Another cause of obesity

Missing neurons in the brain were the cause of obesity – biologists

RIA NewsThe absence or insufficient number of so-called AgRP neurons in the center of metabolism in the brain of mice causes obesity in cases when their diet is excessively saturated with sugar and other carbohydrates, scientists say in an article published in EMBO Journal (Joly-Amado et al., Hypothalamic AgRP-neurons control peripheral substrate utilization and nutrient partitioning – VM).

"Our work shows that the "backbone" chains of neurons in the brain that control appetite and digestion of food also affect how nutrients are used in other organs of the body. This function of AgRP neurons may turn out to be a key mechanism associated with the development of obesity and concomitant diseases," said Serge Luquet, head of the group of biologists from Diderot University in Paris (France).

The authors of the article studied the work of the so–called arcuate nucleus of the hypothalamus - a special area in the mammalian brain that controls many metabolic processes, digestion and the endocrine system. In this part of the hypothalamus there are many nerve cells that produce and absorb molecules of the AgRP signaling protein. An overabundance of this substance is associated with the development of "wolfish appetite" and obesity, and a lack of it is associated with nutritional problems and stress "jamming".

Lucke and his colleagues suggested that neurons with AgRP receptors may have other functions besides appetite control. They tested this hypothesis by growing a population of mice whose genome lacked a gene responsible for the production of receptors that read AgRP molecules.

It turned out that mice with damaged neurons quickly gained excess weight when eating a carbohydrate diet. This effect persisted even in cases when the number of calories in the diet of rodents did not exceed the values corresponding to a balanced diet. In the blood of such rodents, there was an increased level of insulin and a relatively normal concentration of glucose – in other words, the body of mice absorbed and processed more glucose than is required for normal functioning.

On the other hand, fatty foods did not have such a negative impact – the wards of Luke and his colleagues did not gain excess weight with the usual amount of calories in a diet of fatty foods. Moreover, rodents fed on high–calorie fatty foods gained weight more slowly than mice on a carbohydrate diet, and their blood contained a relatively low proportion of glucose.

Biologists believe that their research can help nutritionists and other scientists understand how the brain controls metabolism and develop appropriate measures to treat metabolic disorders.

Portal "Eternal youth" http://vechnayamolodost.ru20.09.2012