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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.
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Abstract |
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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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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Healthy volunteers (n = 12) were recruited by advertisement and gave written informed consent after all procedures and potential risks were explained. The protocol was approved by the University of Minnesota Human Subjects Committee (University of Minnesota Institutional Review Board no. 9908M15861). All subjects were nonsmoking, healthy males, age 20–55 yr, with stable body weight (ranging between 80 and 130% as per Metropolitan Weight Tables), normal exercise and activity patterns, and consumed less than 20 g of alcohol per week. Screening blood draws were performed on two occasions (approximately 2 wk apart) at the University of Minnesota General Clinical Research Center at Fairview University Medical Center (Minneapolis, MN). Subjects who had fasted for at least 12 h and abstained from alcohol for at least 48 h had blood drawn to verify health status (liver enzymes, hematocrit, etc.) and measure concentrations of fasting glucose, total serum TG, and insulin concentrations. Heights and weights were also measured. Subjects were excluded by the following criteria: fasting concentrations of blood glucose more than 7.17 mmol/liter (129 mg/dl) or serum total cholesterol more than 7.76 mmol/liter (300 mg/dl); or aerobic activity more than 5 h/wk, vegetarian, or other restrictive dietary habits, history of diabetes, or other metabolic disease or medication use known to affect lipid metabolism. With regard to ethnicity, the subjects were 11 Caucasians and one Indian. Fasting glucose, insulin, and TG concentrations obtained during screening were 4.73 ± 0.57 mmol/liter, 4.1 ± 1.2 µU/ml, and 1.03 ± 0.67 mmol/liter, respectively.
Study design
Subjects were placed on weight-maintaining diets, based on the Harris-Benedict equation multiplied by an activity factor, with comparison with 3-d dietary recalls of usual intake and food frequency questionnaires administered during the screening visits. The run-in diet was consumed for 3 d immediately before the metabolic test and was prepared by the subject’s themselves as directed and monitored by a registered dietitian. This diet plan provided 30% of energy from fat and 55% from carbohydrate (CHO) and was composed of whole foods normally consumed by each individual subject. Subjects recruited for this study were selected to consume diets typical of an American population (30–32% of energy from fat, 55% from CHO). Thus, the run-in diet reflected the subject’s usual diet, with one exception; alcohol consumption was prohibited during the run-in period. As a result, it was anticipated that the subjects would be in steady state with respect to energy metabolism. As shown in Fig. 1
, on d 1 of the study, the subject was admitted to the Clinical Research Center between 1100 and 1200 h and had a physical exam performed by a physician. Between 1430 and 1600 h, the subject had a size 8 French feeding tube placed into the duodenum via the nasal cavity. Fluoroscopy was used to confirm the accurate placement of the tube, 15 cm distal from the pyloric sphincter. An iv line was placed into the antecubital vein of each arm; one iv line was used for the administration of both acetate [1 13C1]-Na acetate and [1,2,3,4-13C4] potassium palmitate as shown in Fig. 1 and as described previously (8). The other iv was used to obtain blood samples. Between 1730 and 1900 h, an evening meal consisting of whole foods was consumed by mouth, representing one third of daily energy intake. After this meal, no food or energy-containing beverages were allowed until 0900 h on d 2, at which time a liquid formula was administered continually through the feeding tube for 11 h (i.e. until 2000 h). Indirect calorimetry was performed for 30 min while subjects were fasted (0800–0830 h) and at 5.5 h after the initiation of feeding (1430–1500 h). A metabolic cart (Sensor Medix, Yorba Linda, CA) in the hooded mode was used. Subjects rested, read, or watched television for the duration of the study.
