Vitamin B against advanced non-alcoholic fatty liver disease? – healing practice

Better understanding of the development of fatty liver disease

Researchers have a new mechanism for the development of advanced forms of the fatty liver disease identified. Fortunately, the process can go through Vitamin B12 and folic acid supplements be reversed.

In a new study involving experts from Peking University were the effects of amino acid homocysteine examined for the progression of non-alcoholic steatohepatitis, metabolism and autophagy. The results are in the “Journal of Hepatology” released.

What is non-alcoholic fatty liver disease?

One non-alcoholic fatty liver disease (NAFL) describes fat deposits in the liver that are not related to alcohol consumption. Worldwide are about 25 percent of all adults are affected, the researchers report.

Non-alcoholic fatty liver disease is one of the leading causes of liver transplants worldwide, the team said. The high prevalence is due to the connection with diabetes and obesity attributed.

When the disease then progresses to inflammation and scarring, it’s called nonalcoholic steatohepatitis (NASH).

Liver dysfunction caused by NASH

“While fat deposition in the liver is reversible in the early stages, progression to NASH leads to liver dysfunction, cirrhosis, and increases the risk of liver cancer‘ explains the author of the study dr Madhulika Tripathi in a press release the Duke-NUS Medical School.

So far, according to the team, there is a lack of understanding of the mechanisms of the disease no pharmacological treatments for NASH. Although it is known that NASH has elevated blood levels of the amino acid homocysteine, its role in the development of the disease has so far remained unclear.

role of homocysteine

However, the researchers have now been able to confirm the link between homocysteine ​​and the progression of NASH in preclinical models and in humans. In addition, the team found that when homocysteine ​​levels in the liver increased, the amino acid turned to different proteins accumulates liver proteinswhose Structure changed and their function impaired.

The researchers report that homocysteine ​​turns when it attaches itself to a protein called Syntaxin 17 attaches, this prevents it from fulfilling its task of transport and digestion of fat in fatty acid metabolism, in mitochondrial turnover and in the prevention of inflammation.

The cellular process of autophagy is disrupted, in which cells remove malformed proteins or damaged organelles, the team explains. This leads to the progression of fatty liver disease to a non-alcoholic steatohepatitis.

Vitamin B12 and folic acid prevent NASH

However, the study also showed that dietary supplementation in the preclinical models with vitamin B12 and folic acid increased levels of syntaxin 17 in the liver and its role in autophagy restored. In addition, the progression of the disease and the Hepatic inflammation and fibrosis decreased.

“Our results are both exciting and important as they suggest that a relatively inexpensive therapy, namely vitamin B12 and folic acid, could be used to prevent and/or delay the progression of NASH‘ reports the author of the study dr Brijesh Singh.

The expert adds that the homocysteine ​​levels in the serum and in the liver are also biomarkers for the severity of NASH be able. Similarly, homocysteine ​​could also affect other liver proteins. The team plans to investigate further in the future which liver proteins it is about.

Therapy of NASH in prospect

Experts are hopeful that this research will lead to the development of Therapies against NASH will lead.

The ability to use vitamin B12 and folic acid as first-line therapies for the prevention and treatment of NASH could result in huge cost savings and reduce the health burden of NASH in both developed and developing countries, adds dr singh. added.

So far, the only way to treat end-stage liver disease is one transplantation. But the study shows that a simple, affordable, and easily accessible intervention can reduce liver damage stop or undo could. (as)