Abstract
The liver is an essential organ for body energy homeostasis, controlling the biosynthesis, uptake and the disposal of carbohydrates and lipids. The hepatic steatosis is a common condition frequently associated with metabolic diseases and is characterized by the excessive accumulation of triglycerides in the liver. In recent years, many efforts have been devoted to prevent and treat the hepatic steatosis, but it remains being pointed out as the major cause for chronic hepatic diseases in Western countries. A considerable part of the knowledge about the physiopathology of hepatic steatosis, the effects of diets and drugs on the metabolic capacity of the liver to metabolize fatty acids, as well as the potential therapeutic approaches for hepatic steatosis derived from experimental animal models using rodents. Here, in this article, we present the details of some of the most common techniques used to evaluate fatty acid metabolism in liver of rats, including quantification of total lipid content, measurement of fatty acid oxidation in isolated subcellular fractions and procedures to measure the activities of important lipogenic enzymes. Classical protocols previously described to be performed using samples from other tissues were adapted to liver samples and different techniques with equivalent aims were compared. The principles and the advantages in terms of reliability and costs were discussed and the procedures here described can be applied for a low-cost broad evaluation of the fatty acid metabolism in liver of rats submitted to different experimental conditions.
Highlights
The liver plays fundamental roles on body energy metabolism, controlling the biosynthesis, uptake and disposal of lipid and glucose (Zakim, 1990)
Excessive fatty acids (FA) overload leads to excessive esterification and accumulation as triglycerides (TG) in the cytosol of hepatocytes, a condition defined as hepatic steatosis (HS)
We reviewed techniques of measurement of the activities of the two most important enzymes involved in liver lipogenesis, namely, Fatty Acid Synthase (FAS) and Glucose-6Phosphate Dehydrogenase (G6PD), in the supernatants of crude liver homogenates
Summary
The liver plays fundamental roles on body energy metabolism, controlling the biosynthesis, uptake and disposal of lipid and glucose (Zakim, 1990). The oxidative damage associated with the accumulation of TG in the liver leads to cell death and inflammation, which in turn contribute to the progression of HS to more severe forms of liver diseases (Charlton et al, 2001). The late diagnosis of HS is associated with a worse prognosis and HS is the most frequent cause of chronic liver diseases in Western countries (Rector, Thyfault, Wei, & Ibdah, 2008). For these reasons, many efforts have been diverted to the investigation of mechanisms involved in the pathogenesis of HS and the search for new therapeutic targets. Several drugs which induce hepatotoxicity by impairing the FA oxidation can cause HS (Berson et al, 1998; Kennedy, Unger, & Horowitz, 1996; Natarajan, Eapen, Pullimood, & Balasubramanian, 2006; Ulrich et al, 1998)
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