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Glyceryl tri(palmitate-d31) was incorporated into a liquid formula for duodenal infusion of nutrients. The liquid formula supplied approximately two thirds of the daily energy intake for each subject with a final macronutrient composition similar to the 3-d run-in diet. The average macronutrient profile of the formulas was 54 ± 1% CHO, 32 ± 1% fat, and 14 ± 2.5% protein. The majority of the CHO (99.7%) was glucose, present as maltodextrin, in the base formula (Boost, Mead Johnson, Evansville, IN); the cream added less than 0.3% of the total CHO as lactose. The enteral formula (Boost, Mead Johnson Nutritionals) was mixed with egg yolk, heavy cream, vegetable oil, and glyceryl tri(palmitate-d31). Glyceryl tri(palmitate-d31) was heated to its melting point (69 C), whereas the remaining ingredients were blended together and heated to the same temperature. All components were combined immediately after heating and blended at high speed. To ensure homogeneity, the solution was passed through a microfludizer (Model 110 Y, Microfluidics Corp., Newton, MA). The primary FAs in the final formula were 18.7% palmitate, 1.5% palmitoleic, 7.2% steric, 45.7% oleic, 23.3% linoleic, and 3.7% linolenic. The amount of glyceryl tri(palmitate-d31) added was estimated to provide a 20% enrichment of the unlabeled palmitic acid contained in the food products. The final enrichments of the TG-palmitate in the formula, as analyzed by gas chromatography/mass spectrometry (GC/MS), were confirmed to be 18.2 ± 2.4% (mean ± SD) and resulted in an average chylomicron-TG palmitate enrichment of 18.5 ± 7.4%. The dietary TG enrichment was used as the precursor enrichment for the calculations of VLDL-TG FAs derived from the diet. For the administration of other isotopes, just before the evening meal on d 1, an iv infusion of [1 13C]-acetate (15 g in 1 liter normal saline) was started at a constant rate of 37 ml/h and continued until 2000 h on d 2. At 2400 h on d 1, an infusion of [1,2,3,4 13C4]-palmitic acid, complexed with human albumin in a 2:1 molar ratio, was started at a constant rate of 50 ml/h (7 µg/kg·min) and continued until 2000 h on d 2. Stable isotopes were purchased from Cambridge Isotope Laboratories, Inc. (Andover, MA) and Isotec Inc. (Miamisburg, OH), and isotopic purity was greater than 98% for all isotopes. All iv solutions were prepared under sterile conditions at the Medical Center Investigational Pharmacy.
Sample analysis isolation and GC/MS
Blood samples were obtained periodically between 2400 h on d 1 and 2000 h on d 2. Serum was separated immediately and kept on ice, whereas EDTA, gentamicin sulfate, chloramphenicol, and phenylmethyl-sulfonylfluoride were added as a preservation cocktail (20). Concentrations were measured enzymatically for glucose on a Vitros Analyzer 950 (Ortho-Clinical Diagnostics, Rochester, NY), NEFA (NEFA kit no. 994-75409 E, Wako Chemicals USA, Inc., Richmond, VA), and TG (kit no. 336, Sigma Diagnostics, St. Louis, MO); insulin concentration was measured via chemiluminescent immunoassay (Diagnostic Products Corp., Los Angeles, CA). Serum samples used for NEFA compositional analysis were extracted immediately and derivatized as described previously (8). Within 24 h of each infusion study, total TRLs were isolated by fixed-angle ultracentrifugation at 40,000 rpm for 20 h in a 50.3Ti rotor (Beckman Instruments, Palo Alto, CA) at 10 C (8). Lipoprotein fractions with Svedberg unit (Sf) >400 and Sf 60–400 were then isolated as previously described (21). Lipoproteins Sf >400 were used as indicators of chylomicron enrichment to determine how well the labeled liquid formula was being absorbed. The primary purpose of the lipoprotein fractionation procedure was to isolate large VLDL (8, 22), a buoyant particle with Sf 60–400 and an average diameter of 70–400 nm. Although these particles represent a small proportion of all TRLs (see TG contents in Table 1), Sf 60–400 particles have a very short half-life and thus reflect the most recently secreted particles by the liver (8). Lipids were extracted from lipoprotein particles, followed by separation of TG. GC/MS was performed on an HP 6890 with a Mass Selective Detector HP 5973 fitted with an ETP electron multiplier (SGE, Incorporated, Austin, TX) using a HP-1, 25-m column, as described previously (21). Electron impact was used to selectively monitor ions with mass to charge ratios 270, 271, 272, 274, 300, and 301. Comparable ion peak areas between standards and biological samples were achieved by either adjusting the volume injected, diluting, or concentrating the sample. For the calculation of rate of appearance (Ra) of NEFA and absolute pools sizes, the proportion of FAs that was palmitate was determined by GC using flame-ionization detection. Individual FAs were identified by retention time and compared with an internal standard for quantification.
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For the formula and infusate enrichments, the calculations were adjusted for the amount of unlabeled FAs present, which had been derived from less than 100% purity of the isotope or from FAs present on the albumin used in the infusion. The inputs of these FAs were subtracted from the final calculated values of RaNEFA and dietary spillover. The formulas and assumptions for the calculations are presented in detail as supplemental data on The Endocrine Society’s Journals Online web site at http://jcem.endojournals.org. Mass isotopomer distribution analysis was used to calculate the percentage of newly made palmitate in lipoproteins (23). Our hypothesis was that many sources of palmitic acid (NEFA, lipogenesis, diet) could contribute to VLDL TG in the fed state; thus, our goal was to determine the relative contributions of FA sources to this TG pool. However, in post hoc analysis, eight of the 12 subjects had a sufficient number of fasted-state data points to use the kinetics of 13C4-palmitate incorporation to calculate VLDL-TG secretion rate during fasting. Furthermore, the isotopic enrichment of the liquid formula was maintained throughout feeding, and fed-state VLDL-TG production rate was determined by analyzing the incorporation of d31-palmitate into the VLDL-TG pool from 0930–2000 h. Calculations were performed using Microsoft Excel (2000, Microsoft, Seattle, WA) and statistical analyses using MacAnova for Windows (version 4.13, University of Minnesota, St. Paul, MN). Unless otherwise noted, data are presented as mean ± SE. P < 0.05 was considered statistically significant.
