We took great pains to introduce the harm of alcohol to health. In addition to the well-known liver injury caused by drinking, the latest research evidence reveals that alcohol can also destroy stem cells and accelerate the induction of a large number of gene mutations. Even a small amount of drinking will increase the risk of cancer.
▲ There is no such thing as "moderate drinking", and "drinking" will also induce a large number of genetic mutations.
Although people often advise to drink less or not, it is not easy to quit after drinking for a while. A new study recently published in Nature, a top academic magazine, shows a way in which alcohol affects the brain. Scientists have found that alcohol metabolized by the liver can quickly regulate gene expression in the brain and affect learning and memory functions. This is probably the reason behind some people's addiction to alcohol.
The study was led by Dr Shelley Berger, professor of epigenetics at the University of Pennsylvania's perelman School of Medicine.
Scientists tracked the position of alcohol and its decomposition products in mice by isotope labeling experiment and mass spectrometry analysis. They found that after the ingested alcohol is decomposed in the liver, acetate produced by metabolism will enter the brain.
Subsequently, in the center of learning and memory-hippocampus and prefrontal cortex, researchers found that histone acetylation of genes was affected.
What does this mean? In the nucleus, long DNA chains are wound around histones, and together they form dense chromatin. The process of histone acetylation is to attach acetyl group to histone. This process will loosen the chromatin structure at a specific location. Just as you can only see the words in a book when you open it, after the chromatin is untied, the gene can also be "read", thus making the protein encoded by the gene.
Another work previously published by the research team in Nature shows that the process of histone acetylation in neurons is directly affected by a key metabolic enzyme called ACSS2. This enzyme combines with chromatin to convert acetate into acetyl which can be deposited on histone, thus affecting key genes related to memory.
▲ In the nucleus, ACSS2 promotes histone acetylation and regulates gene expression.
"Past work tells us that the metabolic factor ACSS2 is necessary to produce new memories." The first author, Dr. Phillips Morse, said. However, after drinking alcohol, due to the rapid increase of acetate content in blood, acetylation occurred rapidly in nerve cells under the action of ACSS2.
Does this mean that the changes in gene expression caused by alcohol will eventually affect the memory related to drinking? In order to test this conjecture, the researchers designed a set of experiments to detect the behavior of mice.
They put different "drinks" in the living environment of mice, some of which are alcohol and some are physiological saline. After a period of training, when mice can move freely, their preference for different spaces is obvious: they spend more time in "bars". In contrast, mice with artificially reduced levels of ACSS2 protein in their brains have no obvious preference for alcohol and normal saline. In other words, due to the regulation of gene expression by ACSS2, the alcohol-related memory of drinking mice was strengthened.
▲ Alcohol affects spatial preference of mice through ACCS2.
"This result is very important," Dr. Mews explained, because in many people with problems such as alcoholism and alcohol dependence, "the memory of alcohol-related clues is the main driving factor for the recurrence of alcoholism." Some people have obviously given up drinking for a long time, and passing by the bar they used to know will fall short and relapse, which may be the reason.
Therefore, researchers believe that metabolic enzyme ACSS2 may be a promising intervention target for the treatment of alcoholics.
It is worth mentioning that although alcohol is the main source of acetate in this study, the author pointed out at the end of the paper that other acetate sources may also participate in the acetylation of brain histones in a similar way and affect brain function. For example, intestinal microbes are a source-intestinal bacteria. How can it be you?
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