How neurons reshape inside body fat to boost its calorie-burning
capacity

Date:
July 22, 2020
Source:
Rockefeller University
Summary:
Scientists have found that a hormone tells the brain to dramatically
restructure neurons embedded in fat tissue. Their work widens our
understanding of how the body regulates its energy consumption,
and how obesity might be treated in the future.



FULL STORY ========================================================================== There's no doubt that you can lose fat by eating less or moving more --
yet after decades of research, the biology underlying this equation
remains mysterious. What really ignites the breakdown of stored fat
molecules are nerves embedded in the fat tissue, and a new study now
reveals that these fat- burning neurons have previously unrecognized
powers. If they receive the right signal, they have an astonishing
capacity to grow.


==========================================================================
That signal is the hormone leptin, which is released by the fat cells themselves. In experiments with mice described on July 22 in the journal Nature, the researchers found that the normally bushy network of neural
fibers within fat tissue shrinks in the absence of leptin and grows
back when the hormone is given as a drug. These changes were shown to
influence the animals' ability to burn the energy stored in fat.

"While the architecture of the nervous system can change significantly
as a young animal develops, we did not expect to find this profound
level of neural plasticity in an adult," says . Jeffrey M. Friedman,
a molecular geneticist at The Rockefeller University.

If confirmed in humans, the findings could advance research on obesity
and related diseases, and potentially open the door to developing new treatments that target neurons in fat.

Homing in on neurons in fat The team began by looking at what happens
to mice who do not produce leptin on their own, and how they respond
when treated with it.



========================================================================== Discovered in Friedman's lab in 1994, the hormone relays signals between
fat deposits and the brain, allowing the nervous system to curb appetite
and boost energy expenditure to regulate body weight. When mice are
genetically engineered to stop producing leptin, they grow three times
heavier than normal mice. They eat more, move less, and cannot survive in
what should be tolerable cold because their body can't properly utilize
fat to generate heat.

Give these mice a dose of leptin, however, and they quickly begin to
eat less and move more. But when the researchers treated them longer,
for two weeks, more profound changes occurred: the animals started to
break down white fat, which stores unused calories, at normal levels,
and regained the ability to use another form of fat tissue, brown fat,
to generate heat.

It was this slower change that interested the research team, including
the first authors of the Nature paper, Putianqi Wang, a graduate student
in the lab, and Ken H. Loh, a postdoctoral fellow. They suspected that
changes in neurons outside the brain -- those that extend into fat --
might explain why this part of the response to leptin took some time.

To the brain and back Using an imaging technique developed by the lab of Rockefeller's Paul Cohen to visualize nerves inside fat, the researchers
traced leptin's effects on the fat-embedded neurons up to the brain's hypothalamus region. From here, they found, leptin's growth-promoting
message travels via the spinal cord back to the neurons in fat. "This
work provides the first example of how leptin can regulate the presence
of neurons in fat, both white and brown," adds Cohen.

Through this pathway, fat appears to be telling the brain how much
innervation it needs to function properly. "Fat is indirectly controlling
its own innervation and thus function," Friedman says. "It is an exquisite feedback loop." Future research will analyze the role of this pathway
in human obesity and possibly provide a novel approach for therapy. Most
obese people produce high levels of leptin, and show a diminished response
to hormone injections, suggesting that their brain is resistant to the
hormone. Thus, bypassing leptin resistance could have a therapeutic
benefit for these patients. "In the new study we see that similar
to animals lacking leptin, obese, leptin-resistant animals also show
reduced fat innervation," Friedman says. "So we speculate that directly activating the nerves that innervate fat and restoring a normal ability to
use stored fat could provide a possible new avenue for treating obesity.


========================================================================== Story Source: Materials provided by Rockefeller_University. Note:
Content may be edited for style and length.


========================================================================== Journal Reference:
1. Putianqi Wang, Ken H. Loh, Michelle Wu, Donald A. Morgan, Marc
Schneeberger, Xiaofei Yu, Jingyi Chi, Christin Kosse, Damian Kim,
Kamal Rahmouni, Paul Cohen, Jeffrey Friedman. A leptin-BDNF pathway
regulating sympathetic innervation of adipose tissue. Nature,
2020; DOI: 10.1038/ s41586-020-2527-y ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2020/07/200722112650.htm

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