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Attenuation of NASH by stimulation of free fatty acid metabolism
Date:10/26/2007

Medically-complicated obesity is a societal problem that needs to be solved. Liver disease, specifically non-alcoholic steatohepatitis or NASH, is just one of the many complications of increased body weight. Treatment options for NASH are limited, and therefore there is an unmet need for pharmacologic treatment of this liver disease. A recent article in World Journal of Gastroenterology by Dr. Baski-Bey et al. offers a helping hand to potentially aid in abolishing the occurrence of NASH in the population. The article describes how administration of a constitutive androstane receptor (CAR) agonist (TCPOBOP) can induce genes involved in fatty acid microsomal omega-oxidation and beta-oxidation pathways, resulting in a reduction in the occurrence of NASH in mice fed the methionine choline deficient (MCD) diet. The MCD diet, when fed to rodents, rapidly produces hepatic steatosis and steatohepatitis by blocking fatty acid oxidation.

Currently, the etiopathogenesis of NASH remains to be defined. In hepatic steatosis, an excess of non-esterified fatty acids are released from peripheral tissues into the serum. These excess serum-free fatty acids are discharged by the liver, where they are esterified and accumulate as neutral fat, secondary to a limited capacity to oxidize excess fatty acids. A potential strategy to protect the liver from hepatic steatosis would involve mechanisms to enhance hepatic fatty acid oxidation. Hepatic fatty acid oxidation occurs by three pathways: beta-oxidation is the predominant pathway; peroxisomal beta-oxidation occurs within peroxisomes and is rate-limited by the peroxisomal L-bifunctional enzyme (L-PBE), acetyl-COA oxidase (ACO) and urate oxidase (UO); the third pathway is omega-oxidation, which occurs in the endoplasmic reticulum. This pathway is dependent upon expression of the cytochrome enzymes CYPA410 and CYP4A14. Stimulation of these pathways either individually or collectively could help remove excess free fatty acid
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Contact: You-De Chang
y.d.chang@wjgnet.com
0086-108-538-1892
World Journal of Gastroenterology
Source:Eurekalert

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