The liver is a major component of the body's digestive system and has the ability to break down and detoxify. Although the liver is powerful, its weakness is that it has no painful nerves and once a major disease has occurred, it is difficult to be detected in the early stages and once detected it is often in the late stages of the disease leading to delays.
Liver problems are a quantitative to qualitative process and accumulate over a long time scale to assemble and eventually explode. In the early stages, the liver is only in a sub-healthy state which is the most important window of time to intervene and protect the liver, using animal fatty liver and alcoholic liver as models respectively, scientists have found that NMN can play an effective role in protecting the liver.
NMN may be used to prevent liver cancer
As the global wave of ageing expands, anti-ageing research is gaining more and more attention, and some new insights into the efficacy of NMN in fighting liver cancer have been gained.
New findings from a Tsinghua University team on NMN are out: NMN can protect the liver, prevent liver fibrosis and prevent liver cancer.
The Free Radical Biology and Medicine recently published a new study by Professor Deng Haiteng's team from Tsinghua University, which showed that NMN supplementation can prevent liver fibrosis by regulating prostaglandin E2 (PGE2) and 15-PGDH, controlling the activity of hepatic stellate cell LX-2, and thus reducing the damage caused by bad lifestyle habits and other It also reduces the risk of liver cancer.
The data from this study, according to the researchers, demonstrates the potential of NMN as a novel liver fibrosis prevention strategy. Liver fibrosis is one of the liver's responses to both acute and chronic injury and, if left unprevented, is highly susceptible to serious diseases such as cirrhosis and liver cancer.
NMN is an effective antidote to alcohol and liver problems
The Lancet, the world's leading medical journal, has published a major study showing that long-term alcohol consumption can cause liver damage initially in the form of fatty liver, which can progress to alcoholic hepatitis, liver fibrosis, cirrhosis and liver cancer, and can lead to liver failure in severe alcohol abuse.
French, S.W., Professor of Pathology at the University of California, Los Angeles, gives us an insight into the underlying mechanism of the damage caused by chronic alcohol abuse, which results in a decrease in NAD+ levels when large amounts of alcohol are consumed over a long period of time. When the NAD+ supply is not sufficient, the normal function of the liver and other organs is affected, disrupting the body's circadian rhythm and metabolic levels, which in turn leads to alcoholic fatty liver and other organ and systemic diseases.
According to the chemistry associated with alcohol metabolism, the metabolism of both ethanol and acetaldehyde involves the involvement of the key coenzyme, NAD+, in the body.
There are three main steps in the catabolism of alcohol:
1. the conversion of alcohol (ethanol) to acetaldehyde by the action of ethanol dehydrogenase (ADH) and NAD+;
2. the conversion of acetaldehyde to acetic acid by the action of acetaldehyde dehydrogenase 2 (ALDH2) and NAD+;
3. acetic acid enters the tricarboxylic acid cycle and is converted to carbon dioxide and water.
NMN can rapidly increase NAD+ levels in the liver and accelerate the metabolism of alcohol, thus providing a rapid detoxification effect. In addition, it was found that NMN was able to increase liver NAD+ levels, which is important for the treatment of alcoholic fatty liver by blocking ethanol-induced increases in ALT and AST and altering the expression of 25% of the genes regulated by ethanol metabolism.
The key to liver protection for long-term drinkers is therefore to increase the level of NAD+, an important coenzyme in the metabolism of alcohol. When alcohol is consumed, the presence of sufficient NAD+ in the body can increase the rate of alcohol metabolism several times, reducing the time that alcohol and its metabolites remain in the body and eliminating the harmful effects of alcohol consumption.
NMN can slow down liver aging
The latest research findings published by a Tsinghua University research team in the top journal Cells have unlocked a new function of NMN for delaying liver aging, which is considered good news for people suffering from fatty liver, brain aging, high blood pressure and other physical subhealth.
The article simply states that aging-related protein acetylation in the liver increases dramatically with age, and that NMN stops this increase in just 4 weeks.
What is protein "acetylation"?
This study from Tsinghua University explores the anti-aging effects of NMN from the perspective of protein acetylation.
Acetylation is a post-translational modification of proteins that can affect their catalytic activity, their ability to stabilise. Protein acetylation plays a crucial role in the regulation of the ageing process and age-related diseases.
The main players involved in this regulation are deacetylases (i.e. deacetylases), of which the well-known longevity protein "Sirtuins" is one, and the expression of sirtuins is dependent on NAD+, so supplementation with the NAD+ precursor NMN boosts NAD+ levels and improves age-related physiological decline. Therefore, supplementation with the NAD+ precursor NMN can increase NAD+ levels and improve age-related physiological decline.
NMN supplementation reduces acetylation in the aged liver.
The study compared liver protein acetylation levels in young mice at 8 weeks of age with those in older mice at 96 weeks of age, and controlled observations in older mice after treatment with NMN intraperitoneally. The results revealed that NMN supplementation inhibited the increase in protein acetylation associated with ageing.
1. Protein acetylation was significantly enhanced in older livers compared to younger livers, whereas NMN reduced age-related protein acetylation.
2. NAD (P) transhydrogenase is significantly hyperacetylated at K70 in aged livers and NMN reduces the intensity of acetylation and does not affect protein levels. Acetylation of cytochrome 3a25 (Cyp3a25) was also significantly increased in the ageing liver, and NMN also prevented acetylation of cytochromes.
3. NMN also regulates fatty acid beta-oxidation, the tricarboxylic acid (TCA) cycle and the degradation of valine. As we age, enzymes involved in the tricarboxylic acid cycle are highly acetylated in the ageing liver, whereas NMN supplementation prevents age-related high acetylation.
(Human consumption of food undergoes three stages that provide more than 95% of the body's energy for vital activities: glycolysis, the tricarboxylic acid cycle and fatty acid oxidation.
The tricarboxylic acid cycle is a common metabolic pathway in aerobic organisms and is the final metabolic pathway for the three major nutrients, and the hub for the metabolic linkage of sugars, lipids and amino acids.)
The three points mentioned above are similar and ultimately confirm that ageing increases the level of acetylation and oxidative stress in the body, and that NMN can improve ageing and loss of organs by converting into NAD+ and participating in cellular metabolism in the body, supplying energy to the organism.
Although the present pilot study mainly explores the relationship between NMN and liver health from the perspective of various acetylations in vivo, it makes the pathways of action of NMN more clear and its uses are again expanded. It not only accelerates alcohol metabolism in the liver, but also enhances adaptive endostasis and delays liver ageing. When the liver is healthy, toxins can be excreted from the body more quickly, and the body can be healthier and anti-ageing is more likely.
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