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Results |
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). As shown in Fig. 2, metabolite concentrations remained constant during feeding (slopes during the last 5 h of the experiment were not different from zero). The total serum TG concentration increased (Fig. 2B), as did the TG concentration of the total TRL fraction, which increased 25% primarily due to a 5.5-fold increase in chylomicron-TG concentration (Table 1). VLDL-TG (Sf, 60–400) concentration did not change significantly with feeding (Fig. 2C), whereas TG in the Sf >400 fraction rose significantly (Fig. 2C). As expected, serum NEFA concentration decreased by nearly 50% from fasted to fed states (Fig. 2B and Table 1), and the respiratory quotient rose with feeding; glucose oxidation increased significantly, whereas FA oxidation decreased (Table 1). Dietary-derived FAs in the serum NEFA pool accumulated with feeding, as shown previously (16). At steady state, 22.9 ± 3.4% of serum NEFAs were derived from spillover of TRL lipid.
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). Although not the primary goal of this study, a sufficient quantity of data points was available to model label incorporation into VLDL-TG for eight of the 12 subjects. As shown in Table 2, for RaVLDL-TG, the fasting-state turnover tended to be faster than the fed state, although not significantly so (14.9 ± 6.1 vs. 8.9 ± 2.1 µmol/kg·h, fasted vs. fed, P = 0.167). Despite the constant VLDL-TG pool size and turnover rate, the contributions of different FA sources used for synthesis of VLDL-TG changed significantly with feeding. The steady-state values of FA sources into VLDL-TG are shown in Table 2, and the temporal incorporation into VLDL-TG is shown in Fig. 3. Serum NEFA represented the main FA source used for fasting VLDL-TG synthesis, composing 77.2 ± 4.0% of VLDL-TG palmitate. At the same time, 4.0 ± 1.0% of VLDL-TG were derived from the DNL pathway. In total, 81.2 ± 4.0% of VLDL-TG FAs were accounted for in the fasted state, a result of either incomplete turnover of the VLDL-TG pool or, more likely, due to the use of some unlabeled FAs for VLDL-TG synthesis because the Sf 60–400 fraction turns over in 2–4 h. During the fed state, the reduction in RaNEFA coincided with a 42.8 ± 22.2% reduction in the appearance of NEFA in VLDL-TG (P < 0.003). However, even with this reduction, serum NEFA continued to provide 43.6 ± 5.4% of fed-state FAs appearing in VLDL-TG. Dietary FAs accounted for 25.5 ± 4.5% of VLDL-TG during the fed state. The amount of VLDL-TG derived from diet was greater than could be accounted for by the amount of dietary label that appeared in the NEFA pool. This observation supports the concept of chylomicron-remnant clearance by the liver and dietary FA recycling through incorporation into VLDL-TG (hereafter, this source will be referred to as chylomicron-remnant TG). Thus, during the final hours of feeding, diet-derived NEFA and chylomicron-remnant TG sources composed 10.3 ± 6.9% and 15.2 ± 13.7% of VLDL-TG, respectively (Table 2). The contribution of FAs from DNL increased during feeding and reached 8.2 ± 1.5% of VLDL-TG. In total, 77.9 ± 3.6% of VLDL-TG was accounted for by NEFA, dietary, and newly made FA sources during the fed state.
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). Sf 60–400 VLDL-TG pool size was not increased, and although the percentage of VLDL-TG from NEFA decreased significantly from fasting to feeding, the corresponding reduction in VLDL-TG concentration from NEFA was not significant (P = 0.12). No significant difference was observed between the two routes of dietary input (P = 0.27 for percentage, P = 0.34 for absolute), nor was a significant difference found in either the cumulative percentage or concentration of VLDL-TG accounted for during the fed state compared with fasting (P = 0.47 and P = 0.71, respectively). Finally, the change in RaNEFA from the fasted to fed state was found to correlate with the change in the amount of NEFA found in VLDL-TG (P = 0.037, Fig. 4).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The percentages of VLDL-TG FAs derived from the serum NEFA pool during the fasted state were comparable with previous data (8). A number of previous studies have indicated that fasting NEFA flux regulates VLDL-TG synthesis and secretion, although the sole importance of NEFA flux to VLDL-TG secretion has been questioned (34). The present data support a key role for the serum NEFA pool in contributing to VLDL-TG synthesis in the fed state. Although serum NEFA concentration and flux were reduced with feeding, this pool remained the primary contributor to VLDL-TG. Furthermore, a significant relationship existed between the absolute reduction in adipose NEFA flux and the reduction in its use for TG synthesis. Lastly, based on the existence of dietary FAs present in the NEFA pool, one interpretation of these data could be that the role of NEFA to support liver-TG synthesis may be so important physiologically that the spillover mechanism exists to protect this source as release of adipose NEFA is reduced postprandially. The second source of FAs used for VLDL-TG synthesis was the pathway of hepatic DNL. In the fasting state, newly made FAs represented only 4% of the palmitate found in VLDL-TG, as would be expected (8, 35), and, although the presence of these FAs increased with feeding, this source continued to constitute the smallest fraction of fed-state VLDL-TG. The low level of lipogenesis found postprandially may have been due to the low concentration of insulin elicited by the slow infusion of nutrients. A comparison of the present data with those derived from feeding the formula by mouth has recently been published (36, 37). Similarly, the low rate of formula infusion probably impacted the fate of dietary FAs, the third VLDL-TG FA source.
