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Editor-in-Chief | Xi Chinese wine culture has a long history, and every festive dinner, family and friends gatherings-wine is indispensable.
Everyone knows that drunkenness-related behaviors occur after drinking, but we still don’t know how alcohol causes drunkenness.
In fact, drunkenness-related behaviors after drinking depend on the body's ability to degrade alcohol.
Most experts believe that drunkenness after drinking depends on the metabolic decomposition of alcohol in the liver, because the liver has a large number of alcohol-metabolizing enzymes, especially one called acetaldehyde dehydrogenation.
Enzyme type 2 (aldehyde dehydrogenase 2, ALDH2) is a key enzyme that determines alcohol metabolism and drinking behavior in our body.
Due to the very low content of various alcohol-metabolizing enzymes in the brain, coupled with the lack of precise and specific research tools, the role of the brain in alcohol metabolism has been ignored.
In addition, people lack understanding of the role of acetic acid (commonly known as acetic acid), a lower metabolite of alcohol.
For a long time, acetic acid has been designated as the non-toxic and harmless metabolic end product of alcohol.
On March 22, 2021, Professor Zhang Li's team from the National Institutes of Health Institute of Alcohol Abuse and Alcoholism (NIH/NIAAA) published an article Brain ethanol metabolism by astrocytic ALDH2 drives the behavioural effects of ethanol intoxication in Nature Metabolism ( Astrocyte ALDH2 mediates alcohol metabolism and drunken behavior in the brain).
Nature will also publish a special article introducing this work.
This study reveals for the first time that there is a powerful alcohol metabolism mechanism in the brain and directly regulates alcohol metabolism and the production of acetic acid, and it is acetic acid that mediates the neurotransmitter changes and behavioral effects in the brain caused by alcohol.
In this work, the researchers used highly sensitive RNA in situ hybridization (RNAscope) and other biochemical techniques combined with cell-specific ALDH2 knockout mice to verify that the key enzyme of alcohol metabolism in the central nervous system --- ALDH2 is mainly in It is expressed in astrocytes in the cerebellar cortex, and similar expression characteristics are also observed in other brain regions.
By combining the whole mouse magnetic resonance spectroscopy (MRS) and liquid/gas chromatography-mass spectrometry analysis, it was found that ALDH2 in astrocytes plays a key role in the cerebellar alcohol metabolism, which is responsible for causing the mice to exercise after drinking.
And the main regulatory mechanism of balance dysfunction.
Not only that, even local selective knockout of ALDH2 in cerebellar astrocytes can also play a similar role.
On the contrary, selective knockout of ALDH2 in liver cells did not have much effect on alcohol metabolism and drunken behavior in the brain.
Subsequently, the researchers further studied the cellular and molecular mechanisms of ALDH2 in cerebellar astrocytes that regulate drunken behavior by using single-cell mass spectrometry and neuroelectrophysiological analysis techniques.
It was found that the alcohol metabolite acetic acid promotes the synthesis of the inhibitory neurotransmitter GABA in glial cells, enhances the activity of GABAA receptors in the outer synaptic membrane of small granular neurons in the cerebellar cortex and tonic inhibition.
This brain glial cell ALDH2 mediated alcohol metabolism and signaling system is one of the main mechanisms leading to drunken behavior after drinking.
It is worth mentioning that the researchers also found that although peripheral acetic acid can enter the blood-brain barrier, the efficiency of ingesting astrocytes into GABA is very low, which also explains why it is not easy to get drunk when drinking vinegar.
.
This study revealed for the first time that the central mechanism of alcohol metabolism and its induced motor and balance dysfunction are closely related to the function of ALDH2 astrocytes in the cerebellum.
There are various drunken behaviors, and little is known about their causes in the past.
It can be foreseen that this brain region and cell-specific mode of alcohol metabolism may open up a new direction for the research of specific mechanisms of drunken behavior in the future. This research is particularly important to the Chinese people.
Nearly half of the Han people have ALDH2 gene mutations that will cause the enzyme activity to decrease or even completely lose.
New drugs and treatments that regulate the expression and function of ALDH2 in astrocytes will help in the future "relief" and treat alcohol dependence and alcohol-induced brain damage and degeneration.
It is reported that the first authors of the study are Jin Shiyun, PhD in Anesthesiology from the Second Affiliated Hospital of Anhui Medical University (NIH/NIAAA visiting scholar), Professor Cao Qi from the Department of Radiology and Nuclear Medicine, University of Maryland School of Medicine, and NIH/NIAAA Yang Fanghan (now Peking Union Medical College) Medical school graduate student), this work was also greatly assisted by the team of Professor Xiong Wei from the School of Life Sciences, University of Science and Technology of China.
Original link: https://doi.
org/10.
1038/s42255-021-00357-z Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Reprinting is prohibited without permission.
