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How Stress Causes Obesity
New research at Georgetown University Medical Center, Washington DC, published in the online edition of Nature Medicine, has found a biological process involving neurotransmitters that may reveal people under chronic stress can add on extra weight based on the calories they consume.
The NYP Molecule
Researchers discovered a molecule the body releases when stressed that appears to unlock certain receptors in fat cells, causing them to grow in both size and number. The molecule in question is called NPY.
The Exact Pathway
One the researchers involved, Herbert Herzog, PhD, of the Garvan Institute of Medical Research in Sydney, Australia commented that, for over a decade, scientists have known of a connection between chronic stress and obesity. “Now we have identified the exact pathway, or chain of molecular events, that links chronic stress with obesity."
Neurotransmitters are biochemicals released by neurons to transmit signals to other neurons. In this study, researchers manipulated a neurotransmitter called neuropeptide Y (NPY) and the receptor, neuropeptide Y2 (YR2) that it activates. These biochemicals function in two types of fat tissue cells – endothelial cells that line blood vessels and regular fat cells.
Finding the Trigger
The scientists discovered that these stress sensors reacted to being threatened by aggression, which leads to nerves of the sympathetic nervous system releasing NPY. This release of NPY is received by it receptor (YR2) which then causes the release of more NPY. This feedback effect is what eventually causes the growth of abdominal fat and apple-shaped obesity (where weight gain is concentrated around the waistline).
The stress of aggression was invoked by putting a mouse into the cage of a larger, dominant mouse. This might be the equivalent to a person having a dispute with their boss, or a confrontation by a fellow worker, or several incidents of road rage. It is also significant to point out that following the aggressive stress, the mouse that gained weight were fed a high-fat diet. This is the equivalent of a stressed-out individual pulling into fast food restaurant and ordering a large cheeseburger and fries.
By injecting a YR2 blocker into the abdominal fat, the scientists were then able to break the feedback cycle and prevent the fat build-up. One of the doctors noted that another by-product of the YR2 blocker injection, was that it reduced fat in the liver and skeletal muscle and helped to control insulin resistance, glucose intolerance and inflammation in the experimental mice. Further studies will be needed to prove it performs the same in humans, thought that is exactly what is expected.
The Physiological Response of Fat Tissue
Aside from the groundbreaking discoveries linking stress and obesity, the research also has revealed that in humans, this type of stress-mediated fat increase may prove to have nothing to do with brain function, but rather prove that this stress reaction is a physiological response of the fat tissue. Most likely a primitive defensive that allows the body to store up a fat reserve in anticipation of using that extra energy in a future fight against the aggressor.
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