Want to eat more after eating? This is a "contribution" to weight loss failure

China Science and Technology News Network, December 6 (Qin Chuan) Many people think that being "fat" is just being a little rounder, but in fact obesity is indeed a disease, not a single disease, but a clinical syndrome. When the body consumes more calories than it consumes, the excess calories are stored in the body in the form of fat, and the amount exceeds the normal physiological needs. When it reaches a certain value, it evolves into obesity.

Generally speaking, if obesity is not treated in time, it often causes a series of complications and health problems. Clinically, the most common ones are metabolic syndrome, respiratory diseases, osteoarthritis, cardiovascular and cerebrovascular diseases, etc. Most of the causes of obesity are "eating without moving" or even overeating. What are the factors that affect this?

Some specific nerve nuclei in the hypothalamus and limbic system of humans and many animals control feeding behavior. Some nerves in the hypothalamus are related to satiety. When they are excited, they cause anorexia and refuse to eat, and when they are inhibited, the appetite increases greatly. They are called satiety centers. Some nerves in the hypothalamus are related to hunger. When they are excited, the appetite is strong, and when they are inhibited, the appetite is anorexia and refuse to eat. They are called feeding centers. In addition, the amygdala in the limbic system is also involved in the regulation of feeding behavior.

Studies have shown that the amygdala is highly related to driving overeating. Recently, a related study by Professor Li Bo's team at the Cold Spring Harbor Laboratory in the United States revealed that IPAC-Nts neurons in the amygdala are key nodes in promoting eating after being full and energy metabolism, which is expected to provide new therapeutic strategies for the prevention and treatment of obesity.

Through a large number of experiments, the researchers provided new insights into the amygdala IPAC-Nts neurons that drive hedonic eating, revealing the neural circuit in which IPAC-Nts neurons receive sensory stimulation signals and project to the LHA, thereby inducing eating behavior. This study provides important clues to the regulatory mechanism of overeating and is expected to provide new scientific basis for the prevention and treatment of obesity.