Nonalcoholic fatty liver disease (NAFLD) is currently the most common chronic liver condition in the Western world. Clinical, epidemiological, and biochemical data strongly support the concept that NAFLD is the hepatic manifestation of the metabolic syndrome, the constellation of metabolic abnormalities including obesity, diabetes, dyslipidemia, and insulin resistance. NAFLD incorporates a spectrum of disease ranging from simple steatosis in its most benign form to an intermediate lesion, termed nonalcoholic steatohepatitis (NASH), and sometimes cirrhosis. The hallmark of NAFLD is hepatocyte accumulation of triglyceride. The mechanism responsible for an excessive amount of intrahepatic fat remains unclear but must involve an imbalance between the intrahepatic production of triglyceride (primarily derived from plasma fatty acids delivered to the liver that are not oxidized for fuel) and the removal of intrahepatic triglyceride [primarily exported from the liver within very low density lipoprotein (VLDL)]. To clarify the pathogenesis of NAFLD and identify potential therapeutic targets, an increased understanding of the dynamics of triglyceride metabolism in the liver in relation to whole-body metabolic status is warranted. Therefore, this chapter provides an overview of the fundamental principles of lipid metabolism, and its disturbance in insulin resistance relevant to understanding the mechanism of hepatic steatosis and lipotoxicity in NAFLD (Table 5.1).
|Original language||English (US)|
|Title of host publication||Nutrition, Diet Therapy, and the Liver|
|Number of pages||14|
|State||Published - Jan 1 2009|
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