Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease.

By E. Fabbrini, B. S. Mohammed, F. Magkos, K. Korenblat, B. Patterson, S. Klein. Gastroenterology, 2008

627 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/951c261d8f519f8b0b7b78c06507d31926f8f875

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Citations in the corpus

Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “It is well recognized that unbridled adipocyte lipolysis, such as occurs during prolonged fasting, can send more fatty acids to the liver than the liver can handle.(76,77) Older studies demonstrated the adverse impact of prolonged fasting on accelerating liver injury,(78,79) but newer studies have a”
Excessive Hepatic Mitochondrial TCA Cycle and Gluconeogenesis in Humans with Nonalcoholic Fatty Liver Disease (2011, background): “…from increased adipose lipolysis, de novo lipogenesis, and perhaps saturated lipoprotein TG export (Choi and Ginsberg, 2011; Donnelly et al., 2005; Fabbrini et al., 2008), with sparse in vivo data to address the role of mitochondrial metabolism in the pathogenesis or progression of NAFLD.”
Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease. (2019, methodology): “The contribution of palmitate made de novo in adipose tissue that were incorporated into circulating TRL-TG was estimated by: i) directly measuring the contribution of palmitate made by DNL in adipose tissue TGs; and ii) estimating the relative incorporation of the release of these fatty acids into ”
Non-Alcoholic Fatty Liver Disease (NAFLD) and Its Connection with Insulin Resistance, Dyslipidemia, Atherosclerosis and Coronary Heart Disease (2013, neutral): “both hepatic and systemic lipid oxidation [13], and in VLDL-TG secretion [25,26].”
Mechanisms of Hepatic Triglyceride Accumulation in Nonalcoholic Fatty Liver Disease (2013, positive): “This is in line with the observation that plasma non-esterified fatty acid concentrations are elevated in NAFLD subjects, an effect that is attributable to increased fatty acid release from adipose tissue [23, 24].”
Why Does Obesity Cause Diabetes? (2022, background): “Hepatic steatosis is primarily caused by an increased production of triglycerides, not a decrease in either the oxidation of fatty acids or the export of triglycerides through very-low-density-lipoprotein (VLDL) secretion (Fabbrini et al., 2008; Iozzo et al., 2010).”
Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease (2018, background): “While one molecule of apoB100 is associated with each VLDL particle, and is required for VLDL export, the triglyceride content of the VLDL particle can vary considerably [9, 110].”
Increased de novo Lipogenesis is a Distinct Characteristic of Individuals with Nonalcoholic Fatty Liver Disease (2013, neutral): “Research subjects were recruited from local community health fairs and physician referrals to determine the role of metabolic syndrome in the development of NAFLD.1 The initial screening criteria included characteristics of metabolic syndrome,33 and liver enzyme levels were measured to increase the ”
Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Several mechanisms may lead to a fatty liver: (1) increased free fatty acids supply due to increased lipolysis from both visceral/subcutaneous adipose tissue and/or increased intake of dietary fat; (2) decreased free fatty oxidation oxidation; (3) increased de novo hepatic lipogenesis (DNL) and (4) ”
Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications (2017, background): “From fasting studies in patients with NAFLD, excessive uptake of FA in the liver could be attributed to insulin resistance in adipose tissue (Fabbrini et al., 2008).”
Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity (2009, methodology): “Our data suggest that the increase in VLDL-TG secretion rate in obese subjects who have NAFLD is primarily caused by the availability of nonsystemic fatty acids derived from lipolysis of IHTG, not VAT, because VAT volume was the same in both groups and de novo lipogenesis accounts for up to 20% of t”
Long-Term Pioglitazone Treatment for Patients With Nonalcoholic Steatohepatitis and Prediabetes or Type 2 Diabetes Mellitus (2016, neutral): “without T2DM) is relevant because additional metabolic factors, such as hyperglycemia (15, 16), lower adiponectin levels (17, 18), worse dyslipidemia (19, 20), and more severe insulin resistance and hepatic steatosis (10, 16, 18–21), may account for the higher rates of severe liver disease observed ”
Triglyceride metabolism in the liver (2017, neutral): “In this setting, higher rates of TG accumulation fail to increase VLDL-TG proportionately, suggesting a limited capacity for increasing VLDL production and secretion (81).”