TY - CHAP
T1 - Monounsaturated Fat Enriched with Olive Oil in Non-alcoholic Fatty Liver Disease
AU - Assy, Nimmer
AU - Nassar, Faris
AU - Grosovski, Maria
PY - 2010
Y1 - 2010
N2 - The pathogenesis of non-alcoholic fatty liver disease (NAFLD) includes insulin resistance, lipotoxicity, increased exposure of hepatocytes to TNFα, and increased oxidative stress. Etiologic mechanism of NAFLD includes increased influx of free fatty acids to the liver from dietary triglycerides and from free fatty acids that are released from adipocytes during fasting, reduced free fatty acid β-oxidation, reduced hepatic secretion of triglycerides-rich lipoprotein, and increased lipid per oxidation. An impaired postprandial triglyceride response has been recently reported in patients with NASH (non-alcoholic steatohepatitis) and may play a role by favoring triglyceride accumulation in the liver. Diet and nutrition, in particular the amount and type of fat intake, were recently linked to insulin resistance, increased risk of developing type 2 diabetes, and impaired postprandial lipid metabolism. Moreover, animal and human models suggest that dietary factors can affect fatty infiltration and lipid peroxidation in different types of liver disease including NAFLD. Although few studies of the effects of different diets on NAFLD have been performed in humans, the Mediterranean diet has been proposed for the prevention of metabolic syndrome, hypertension, and cardiovascular disease. The major part of its beneficial effect is a high supply of energy coming from monounsaturated fatty acids (MUFA), mainly from olive oil. This chapter describes dietary sources of MUFA, dietary habits and their relation to insulin resistance and postprandial glucose and triglyceride levels in NASH, the mechanism by which olive oil ameliorates fatty liver, experimental and clinical studies of olive oil and NAFLD, and future perspectives. © 2010
AB - The pathogenesis of non-alcoholic fatty liver disease (NAFLD) includes insulin resistance, lipotoxicity, increased exposure of hepatocytes to TNFα, and increased oxidative stress. Etiologic mechanism of NAFLD includes increased influx of free fatty acids to the liver from dietary triglycerides and from free fatty acids that are released from adipocytes during fasting, reduced free fatty acid β-oxidation, reduced hepatic secretion of triglycerides-rich lipoprotein, and increased lipid per oxidation. An impaired postprandial triglyceride response has been recently reported in patients with NASH (non-alcoholic steatohepatitis) and may play a role by favoring triglyceride accumulation in the liver. Diet and nutrition, in particular the amount and type of fat intake, were recently linked to insulin resistance, increased risk of developing type 2 diabetes, and impaired postprandial lipid metabolism. Moreover, animal and human models suggest that dietary factors can affect fatty infiltration and lipid peroxidation in different types of liver disease including NAFLD. Although few studies of the effects of different diets on NAFLD have been performed in humans, the Mediterranean diet has been proposed for the prevention of metabolic syndrome, hypertension, and cardiovascular disease. The major part of its beneficial effect is a high supply of energy coming from monounsaturated fatty acids (MUFA), mainly from olive oil. This chapter describes dietary sources of MUFA, dietary habits and their relation to insulin resistance and postprandial glucose and triglyceride levels in NASH, the mechanism by which olive oil ameliorates fatty liver, experimental and clinical studies of olive oil and NAFLD, and future perspectives. © 2010
UR - http://www.scopus.com/inward/record.url?scp=84882810129&partnerID=8YFLogxK
U2 - 10.1016/b978-0-12-374420-3.00126-1
DO - 10.1016/b978-0-12-374420-3.00126-1
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AN - SCOPUS:84882810129
SN - 9780123744203
SP - 1151
EP - 1156
BT - Olives and Olive Oil in Health and Disease Prevention
PB - Elsevier Inc.
ER -