SAMe API

SAMe, as a methyl donor (transmethylation) and a precursor of physiological sulfur compounds (such as cysteine, taurine, glutathione and coenzyme A, etc.) biochemical reactions. In the liver, the fluidity of the liver cell membrane is regulated by methylating the plasma membrane phospholipids, and the synthesis of sulfurized products in the detoxification process can be promoted through the transsulfuration reaction.

The synthesis of hepatic adenosylmethionine (SAMe) is significantly decreased in liver damage such as cirrhosis, which is due to the significant decrease (about 50%) of the activity of adenosylmethionine synthase (catalyzing the conversion of the essential amino acid methionine to adenosylmethionine). This metabolic disorder reduces the conversion of methionine to adenosylmethionine, thereby impairing the normal physiological processes that prevent cholestasis. As a result, the plasma clearance of methionine in the diet of patients with hepatic impairment is reduced, and the availability of its metabolites, especially cysteine, glutathione and taurine, is reduced. Moreover, this metabolic disorder also causes hypermethioninemia, which increases the risk of hepatic encephalopathy.

Supplementation of SAMe can eliminate the metabolic block caused by the decreased activity of adenosylmethionine synthase and restore the physiological mechanism of bile excretion. In fact, various experimental models have demonstrated that the anti-cholestasis activity of SAMe should be attributed to: 1) Restoration of cell membrane fluidity through the SAMe-dependent synthesis of membrane phospholipids (lowering the ratio of cholesterol to phospholipids); 2) Participation in endogenous Sulfur-containing compounds in the detoxification process. Studies have shown that the accumulation of methionine in the body can lead to an increase in the blood concentration of its degradation products (such as mercaptans, methyl mercaptans), and these degradation products play an important role in the pathogenesis of hepatic encephalopathy. Since adenosylmethionine can increase the synthesis of sulfhydryl compounds without increasing the concentration of methionine in the blood circulation, the supplementation of adenosylmethionine in patients with liver damage can restore endogenous levels of an essential compound whose bioavailability is reduced in liver disease.

In addition, the study also found that SAMe can regulate the production of IL-10 in monocytes, increase the synthesis of IL-6 in monocytes and liver Kupffer cells stimulated by lipopolysaccharides (LPS), and its metabolite 5- Methylthio adenosine also has an important immunomodulatory effect on the inflammatory response of liver cells. Multi-faceted synergistic effects jointly prevent liver cell damage and necrosis. Studies have confirmed that SAMe can effectively treat intrahepatic cholestasis in precirrhosis. It also has a good therapeutic effect on acute and chronic hepatitis.

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