Obesity and Nonalcoholic Fatty Liver Disease: Biochemical, Metabolic and Clinical Implications

By E. Fabbrini, Shelby Sullivan, S. Klein. Hepatology, 2010

2,062 citations recorded by the source corpus.

Obesity is associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). Steatosis, the hallmark feature of NAFLD, occurs when the rate of hepatic fatty acid uptake from plasma and de novo fatty acid synthesis is greater than the rate of fatty acid oxidation and export (as triglyceride within very low‐density lipoprotein). Therefore, an excessive amount of intrahepatic triglyceride (IHTG) represents an imbalance between complex interactions of metabolic events. The presence of steatosis is associated with a constellation of adverse alterations in glucose, fatty acid, and lipoprotein metabolism. It is likely that abnormalities in fatty acid metabolism, in conjunction with adipose tissue, hepatic, and systemic inflammation, are key factors involved in the development of insulin resistance, dyslipidemia, and other cardiometabolic risk factors associated with NAFLD. However, it is not clear whether NAFLD causes metabolic dysfunction or whether metabolic dysfunction is responsible for IHTG accumulation, or possibly both. Understanding the precise factors involved in the pathogenesis and pathophysiology of NAFLD will provide important insights into the mechanisms responsible for the cardiometabolic complications of obesity. (HEPATOLOGY 2009.)

Subfields: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism, Epidemiology

View Paper: https://www.semanticscholar.org/paper/a3e72ae2c6b5d38153efa3e8aec357c86d22cdf7

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Citations in the corpus

Non Alcoholic Fatty Liver Disease, Hepatic Insulin Resistance and Type 2 Diabetes (2014, background): “The most common cause of NAFLD in developed countries can most likely be attributed to increased caloric intake exceeding rates of caloric expenditure.(3,9,39) This relationship between the nutritional state and NAFLD is reflected by the high prevalence of NAFLD and IR among obese individuals.”
Multi-dimensional roles of ketone bodies in fuel metabolism, signaling, and therapeutics (2017, background): “These changes partly reflect the alterations encountered in NAFLD, in which the liver exhibits increased esterification to and lipolysis from lipid droplets, increased b-oxidation of fatty acids, increased terminal oxidation, and increased gluconeogenesis but diminished ketogenesis relative to the a”
Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, methodology): “Fatty acids used for IHTG production are derived from: i) fatty acids released into the systemic and portal circulations by lipolysis of TGs in subcutaneous and intra-abdominal adipose tissues, ii) fatty acids released into the systemic circulation by postprandial lipolysis of TGs in chylomicrons, i”
Triglyceride metabolism in the liver (2017, neutral): “In nondiabetic obese NAFLD subjects, VLDL-TG secretion rates are elevated up to two times in comparison to normal subjects (82).”
Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “9, the prevalence rates were 65% and 20%, respectively, and in extremely obese subjects with BMI ‡40, the rates were 85% and 40%, respectively.(175) Racial/ethnic background and genetic variation in specific genes can influence the relationship between BMI and NAFLD.”
Mechanisms of Hepatic Triglyceride Accumulation in Nonalcoholic Fatty Liver Disease (2013, neutral): “NAFLD is strongly associated with obesity, and increased fat mass contributes directly to greater fatty acid release from adipose tissue [25].”
Economic Burden of Obesity: A Systematic Literature Review (2017, background): “[31], included obesity-related liver diseases, such as non-alcoholic fatty liver disease (NAFLD), liver fibrosis and cirrhosis of the liver, which are also associated with obesity [75,76].”