A collection of sticky substance, the neurons in a Appetite control center in the brain href = "https://www.nature.com/articles/d41586-023-00676-z" Data-Track = "Click" Data-Label = "https://www.nature.com/articles/d41586-023-00676-z" Data-track-category text Link "> Diabetes and obesity associated, as a study on mice shows 1 .

This substance also prevents insulin from reaching the neurons in the brain that control the feeling of hunger. The inhibition of the production of this substance led to weight loss in the mice, the experiments found out. These results show that there is a new trigger for metabolic disorders gives what could help scientists to identify target structures for medication for the treatment of these diseases.

These results were published today in the journal Nature

hunger regulator in the brain

metabolic diseases such as Type 2-diabetes and obesity can occur if the cells of the body become insensitive to insulin, a hormone that regulates the blood sugar level. Scientists who are looking for the mechanism that causes this insulin resistance have concentrated on part of the brain, which as Arcuate Nucleus of Hypothalamus is known. This area recognizes the insulin levels and fits in accordance with the energy consumption and The feeling of hunger an.

When the animals developed an insulin resistance, a kind of Cellular scaffolding , called extracellular matrix, which holds the hungerurons in their place, into an unorganized substance. Earlier research had shown that this scaffolding has changed when mice received a high-fat diet 2 .

The researchers wanted to find out whether these changes in the brain may cause insulin resistance instead of just acting at the same time. They feeded a high -fat and sugar diet for 12 weeks and monitor the scaffolding around the hungerurons by removing tissue samples and monitoring gene activity.

They found that this scaffolding became thicker and stickier within a few weeks after the unhealthy diet began. While the animals increased in weight, their hypothalamus neurons were less able to process insulin normally, even if the hormone was injected directly into their brain. This suggests that the stickiness of the scaffold prevents insulin from getting into the brain. Instead, "it gets stuck," says co -author Garron Dodd, a neuroscientist at the University of Melbourne in Australia.

loss of the substance leads to weight loss

In order to undo these changes, the researchers either injected the mice an enzyme that reduces the substance, or a molecule called fluorosamine that inhibits the formation of the scaffolding. Both approaches successfully led to the sticky obstacle in the animals' brain, which increased the insulin intake. Fluorosamine even led to the animals lost weight and increased their energy consumption. Treatment of insulin resistance by the targeted address of the support sciper for the neurons could be safer than to target the neurons, says Dodd.

This "high -quality" study "repeatedly" proves that this cellular scaffolding regulates the hormonal signal transmission, which has a direct impact on the body's metabolism and drives diseases, says Kimberly Alonge, a biochemist at the University of Washington School of Pharmacy in Seattle, which was not involved in the study. It also draws attention to the need not only to look at individual cells and cell types, but also the "packaging material in which the cells are located," she adds.

The experiments of the team also showed that inflammation in hypothalamus drives the disorder of the scaffolding. However, the study does not clarify what the inflammation originally triggers, says Alonge. Earlier research has shown that brain cells that are called GLIA can influence the structural integrity of the creation, and Alonge wants to know whether glia cells contribute to the inflammation in the study.

It is still unclear what role dysfunctional scaffolding plays in the development of metabolic diseases compared to other well -established triggers, says Dodd. He and his colleagues hope to tackle this question later.

Further research is required to examine whether this sticky material is created in people with the development of metabolic diseases. This could be a challenge, says Dodd, since there is no non-invasive access to the hypothalamus that is deep in the brain, and it is difficult to remove tissue samples from donated organs.