Obesity and the pathogenesis of nonalcoholic fatty liver disease
Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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Obesity and the pathogenesis of nonalcoholic fatty liver disease. / Fabbrini, Elisa; Magkos, Faidon.
Treatment of the Obese Patient. 2. ed. New York : Springer New York, 2014. p. 121-135.Research output: Chapter in Book/Report/Conference proceeding › Book chapter › Research › peer-review
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TY - CHAP
T1 - Obesity and the pathogenesis of nonalcoholic fatty liver disease
AU - Fabbrini, Elisa
AU - Magkos, Faidon
N1 - Publisher Copyright: © 2014 Springer Science+Business Media New York. All rights are reserved.
PY - 2014
Y1 - 2014
N2 - Obesity is associated with increased deposition of fat in the liver (nonalcoholic fatty liver disease; NAFLD), which develops when hepatic fatty acid availability from plasma and de novo synthesis exceeds hepatic fatty acid disposal by oxidation and triglyceride export. Therefore, an increase in intrahepatic triglyceride content (steatosis) results from an imbalance between interacting metabolic events. Hepatic steatosis is associated with an array of adverse changes in glucose, fatty acid and lipoprotein metabolism, not only locally (in the liver) but also at the whole body level. These metabolic abnormalities are likely responsible for many cardiometabolic risk factors associated with NAFLD, such as insulin resistance and dyslipidemia. However, whether NAFLD is the cause of metabolic dysfunction or whether metabolic dysfunction is responsible for excessive intrahepatic triglyceride accumulation remains unclear at this time. Understanding the factors involved in the pathogenesis and pathophysiology of NAFLD will lead to a better understanding of the mechanisms responsible for the metabolic complications of obesity.
AB - Obesity is associated with increased deposition of fat in the liver (nonalcoholic fatty liver disease; NAFLD), which develops when hepatic fatty acid availability from plasma and de novo synthesis exceeds hepatic fatty acid disposal by oxidation and triglyceride export. Therefore, an increase in intrahepatic triglyceride content (steatosis) results from an imbalance between interacting metabolic events. Hepatic steatosis is associated with an array of adverse changes in glucose, fatty acid and lipoprotein metabolism, not only locally (in the liver) but also at the whole body level. These metabolic abnormalities are likely responsible for many cardiometabolic risk factors associated with NAFLD, such as insulin resistance and dyslipidemia. However, whether NAFLD is the cause of metabolic dysfunction or whether metabolic dysfunction is responsible for excessive intrahepatic triglyceride accumulation remains unclear at this time. Understanding the factors involved in the pathogenesis and pathophysiology of NAFLD will lead to a better understanding of the mechanisms responsible for the metabolic complications of obesity.
U2 - 10.1007/978-1-4939-1203-2_9
DO - 10.1007/978-1-4939-1203-2_9
M3 - Book chapter
AN - SCOPUS:84929907713
SN - 9781493912025
SP - 121
EP - 135
BT - Treatment of the Obese Patient
PB - Springer New York
CY - New York
ER -
ID: 302382089