Fat burning is not active, nerve problem? The leptin finder team Nature has published its latest report.

Losing weight is a topic that modern people are paying more and more attention to.so far, perhaps the most effective way to lose weight is dieting, liposuction, "shut your mouth, open your legs."While dieting and exercise to lose weight seem common sense to the general public, it's interesting to scientists why doing so promotes fat-burning, and the causality behind it remains a mystery, creating difficulties in developing effective weight-loss therapies., however, in a recent paper published in Nature, a team from The Rockefeller University used mouse models to discover the mystery of fat burning.the study suggests that the real igniting of the body's stored fat is a type of nerve embedded in adipose tissue.without the right stimulation, these fat-dominated nerves will shrink collectively; "This finding, if subsequently confirmed in humans, will lead to research into obesity and obesity-related diseases, and may lead to the development of new treatments for nerves in fat," theresearch agency said." led the study by renowned geneticist and leptin gene discoverer Professor Jeffrey Friedman.leptin, as the name suggests, is associated with "thin" and is an important molecule that regulates energy balance and weight.1994, Professor Friedman's team first discovered the hormone, which is secreted mainly by fat cells in white adipose tissue and reports the body's fat content to the brain, causing the nervous system to suppress appetite and increase energy consumption.the team found that if mice were unable to produce leptin on their own, such as the O-gene, which encodes leptin, they would become "lazy" and gain more than three times the weight of normal mice.even more strange, they say that fat people bring their own "heat shield" not afraid of cold, but the Ob gene defecttype mouse than normal mice are afraid of cold.and it's all because of the absence of leptin, which doesn't produce heat by burning fat properly.at this point, as long as a shot of leptin, the mice began to eat less, move more, and more cold.However, the real magic change will not take until two weeks after the continued injection of leptin, the white fat stored in the mice begins to break down normally, and another type of fat tissue, brown fat, returns to fat-burning heat, and the animals begin to lose weight.infusion of leptin can quickly make animals eat less and move more, but its fat-burning weight loss effect is not immediate? This "lag" often discourages people who are just starting to lose weight, but scientists are curious about the reasons behind it.they suspect that the relatively slow response may be related to neurological changes outside the brain. , the team used a newly developed neuronal imaging technique to look at nerves in fat and track their connections to the regions associated with the brain. this led them to discover that leptin injection swells the development of sympathetic nerves in adipose tissue. reason, it turns out that leptin transmits fat content information to the hypothalamus region of the brain, where the neural loop senile sepulrates produce the growth-promoting signal inglision molecule BDNF, which is transmitted back through the spinal cord to the neurons that dominate the fat. has this feedback mechanism, leptin is like a messenger of fat, telling the brain exactly how many nerves it needs to process excess fat. "Usually we know that the structure of the nervous system changes significantly during the development of animals in their early years, but we didn't expect that adult animals would find such intense neuroplasticity, " . ," Professor Friedman stressed. discovery gives scientists a new insight into the development of weight-loss therapies. the past people noticed a strange phenomenon: Since leptin molecules are mainly produced by fat cells, fat people have full fat cells and should produce more leptin, why are they still obese? Moreover, some early clinical trials have shown that some people may have "resistance" to leptin after adding leptin to obese patients. looks, the brain gives up on this persistent overdose of signals, as if to say, "Eat, you're fat!" Now, we might be able to consider new ways to bypass the brain's resistance to leptin. "We observed in this study that leptin-resistant obese mice were similar to animals that lacked leptin, with less nerve power over fat, " . , " says Professor Friedman, "so we speculate that if the nerves that dominate fats can be activated directly, allowing them to regain their ability to burn fat, using stored fat would be a new way to treat obesity." " ()