Because the quantitation of dietary FAs flowing to VLDL-TG had not been published before this project was begun, it was unknown just how many of these FAs would be recycled through the liver. The present data demonstrate that dietary lipid can constitute a significant portion of VLDL-TG. The spillover of dietary FAs found here using endogenous chylomicron labeling confirms data from prior studies in which chylomicrons or chylomicron-like lipid emulsions were iv administered during fasted conditions (14, 38) as well as after consumption of a high-fat meal (16). Furthermore, if the insulin concentration was sufficient to stimulate adipose LPL activity, but not high enough to completely up-regulate adipose tissue FA reesterification, this may have increased spillover. Whether this effect may be more pronounced in individuals whose adipose tissue is insulin resistant will be important to determine. The present findings show that, on average, over 25% of VLDL-TG in healthy men can be derived from dietary FAs during slow infusion of lipid, a result suggesting an efficient hepatic removal of chylomicron remnants and the use of chylomicron FAs for production of newly formed VLDL particles. However, because VLDL particles are not as readily lipolyzed as chylomicrons (39), maintenance of VLDL-TG concentration by dietary FAs may prolong postprandial lipemia and contribute to the atherogenic potential of postprandial TRL particles. The fasting RaVLDL-TG in this study was comparable with previous data using stable isotope tracers and lipoprotein fractionation in healthy subjects (8). Our data support the concept that fasting NEFA flux may regulate VLDL-TG production.
A number of limitations of the study design should be mentioned. First, as described in the supplemental data, the Sf 60–400 lipoprotein fraction primarily contains large VLDL particles but can also contain some chylomicron remnants. In the present study, the ratio of these particles was 25:1 during feeding. The presence of a small number of chylomicrons carrying the dietary label would tend to cause an overestimation of the percentage of dietary FAs attributed to VLDL-TG (those presumed to enter VLDL through chylomicron clearance to the liver). Second, the use of the duodenal feeding tube resulted in steady-state postprandial metabolism so that determination of VLDL-TG FA sources could be made with a high degree of accuracy. The drawback of this protocol was that the mode of feeding was not physiological. Furthermore, the use of the feeding tube required administration of a formula diet. On the other hand, the protocol does shed light on metabolism that occurs when individuals eat continuously, particularly when calories are consumed in liquid form. Lastly, a limitation to consider was the potential for stress associated with the use of a feeding tube in healthy subjects. The tube was put in by an experienced radiologist who preformed the procedure the day before the study to increase the amount of time that elapsed before data collection. We anticipated that the result of such stress would be to amplify the flux of adipose FAs; however, the NEFA fluxes measured the next morning in the fasting state were within normal ranges, as were the NEFA and glucose concentrations.
In summary, these data highlight two concepts for future study of VLDL-TG regulation: dysregulation of adipose FA release and the inability of extrahepatic tissues to remove dietary FAs from the circulation. In persons with hyperlipidemia and insulin resistance, sustained lipolysis of adipose TG occurs and adipose tissue lipoprotein lipase activity has been found to be diminished (40, 41). Data from the healthy subjects studied here demonstrate the unique characteristic of the liver to flexibly use the FAs that are presented to it postprandially. How this flexibility is impacted by insulin resistance will be an important topic for future investigation.
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Acknowledgments |
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Footnotes |
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Neither B.R.B. nor E.J.P. has any conflicts of interest.
First Published Online January 31, 2006
Abbreviations: CHO, Carbohydrate; DNL, de novo lipogenesis; FA, fatty acid; GC/MS, gas chromatography/mass spectrometry; NEFA, nonesterified FA; Ra, rate of appearance; Sf, Svedberg unit; TG, triacylglycerol; TRL, TG-rich lipoprotein; VLDL, very low-density lipoprotein.
Received August 1, 2005.
Accepted January 19, 2006.
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