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New Study - SAMe

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Published Online:

26 Apr 2007

Role of S-adenosyl-L-methionine

in liver health and injury

José M. Mato, C. Lu

CIC-Biogune, Center for

ative Research in Biosciences, CIBER-HEPAD, Parque

Tecnológico de Bizkaia, Derio, Bizkaia

USC Research Center for Liver Diseases, USC-UCLA

Research Center for Alcoholic Liver and Pancreatic Diseases, Keck School of

Medicine USC, Los Angeles, CA

Funded by:

NIH; Grant Number: DK51719, AA12677, AA013847, AT1576

USC-UCLA Research

Center for Alcoholic Liver and

Pancreatic Diseases; Grant Number: P50 AA11999

USC Research

Center for Liver Diseases; Grant

Number: P30 DK48522

Plan Nacional of I+D SAF2005-00855

HEPADIP-EULSHM-CT-205

ISCiii CIBER-HEPAD

ETORTEK 2005

Abstract

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. (HEPATOLOGY 2007;45:1306-1312.)

Barb in Texas - Together in the Fight, Whatever it Takes!

Son Ken (33) UC 91 - PSC 99 Listed 7/21 @ Baylor Dallas

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