title: Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver disease.
abstract: OBJECTIVE
  Steatosis in patients with nonalcoholic fatty liver disease (NAFLD) is due to an imbalance between intrahepatic triglyceride (IHTG) production and export. The purpose of this study was to evaluate TG metabolism in adipose tissue and liver in NAFLD.
  
  
  METHODS
  Fatty acid, VLDL-TG, and VLDL-apolipoprotein B-100 (apoB100) kinetics were assessed by using stable isotope tracers in 14 nondiabetic obese subjects with NAFLD (IHTG, 22.7% +/- 2.0%) and 14 nondiabetic obese subjects with normal IHTG content (IHTG, 3.4% +/- 0.4%), matched on age, sex, body mass index, and percent body fat.
  
  
  RESULTS
  Compared with the normal IHTG group, the NAFLD group had greater rates of palmitate release from adipose tissue into plasma (85.4 +/- 6.6 and 114.1 +/- 8.1 micromol/min, respectively; P = .01) and VLDL-TG secretion (11.4 +/- 1.1 and 24.3 +/- 3.1 micromol/min, respectively; P = .001); VLDL-apoB100 secretion rates were not different between groups. The increase in VLDL-TG secretion was primarily due to an increased contribution from "nonsystemic" fatty acids, presumably derived from lipolysis of intrahepatic and intra-abdominal fat and de novo lipogenesis. VLDL-TG secretion rate increased linearly with increasing IHTG content in subjects with normal IHTG but reached a plateau when IHTG content was >/=10% (r = 0.618, P < .001).
  
  
  CONCLUSIONS
  Obese persons with NAFLD have marked alterations in both adipose tissue (increased lipolytic rates) and hepatic (increased VLDL-TG secretion) TG metabolism. Fatty acids derived from nonsystemic sources are responsible for the increase in VLDL-TG secretion. However, the increase in hepatic TG export is not adequate to normalize IHTG content.
authors.affiliation: Center for Human Nutrition, Washington University School of Medicine, St. Louis, Missouri, USA.
authors.forename: Elisa
authors.initials: E
authors.lastname: Fabbrini
authors.forename: B Selma
authors.initials: BS
authors.lastname: Mohammed
authors.forename: Faidon
authors.initials: F
authors.lastname: Magkos
authors.forename: Kevin M
authors.initials: KM
authors.lastname: Korenblat
authors.forename: Bruce W
authors.initials: BW
authors.lastname: Patterson
authors.forename: Samuel
authors.initials: S
authors.lastname: Klein
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism* / Q000503:physiopathology; D000328:Adult; D053299:Apolipoprotein B-100 / Q000378:metabolism; D001823:Body Composition / Q000502:physiology; D016022:Case-Control Studies; D005227:Fatty Acids / Q000378:metabolism; D005234:Fatty Liver / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D006801:Humans; D050356:Lipid Metabolism / Q000502:physiology*; D008074:Lipoproteins / Q000378:metabolism; D008079:Lipoproteins, VLDL / Q000378:metabolism; D008099:Liver / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D014280:Triglycerides / Q000378:metabolism
chemical_list: D053299:Apolipoprotein B-100; D005227:Fatty Acids; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride