title: Contributions of different fatty acid sources to very low-density lipoprotein-triacylglycerol in the fasted and fed states.
abstract: BACKGROUND
  The liver's regulation of fatty acids (FAs) postprandially may contribute to risk of metabolic diseases.
  
  
  OBJECTIVE
  Measurements of steady-state metabolism were used to investigate sources of FAs used for very low-density lipoprotein (VLDL)-triacylglycerol (TG) synthesis during fasting and feeding in vivo.
  
  
  METHODS
  Subjects were duodenally fed a formula labeled with the stable isotope glyceryl tri-palmitate-d(31) and iv infused with [1,2,3,4-(13)C(4)]-palmitatic acid and [1-(13)C(1)]-acetate to quantitate the liver's use of FAs originating from adipose tissue and de novo lipogenesis.
  
  
  METHODS
  This study of healthy men (n = 12; body mass index, 24.4 +/- 2.7 kg/m(2)) was conducted at a General Clinical Research Center.
  
  
  METHODS
  Concentrations of metabolites during fasting and feeding, sources of FAs used for lipoprotein synthesis, rate of appearance of serum nonesterified FA (NEFA), and VLDL-TG were measured.
  
  
  RESULTS
  During fasting, 77.2 +/- 14.0% of VLDL-TG was derived from adipose FA recycling and 4.0 +/- 3.6% from lipogenesis; with feeding, 43.6 +/- 18.6% came from adipose FAs (P < 0.001), 8.2 +/- 5.1% from lipogenesis (P < 0.001), 15.2 +/- 13.7% from uptake of chylomicron-remnant TG, and 10.3 +/- 6.9% from dietary FA spillover into the serum NEFA pool. Fed-state VLDL-TG from NEFA reesterification decreased in proportion to the reduction in adipose NEFA appearance.
  
  
  CONCLUSIONS
  These data: 1) quantify the extent to which the healthy liver manages its use of different sources of FAs that flow to it, 2) demonstrate how the postprandial reduction in adipose-NEFA flux may be partially replaced by other sources, and 3) highlight the potential for dietary FA spillover to support the continued dominance of NEFA as a substrate for VLDL-TG synthesis.
authors.affiliation: Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9052, USA.
authors.forename: Brian R
authors.initials: BR
authors.lastname: Barrows
authors.forename: Elizabeth J
authors.initials: EJ
authors.lastname: Parks
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D002914:Chylomicrons / Q000378:metabolism; D004032:Diet; D005215:Fasting / Q000378:metabolism*; D005227:Fatty Acids / Q000493:pharmacokinetics / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D006801:Humans; D007328:Insulin / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D014280:Triglycerides / Q000097:blood*
chemical_list: D001786:Blood Glucose; D002914:Chylomicrons; D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D008079:Lipoproteins, VLDL; D019275:Radiopharmaceuticals; D014280:Triglycerides