Insulin is linked to the brain reward circuit and obesity
A team of researchers from the Max Planck Institute for Neurological Research, in Germany, contributes in the latest issue of Cell Metabolism which it is, in his opinion, one of the first solid evidence that insulin has a direct effect on the brain circuits ofreward.
Researchers have worked on a mouse model to determine that animals whose neurological reward mechanisms are not able to respond to insulin tend to eat more and to be more obese.This finding suggests that insulin resistance can explain why obese people find more difficult to reduce their food intake and lose weight.
When a person is obese and enters a positive energy balance, insulin resistance in the brain mechanism linked to reward "can lead to a vicious circle. There is still no evidence that this is the principle of obesity, but canContribute to this and the difficulty of abandoning this state, "says Brüning.Previous investigations had focused on the effect of insulin on the hypothalamus, the brain region that controls food behavior.But the Max Planck Institute team believes that neurophysiology is key in the process.
Dopamine centered
With the aim of better understanding the aspects linked to the reward in relation to food, they have focused their study on the release of dopamine, composed of motivation, punishment and reward mechanisms.
When insulin signaling was deactivated in these neurons, mice grew with more weight and volume due to greater food intake.According to the authors, insulin normally causes neurons to be activated more frequently, an answer that is lost in animals that lack insulin receptors.In addition, the mice showed an altered response to cocaine and glucose when they received a low amount of food, which means "more evidence that reward brain centers depend on insulin to function properly."
Brüning points out that, if research is confirmed in humans, clinical implications would be clear.In conclusion, he emphasizes that his work "reveals a critical role of insulin action in catecholaminérgic neurons in the long -term control of food intake."
