▎ Edit of Yao Ming Kangdes content team
Needless to doubt that obesity is inseparable from the excessive accumulation of fat, but many people may not think that in a healthy state, fat tissue is originally the main force to help individuals suppress appetite.As a kind of appetite regulating hormones, the stretching of the source of adipose tissue will enter the brain, adjust the food intake process, and maintain the individuals energy balance .This behavior of adipose tissue can help control the overall quality of individual fat and prevent excessive fat storage.
Many obese individuals cannot respond to the signal of "eating enough" by the adipose tissue because they have almost lost their sensitivity to leptin.And fully understanding the neural mechanism related to leptin is expected to bring more obese therapeutic targets in the future.
Picture Source: 123rf
At present, scientists already know that leiny elements have two main onesRegarding the object, one is Previous opioid cytotrophic hormone (POMC) neurons . POMC can activate melanin 4 receptor (MC4R) after hydrolysis, triggering the effects of appetite.A paper in "Cell-Metabolism" in March this year has discovered that as the age increases, the level of MC4R levels of the hypothalamus neurons will decline, which will cause increased appetite and "blessing".
Another object of leptin is Steaming Rat Associated Protein (AGPR)/Nurgeon Y (NPY) Neuron , this type of neurons not only playTo promote appetite effect, it can also inhibit POMC neurons, so leptin can selectively suppress their activity.In the past, POMC neurons and AGPR/NPY neurons were considered a model of "yin and yang" regulation, but recent studies have found that there may be hidden mystery.
According to a new paper based on the "Nature" magazine, when directly stimulating the AGPR neurons, it can indeed quickly promote appetite. HoweverEffect, this shows that there are other regulatory objects in terms of appetite.Scientists from the Institute of Medical Research in Howard found that a neuron that expresses alkaline nucleoprotein 2 (BNC2) can also respond to leptin signals, play a fast appetite inhibitory effect, and can inhibit AGPR/NPY neuron in neurons.Activation , this new discovery also fills a big gap in leptin regulating neural mechanism.
In the study, the author first obtained the mouses hill brain bow nucleus (ARC) sample.The brain area enriched by neurons.Subsequently, they screened the cells through RNA sequencing, mainly to find cells that were positive (LEPR+) of leptin receptor (LEPR+). Some of these cells expressed POMC or AGPR/NPY.
Unexpectedly, although some cells expressed leptin, the above two types of gene expression levels are very low.In a small cluster cell, the author found that they actually had a high -level BNC2, which was never seen before, which also means that they reveal the new subtype of LEPR+cells for the first time .
▲ A new neuron subtype that responds to leptin can help suppress appetite (Image source: Reference Data [1])
Subsequent research focuses on the connection between mice and BNC2 neurons.After fasting the food again, the BNC2 neuron will gradually respond and activate.In addition, injection of leptin directly to mice can also achieve the same effect.According to the tracking results in time, BNC2 activation can quickly suppress appetite. After the BNC2 neurons are activated through optical genetic means for 20 minutes, even mice will respond quickly even after fasting overnight to reduce feeding behavior.
