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Submitted on August 1, 2005
Accepted on January 19, 2006
Department of Food Science and Nutrition and Division of Endocrinology and Diabetes University of Minnesota, St. Paul, MN, 55108
* To whom correspondence should be addressed. E-mail: Elizabeth.Parks{at}UTSoutwestern.edu.
Context: The liver's regulation of fatty acids (FAs) postprandially may contribute to risk of metabolic diseases.
Objective : Measurements of steady-state metabolism were use to investigate sources of FAs used for VLDL-triacylglycerol (TG) synthesis during fasting and feeding in vivo.
Design/Intervention: Subjects were duodenally-fed a formula labeled with the stable isotope glyceryl tri-palmitate-d31, and intravenously infused with [1,2,3,4-13C4]-palmitatic acid and [1-13C1]-acetate, to quantitate the liver's use of FAs originating from adipose tissue and de novo lipogenesis.
Setting/Participants: This study of healthy men (n = 12, BMI 24.4 ± 2.7 kg/m2) was conducted at a General Clinical Research Center.
Main Outcome Measures: Concentrations of metabolites during fasting and feeding, sources of FAs used for lipoprotein synthesis, rate of appearance of serum NEFA and VLDL-TG.
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.
Conclusion: These data 1) quantify the extent to which the healthy liver manages its use of different sources of fatty acids 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 fatty acid spillover to support the continued dominance of NEFA as a substrate for VLDL-TG synthesis.
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