Nat Metab: Children's youth and Beam Gang/Jiang Qingyan cooperation reveal the central control mechanism of "mouth".

Feeding is the basis for the growth and development of animals in the evolution, and obesity caused by excessive intake of human beings has gradually become one of the major epidemics threatening human health due to the progress of human civilization greater than the rate of natural evolution.
Therefore, how to reduce weight by controlling diet has become a hot topic.
but unfortunately the inability to resist the temptation of food has been a major obstacle to weight loss.
the thalamus arch nucleus as the center of appetite regulation, mainly composed of GABA energy neurons.
is now widely regarded as the gold standard for regulating appetite, acute activation of AgRP neurons can significantly increase short-term intake in animals, and the elimination of AgRP neurons in adult mice leads to significant anorexia and weight loss.
but in recent years studies have found that non-AgRP GABA neurons (Th (Tyrosine Hydroxylase), NOS1 (Nitric Oxide Synthetase 1), PDX1 (Pancreas-Duoden Homeum Homebox 1) also play an important role in appetite and weight regulation.
in addition, the elimination of AgRP neurons at an early age does not affect the growth and development of animals.
therefore, it is not clear whether the increase in appetite caused by the activation of AgRP neurons in the arch nucleus is the main cause of obesity, what role non-AgRP GABA neurons play in it, and what the specific central regulatory mechanism for overcoming strong appetite is.
the U.S. UT Health Science Center at Houston Child Youth Task Force, in collaboration with the South China Agricultural University's Tie Gang/Jiang Qingyan Task Force, published a paper entitled Profound and Operations of The Sauate s of Arcuate Neuron in Obesity Development in nature, revealing the key role of arch-nuclear GABA-energy neurons in the development of animal obesity.
the authors first activated the arch-core AgRP neurons or GABA energy neurons for a long time by specifically expressing the Na-channel NachBac, and found that either the activation of AgRP or GABA neurons could cause appetite and extreme obesity symptoms in mice like leptin deficiency (ob/ob).
further analysis of the number of GABA neurons expressing NaChBac and mouse weight analysis found that the obesity level of mice did not depend on the amount of GABA neuron activation, and random one-sided or two-sided activation of GABA neurons contributed to obesity.
suggestthat the function of the bow-core GABA neurons in obesity regulation is repetitive, so that only some of these neurons are activated enough to cause obesity.
the authors then modeled the specific elimination of AgRP neurons in AgRPDTR mice and found that similar traits were present in normal mice that specifically activated the caparp non-AgRP neurons, or in ob/ob mice that eliminated AgRP neurons.
at the same time, injecting leptin into the brain chambers of normal mice and ob/ob mice that activated the bow-nuclear GABA neurons, respectively, did not reduce the amount of food eaten and weight in the mice;
the above results show that neither the activation of the toxoplasmosis GABA neurons caused by obesity, nor the process of leptin inhibiting obesity is not entirely dependent on the involvement of AgRP neurons.
finally, to further confirm the role of GABA neurons in obesity, the authors expressed the activity of these neurons to The K-channel Kir2.1 in AgRP neurons or GABA neurons for a long time.
found that only long-term two-sided suppression of almost all bow-nuclear GABA neurons in both normal mice and ob/ob obese mice significantly reduced the amount of food and weight in the mice.
but surprisingly, even long-term inhibition of almost all of the AgRP neurons did not affect the amount of food eaten and the weight of the mice.
revealthat bow-core GABA neurons play a key role in suppressing appetite and weight in animals.
the study system expounds the central regulatory mechanism of appetite-induced obesity, and random euphoria of GABA energy neurons in the bow nuclear part of the hypothalamus can cause an increase in appetite, which eventually leads to the occurrence of obesity.
, in contrast, by reducing the amount of food to control the weight, the entire bow nuclear GABA neuronal activity needs to be inhibited.
the "redundancy" of bow-nuclear GABA neurons in inducing obesity and the "necessary" function of weight loss, which explains why weight loss is always a failure because of "mouth", and animals are more likely to develop cravings for food than disgust.
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