A study in the mouse model showed that the arrest of insulin action on catecholaminergic neurons that release dopamine causes the onset of obesity.
Jens Bruning of the Max-Planck-Institute led a study on the effects that insulin has on certain brain circuits that regulate the reward. Over the past years have been some studies that monitor the effect of insulin on the hypothalamus, the brain area that monitors a reflection of “stop and go” food behavior.
According to Jens Bruning is however important to note that the super-nutrition depends more on the neuropsychology and to a lesser extent by hunger: in fact, eat according to our mood, continuing to eat even after being fed and according to the company that you see.
For this reason, the research team has chosen to explore the way insulin works and the process of reward. The experiment was conducted on mice and found that inactivation of the insulin signal in those neurons responsible for the release of dopamine, a neurotransmitter involved in reward mechanisms, because murine obesity.
Bruning The researcher explained: “After you have established a positive energy balance and obesity, you can create a vicious circle caused insulin resistance. This seems to be an important factor for the onset of obesity, although is not yet certain that it is the first step towards this condition.
“Our study shows that insulin action on catecholaminergic neurons is critical in long-term control failure. The starting point for potential treatment of obesity in humans is the identification of the precise molecular mechanisms involved in this process,” concluded the researcher.
