Hypothalamic neurons caused the mice to eat more fatty foods

Neurons of the arcuate nucleus of the hypothalamus that Express the neuropeptide preprivatization affect feeding behavior in high-fat diet. Their activation causes mice to eat more, but no animals of such cells gain less weight when eating fatty foods. Article published in the journal Neuron.

A diet high in fat provokes overeating, disrupts the secretion of hormones of the gut and the sensitivity of the sensory fibers of the vagus nerve. How exactly vysokogirna diet affect the Central regulation of food, clearly not up to the end.

For the analysis of the physiological parameters of blood and setting eating behavior meets the hypothalamus. In particular, neurons of the arcuate nucleus of the hypothalamus (including the cell, which is proopiomelanocortin) perceive the energy balance of the organism through receptors for glucose and hormones. These cells generate signals of hunger or satiety and trigger the appropriate behavior. A diet high in fat breaks sensitivity proopiomelanocortin-expressing neurons.

Scientists from Germany, USA and Switzerland under the leadership of Jens brüning (Jens Bruning) from the Institute for the study of the metabolism of the max Planck Society have discovered a subpopulation of neurons in the arcuate nucleus of the hypothalamus, active in mice that three days eating foods that are high in fat. Analysis of the RNA of these cells showed that they synthesized neuropeptide preprivatization and that they secrete inhibitory neurotransmitter gamma-aminomaslana acid.

Activity preprivatization-expressing (PNOC) neurons were recorded during feeding. Animals that were fed normal or high-fat foods, one fed a double portion and watched how nerve cells adapt to an increased number of calories consumed.

To determine whether PNOC sensitive neurons to glucose concentration in the extracellular space, changing the content of the carbohydrate in the medium with the isolated cells. The activity of neurons was recorded using the method of local fixation potential.

The neurons of mice that three days was eating normal food, after re-feeding was significantly less active (p < 0.01). And in animals on high-fat diet, this adaptation has not occurred. In response to reduced extracellular glucose concentration PNEC the activity of isolated neurons was decreased (p < 0.001). And the nerve cells of animals that have consumed a lot of fat, not adapted to low concentrations of glucose (p < 0.05).

The researchers also assessed the effect of PNOC neurons on feeding behavior of mice. This was observed for transgenic animals without the gene preprivatization, destroyed PNOC neurons in the brains of mice by using proteolytic enzymes or stimulated these cells optogenetics.

Transgenic animals in the first three days of a diet a high-fat diet ate less food than control mice (p <0.001), and in the first week gained less weight (p < 0.05). In the end, after four weeks diet weight fat tissue of mice without the gene preprivatization was less (p < 0.001). Click PNOZ neurons were destroyed, gained less weight after five weeks of high-fat diet (p < 0.01) and on average eating significantly less (p < 0.05). When PNOC neurons stimulated optogenetics, the animals begin to eat more and drink like a normal diet (p < 0.001) and high-fat diet (p < 0.01).

Scientists found that the axons of the neurons PNOC go to proopiomelanocortin-expressing cells of the arcuate nucleus. So, as a result of high-fat diet enhanced deactivation stimulation of these cells. Indeed, in animals without PNOC neuronal activity proopiomelanocortin-expressing cells was higher (p < 0.01).

A high diet can lead to overeating and obesity, but the young mice who eat fatty foods during pregnancy, more quick-witted.

Alice Bahareva

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