The study found that the central amygdala inductive amino acid regulates the new mechanism of white fat brownlier

On June 5, the international academic journal Nature Communications published the research paper "Activation of GCN2/ATF4 signals" by the Guo Extraordinary Group of the Shanghai Institute of Nutrition and Health of the Chinese Academy of SciencesThe study found that the lack of leucine can cause the body's white fat to occur brownlionization, and further found that the process is regulated by the central nervous system amygdala PKC-at-tin neurons, such as GCN2/ATF4, by activating the sympathetic nerve to the fat tissue, to promote the occurrence of white fat browningthere are two main types of fats in humans: white fat (WAT) responsible for storing energy and brown fat (BAT) responsible for producing heat consumption, white fat and brown fat that can be converted to each other under certain conditions, i.ethe white-fat browning process and the brown fat whitelise processHowever, the amount of brown fat in the human body is very small, so in recent years, the study of white fat brown liposuction to promote heat production and weight loss has become a hot topicCold stimulation and sympathetic nerve activation are the factors that clearly induce browning in white lipids, and the nutritional regulation and mechanism of the process is very poorly knownAmino acids play an important role in body metabolism, such as leucine in branched chain amino acids, which regulate lipid metabolism, glucose utilization and energy consumptionHowever, whether it can regulate white fat browning is not yet knownhypothalamus neurons of the central nervous system, such as POMC neurons and AgRP neurons, regulate white-lipid brownliation, where the role of other brain regions is rarely reportedThe amygdala is mainly involved in emotional and other regulations, but recent studies have found that the brain region can also participate in metabolic regulation, suggesting that the brain region may have important functions to exploreThe main purpose of the study is to explore whether the central amygdala can sense amino acids and regulate the process of white-fat browningresearchers first found that a lack of leucine diet promoted browning of white fat in miceFurther studies have found that the activity of PKC-stou neurons in the amygdala increases when leucine is lackingThe use of chemicalgenetictechnology to inhibit the activity of PKC-se neurons can prevent the white-fat lactation caused by the lack of leucineBecause the GCN2/ATF4 signal is a key pathway for sensing amino acid deficiency, the researchers found that gcN2/ATF4 signals in the PKC-at-m neurons of the amygdala were activated, and that both GCN2 and ATF4 were able to respond to the brownliation caused by the lack of leucine, respectively, in PKC-Tonic neurons ATF4 as the downstream of GCN2, specific activation can also reverse the role of GCN2 on lactation regulation The central nervous system can transmit signals to the peripheral, the study found that the sympathetic nerve activation of white lipids when leucinin is lacking, the sympathetic nerve of white fat can inhibit the process of lactation after the drug is removed, and in mice that inhibit the activity of PKC-cynta neurons, the injection drug activates the sympathetic nerve pathway to refill the inhibited process of brown lipids , the study found that leucine deficiency can cause the body to produce white-fat brownliation process, which activates neuronal activity through GCN2/ATF4 signals in the central amygdala PKC-at-trium neurons, which in turn activates sympathetic nerves and promotes white fat browning This study is of great significance for understanding the interaction between nutrition, central nervous system and lipid metabolism, and provides more theoretical basis and exploration direction for the study and application of white lipolia brownlier (
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