Excess calories disrupts the brain
In experiments on mice, scientists at the University of Wisconsin (Madison) it was found that excess calories disrupts the work of important brain regions. In this case, the reaction of the hypothalamus, which plays a major role in maintaining energy balance, develops even in the absence of an increase in body weight.
The IKKbeta/NF-kappaB molecule, known for its ability to trigger the process of inflammation in other tissues of the body, participates in the brain's response to overeating. The results obtained by the authors indicate that therapeutic approaches that block this mechanism in the brain can help in the fight against obesity and associated diseases, including diabetes and heart disease.
Usually the IKKbeta/NF-kappaB mediated mechanism in the brain is inactive, however, for unknown reasons, this molecule is always present in brain tissues. The authors suggest that this mechanism was once an important element of innate immunity, whose task is to protect the body from pathogens penetrating from the outside.
In modern man, the studied mechanism is activated by another external factor – overeating. Activation of this mechanism leads to the development of a number of disorders, including resistance to insulin and leptin – important metabolic hormones.
Earlier studies have shown that excessive intake of nutrients can trigger inflammatory reactions in peripheral tissues, including muscles and liver, causing the development of metabolic disorders in them, which are prerequisites for the development of metabolic syndrome and type 2 diabetes. As a result, experts came to the conclusion that IKKbeta/NF-kappaB is a target for anti-inflammatory therapy effective in the treatment of obesity-associated diabetes.
However, whether metabolic inflammation and its mediators affect the central nervous system remained unclear. In the latest work, the authors demonstrated that the constant consumption of fat-rich foods doubles the activity of the mechanism of inflammation in the brain of mice. Its activity is also significantly increased in the brains of mice genetically predisposed to obesity.
The authors claim that the increased activity of the IKKbeta/NF-kappaB-mediated mechanism is not associated with obesity as such, since the launch of this inflammatory reaction in brain tissues caused the introduction of glucose or fat directly into the brain of mice.
Further experiments have shown that the activity of IKKbeta/NF-kappaB leads to the development of insulin and leptin resistance. Insulin lowers the level of glucose in the blood by stimulating its absorption by cells. Leptin is a fat tissue hormone that plays an important role in appetite management.
Moreover, the researchers found that drugs that block the activity of IKKbeta/NF-kappaB in the brain of animals prevent the development of obesity in them.
While chronic inflammation is traditionally considered a consequence of obesity, the new results suggest that inflammatory reactions may be the cause of an imbalance leading to the development of obesity and associated diseases, including diabetes. Apparently, inflammation and obesity are very closely intertwined: excess calories by itself stimulates inflammation, while obesity activates neurons that stimulate inflammation through feedback. As a result, a kind of "vicious circle" is formed.
The authors believe that their results will form the basis of new treatment methods aimed at preventing the formation of this vicious circle. If such a therapeutic strategy can be developed, it will provide an approach to the prevention of obesity, the safety of which is due to the fact that under normal conditions the hypothalamus does not need an IKKbeta/NF-kappaB-mediated mechanism.
Portal "Eternal youth" http://vechnayamolodost.ru / based on ScienceDaily – Brain Pathway Responsible For Obesity Found: Too Many Calories Send Brain Off Kilter 07.10.2008