There is no magical food that can cause weight gain. In any study, those who burn fewer calories than they burn lose weight, while those who burn more gain more. Energy balances like evolution and Einstein have survived all challengers.
Yet, the biology underlying the breakdown of stored fat molecules is not well known. New paper Claims that nerves embedded in adipose tissue have previously unrecognized functions. They have an amazing ability to grow if they receive the right signal. At least in the mouse.
Don’t get excited about this being instantly claimed in supplement bottles and diet books. It does happen, but science doesn’t work that way. Mice are not small people, so these studies should always fall into the “exploratory” category, even if someone claims to sell something.
White fat neurons that store calories grew after treatment with leptin.
Credit: Rockefeller University Institute of Molecular Genetics
The signal is the hormone leptin released by the fat cells themselves. A hormone discovered in 1994 relays signals between fat deposits and the brain, allowing the nervous system to suppress appetite, increase energy expenditure, and regulate weight. Most obese people produce high levels of leptin and show a reduced response to hormone injections, suggesting that their brain is resistant to hormones. Therefore, avoiding leptin resistance may have therapeutic benefits in these patients.
In experiments with mice, researchers found that a network of normally bushy nerve fibers in adipose tissue contracted in the absence of leptin and returned when the hormone was given as a drug. These changes have been shown to affect an animal’s ability to burn energy stored in fat. If confirmed in humans, this finding could advance research on obesity and related disorders, perhaps by spurring research into new therapies that target neurons in fat.
When mice are genetically engineered to stop producing leptin, they grow three times larger than normal mice. They eat more, have less movement, and the body’s inability to properly utilize fat to generate heat prevents it from surviving in an acceptable cold. However, when these mice are given a dose of leptin, they immediately eat less and move more.
But when researchers worked with them for more than two weeks, deeper changes occurred: animals began to break down white fat, which stores unused calories at normal levels, and another form of adipose tissue. Has regained the ability to use brown fat, which produces heat.
These slow changes were of interest to researchers suspected of neuronal changes outside the brain (up to fat), explaining why this part of the response to leptin was time-consuming. It may be.
The researchers used imaging techniques to visualize nerves in fat and tracked the effects of leptin on the brain’s hypothalamus in neurons embedded in fat. From here, they found that the leptin growth-promoting message travels back through the spinal cord to fat neurons. “This study provides the first example of how leptin regulates the presence of neurons in both white and brown fat,” Cohen adds.
Through this pathway, fat seems to convey the amount of innervation needed for the brain to function properly. “Fat works because it indirectly controls its innervation.” To tell Co-author Jeffrey M. Friedman, A molecular geneticist at Rockefeller University. “It’s an exquisite feedback loop.”
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