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This is a sensory neuron, shown here in fluorescence, that starts near the spine and spreads through the abdominal fat tissue.
[Imagem: Scripps Research]
For years, scientists believed that hormones passively floating around in the blood were the way a person’s fat – called adipose tissue – used to send information related to stress and metabolism to the brain.
In recent years, however, the existence of a complex brain-gut communication network has become clear, which has led scientists to begin mapping the neurons of this “abdominal brain”, more recently called the enteric nervous system. This has increased interest in seeking out other nervous system connections.
Now researchers have discovered sensory neurons that carry a flow of messages specifically from adipose tissue to the brain.
“The discovery of these neurons suggests for the first time that your brain is actively searching for your fat, rather than just passively receiving messages about it. The implications of this discovery are profound,” said Li Ye of Scripps Research Institute (USA).
Adipose tissue neurons
In mammals, adipose tissue stores energy in the form of fat cells, and when the body needs energy, it releases these reserves. Adipose tissue also controls a number of hormones and signaling molecules related to hunger and metabolism. In diseases such as diabetes, fatty liver disease, atherosclerosis and obesity, this energy storage and signaling often presents problems.
Scientists have long known that nerves extend to fat tissue, but they thought that the nerves in fat belonged primarily to the sympathetic nervous system—the network responsible for our fight-or-flight response, which activates fat-burning pathways during periods of stress and physical activity. But the methods used to study neurons closest to the surface of the body or the brain do not work well in adipose tissue, where nerves are difficult to see or stimulate, leaving the matter unclear.
Ye and his colleagues have now developed two new methods that allowed them to overcome these research difficulties. First, they created an imaging technique, called HYBRiD, that made the mice’s tissues transparent, allowing them to better follow the paths of neurons as they meander through adipose tissue. To further investigate the role of these neurons in adipose tissue, the group developed a second technique, which they called ROOT, which stands for “retrograde vector optimized for organ tracking”, which selectively destroys small subsets of sensory neurons in adipose tissue using a virus, allowing you to observe what happens.
The researchers found that nearly half of the neurons in the adipose tissue do not connect to the sympathetic nervous system, but rather to the dorsal root ganglia, an area of the brain where all sensory neurons originate.
Sympathetic neurons accelerate, sensory neurons brake
The experiments revealed that when the brain does not receive sensory messages from adipose tissue, programs driven by the sympathetic nervous system – related to the conversion of white fat to brown fat – become overly active in the fat cells, resulting in larger-than-normal fat. , with especially high levels of brown fat, which breaks down other fat and sugar molecules to produce heat. In fact, animals with blocked sensory neurons – and high levels of sympathetic signaling – showed an increase in body temperature.
The findings indicate that sensory neurons and sympathetic neurons may have two opposing roles, with sympathetic neurons needed to activate fat burning and brown fat production, and sensory neurons needed to deactivate these programs.
“This tells us that there is not just a one-size-fits-all instruction that the brain sends to adipose tissue,” said Li. “It’s more subtle than that; these two types of neurons are acting like an accelerator pedal and a brake to burn fat.”
Article: The role of somatosensory innervation of adipose tissue
Authors: Yu Wang, Verina H. Leung, Yunxiao Zhang, Victoria S. Nudell, Meaghan Loud, M. Rocio Servin-Vences, Dong Yang, Kristina Wang, Maria Dolores Moya-Garzon, Veronica L. Li, Jonathan Z. Long, Ardem Patapoutian, Li Ye
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