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Contributions of Different Fatty Acid Sources to Very Low-Density Lipoprotein-Triacylglycerol in the Fasted and Fed States

Department of Food Science and Nutrition and Division of Endocrinology and Diabetes, University of Minnesota, St. Paul, Minnesota 55108

Address all correspondence and requests for reprints to: Elizabeth J. Parks, Ph.D., Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9052. 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 used to investigate sources of FAs used for very low-density lipoprotein (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 iv 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; body mass index, 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 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.

Conclusion: 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.

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