The author has all legal rights , The offender must be investigated.
Everyone knows that drunkenness-related behaviors occur after drinking, but we still don’t know how alcohol causes drunkenness.
In fact, drunkenness-related behaviors after drinking depend on the body's ability to degrade alcohol.
Most experts believe that drunkenness after drinking depends on the metabolic decomposition of alcohol in the liver, because the liver has a large number of alcohol-metabolizing enzymes, especially one called acetaldehyde dehydrogenation.
Enzyme type 2 (aldehyde dehydrogenase 2, ALDH2) is a key enzyme that determines alcohol metabolism and drinking behavior in our body.
Due to the very low content of various alcohol-metabolizing enzymes in the brain, coupled with the lack of precise and specific research tools, the role of the brain in alcohol metabolism has been ignored.
In addition, people lack understanding of the role of acetic acid (commonly known as acetic acid), a lower metabolite of alcohol.
For a long time, acetic acid has been designated as the non-toxic and harmless metabolic end product of alcohol.
On March 22, 2021, Professor Zhang Li's team from the National Institutes of Health Institute of Alcohol Abuse and Alcoholism (NIH/NIAAA) published an article Brain ethanol metabolism by astrocytic ALDH2 drives the behavioural effects of ethanol intoxication in Nature Metabolism ( Astrocyte ALDH2 mediates alcohol metabolism and drunken behavior in the brain).
Nature will also publish a special article introducing this work.
This study reveals for the first time that there is a powerful alcohol metabolism mechanism in the brain and directly regulates alcohol metabolism and the production of acetic acid, and it is acetic acid that mediates the neurotransmitter changes and behavioral effects in the brain caused by alcohol.
In this work, the researchers used highly sensitive RNA in situ hybridization (RNAscope) and other biochemical techniques combined with cell-specific ALDH2 knockout mice to verify that the key enzyme of alcohol metabolism in the central nervous system --- ALDH2 is mainly in It is expressed in astrocytes in the cerebellar cortex, and similar expression characteristics are also observed in other brain regions.
By combining the whole mouse magnetic resonance spectroscopy (MRS) and liquid/gas chromatography-mass spectrometry analysis, it was found that ALDH2 in astrocytes plays a key role in the cerebellar alcohol metabolism, which is responsible for causing the mice to exercise after drinking.
And the main regulatory mechanism of balance dysfunction.
Not only that, even local selective knockout of ALDH2 in cerebellar astrocytes can also play a similar role.
On the contrary, selective knockout of ALDH2 in liver cells did not have much effect on alcohol metabolism and drunken behavior in the brain.
Subsequently, the researchers further studied the cellular and molecular mechanisms of ALDH2 in cerebellar astrocytes that regulate drunken behavior by using single-cell mass spectrometry and neuroelectrophysiological analysis techniques.
It was found that the alcohol metabolite acetic acid promotes the synthesis of the inhibitory neurotransmitter GABA in glial cells, enhances the activity of GABAA receptors in the outer synaptic membrane of small granular neurons in the cerebellar cortex and tonic inhibition.
This brain glial cell ALDH2 mediated alcohol metabolism and signaling system is one of the main mechanisms leading to drunken behavior after drinking.
It is worth mentioning that the researchers also found that although peripheral acetic acid can enter the blood-brain barrier, the efficiency of ingesting astrocytes into GABA is very low, which also explains why it is not easy to get drunk when drinking vinegar.
.
This study revealed for the first time that the central mechanism of alcohol metabolism and its induced motor and balance dysfunction are closely related to the function of ALDH2 astrocytes in the cerebellum.
There are various drunken behaviors, and little is known about their causes in the past.
It can be foreseen that this brain region and cell-specific mode of alcohol metabolism may open up a new direction for the research of specific mechanisms of drunken behavior in the future. This research is particularly important to the Chinese people.
Nearly half of the Han people have ALDH2 gene mutations that will cause the enzyme activity to decrease or even completely lose.
New drugs and treatments that regulate the expression and function of ALDH2 in astrocytes will help in the future "relief" and treat alcohol dependence and alcohol-induced brain damage and degeneration.
It is reported that the first authors of the study are Jin Shiyun, PhD in Anesthesiology from the Second Affiliated Hospital of Anhui Medical University (NIH/NIAAA visiting scholar), Professor Cao Qi from the Department of Radiology and Nuclear Medicine, University of Maryland School of Medicine, and NIH/NIAAA Yang Fanghan (now Peking Union Medical College) Medical school graduate student), this work was also greatly assisted by the team of Professor Xiong Wei from the School of Life Sciences, University of Science and Technology of China.
Original link: https://doi.
org/10.
1038/s42255-021-00357-z Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Reprinting is prohibited without permission.
The author has all legal rights , The offender must be investigated.
