Study - - SAMe

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Hepatology. 2007 May;45(5):1306-12.

Role of S-adenosyl-L-methionine

in liver health and injury.

Mato JM, Lu SC.

CIC-Biogune, Center for ative

Research in Biosciences, CIBER-HEPAD, Parque Tecnológico de Bizkaia, Derio, Bizkaia.

S-adenosylmethionine (SAMe) has rapidly moved from

being a methyl donor to a key metabolite that regulates hepatocyte

growth, death, and differentiation. Biosynthesis of

SAMe occurs in all mammalian cells as the first step in methionine

catabolism in a reaction catalyzed by methionine adenosyltransferase (MAT). Decreased

hepatic SAMe biosynthesis is a consequence of all forms of chronic liver injury. In an animal model of chronic liver SAMe deficiency, the

liver is predisposed to further injury and develops spontaneous steatohepatitis and hepatocellular

carcinoma. However, impaired SAMe metabolism, which

occurs in patients with mutations of glycine N-methyltransferase (GNMT), can also lead to liver injury. This suggest that hepatic SAMe level needs to be

maintained within a certain range, and deficiency or excess can both lead to

abnormality. SAMe treatment in experimental animal

models of liver injury shows hepatoprotective

properties. Meta-analyses also show it is

effective in patients with cholestatic liver diseases. Recent data show that exogenous SAMe can

regulate hepatocyte growth and death, independent of

its role as a methyl donor. This raises the question

of its mechanism of action when used pharmacologically. Indeed,

many of its actions can be recapitulated by methylthioadenosine

(MTA), a by-product of SAMe that is not a methyl donor. A

better understanding of why liver injury occurs when SAMe

homeostasis is perturbed and mechanisms of action of pharmacologic doses of

SAMe are essential in defining which patients will benefit from its use.

PMID: 17464973 [PubMed - indexed for

MEDLINE]

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