What really ignites the breakdown of fat molecules nerves embedded in fat, and new research now suggests that these fat burning of neurons previously unrecognized powers. If they get the right signal, they have the amazing ability to grow. This signal is the hormone leptin, which is secreted by fat cells.
In experiments with mice, the results of which are published in the journal Nature, the researchers found that, as a rule, a dense network of nerve fibers in adipose tissue is reduced in the absence of leptin and increases the hormone as a drug. These changes were shown to influence the ability of animals to burn energy stored in fat.
“While the architecture of the nervous system can significantly change how a young animal develops, we did not expect to find in this deep level of neural plasticity in an adult,” says Jeffrey M. Friedman, molecular geneticist of the Rockefeller University.
If confirmed in humans, this information can advance research on obesity and related diseases, and potentially opens the way for the development of new therapies, which target neurons in the adipose tissue.
The team began looking at what happens to mice that do not produce leptin on their own, and how they react when you speak with him.
Found in Friedman’s laboratory in 1994, the hormone relay signals from adipose tissue and the brain, allowing the nervous system to curb appetite and increase energy expenditure to control body weight. When mice are genetically engineered to stop the production of leptin, they grow three times heavier than a normal mouse. They eat more, move less, and can survive in what should be tolerated the cold because their body cannot properly use fat to generate heat.
Giving these mice leptin doses, however, and they quickly begin to eat less and move more. But when the researchers processed them longer, within two weeks, more profound changes have occurred: the animals began to break down white fat, which stores unused calories at a normal level and regained the ability to use another form of fat, brown fat, to produce heat.
It was slower than the changes that interested the research team, including first authors on the nature paper, Putianqi Wang, a graduate student in the lab, and Ken H. Luo, postdoctoral fellow. They suspect that changes of neurons outside of the brain-those that are distributed in fat … might explain why this part of the response to leptin it took some time.
Using the imaging technique, developed in the laboratories of the Rockefeller and Paul Cohen to visualize the nerves inside the body fat, researchers have traced the influence of leptin on fat-built-in neurons of the brain the hypothalamus region. Hence, they are found contributing to the growth of Leptin that message goes through the spinal cord back to the neurons to fat.
“This work is the first example of how leptin can regulate the presence of neurons in adipose tissue, white and brown,” added Cohen.
In this way, fat seems to be telling the brain how much nerve supply it needs to function properly. “Fat is indirectly controlled by its own innervation and hence function,” says Friedman. “It is an exquisite feedback loop”.
Future research will analyze the role of this pathway in human obesity and may provide a new approach to therapy. Most of the obese people produce high levels of leptin and showed a decrease of response to hormone injection, suggesting that their brains are resistant to the hormone. Thus, the bypass resistance leptin may have a therapeutic effect for these patients.
“In the new study, we see that similar to animals lacking leptin, obese leptin-resistant animals also show a low-fat innervation. Therefore, we assume that directly stimulating the nerves that Innervate fat and restoring the normal ability to use stored fat can create new opportunities for the treatment of obesity,” said Friedman.