effects on the body.   The proopiomelanocortin(POMC) receptor when activated by insulin and leptin secrete a molecule called alpha-MSH that causes your body to reduce its food intake and increase the amount of energy that it uses.  The neuropeptide Y(NPY) and agouti related protein(AgRP) receptor on the other hand cause your body to increase its food intake and make its uses of energy more efficient.

Here’s where the article turns to obesity.  If there is any sort of malfunction within this system, we see continued food intake even with ample fat stores.  The article says that there are mutations where certain parts of the system were never created by your body, the more common reason why the system ceases to function is that neurons within the hypothalamic arcuate nucleus develop a resistance to leptin and insulin.  This happens because that the receptors activated by leptin and insulin lose their ability to activate a molecule called PI3K.  In insulin signaling PI3K is activated by insulin-receptor-substrate(IRS) proteins.  These proteins are activated when they recieve a phosphate molecule from the insulin receptor itself.  It can be assumed that something similar is happening in leptin signaling.

For our discussion this week we talked exclusively about the relationship between this system and America’s obesity epidemic.  We agreed that it would probably be best that we didn’t focus on a silver bullet solution to this problem, aka some sort of anti-obesity medication.  We said that instead we should really focus on instilling an active lifestyle in people as if you removed the one outward sign of overeating, you would not encourage people to eat anymore healthily.  On a similar note we also agreed that the food industry is somewhat to blame in the obesity epidemic as it is not their responsibility to make people make healthier choices, but to make people buy more of their product.  The use of high fructose corn syrup for one is a huge problem as it is very cheap and has been found to negatively interact with your appetite.  For sure, this is definitely going to be a problem with no easy answer and it is probably going to have to come down to people taking responsibilities for their actions.  I mean, this is probably the first time that average life expectancy for a generation is going to be less than the generation before it, I don’t think that that is a legacy that a generation wants to leave behind.

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