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Department of Foods and Nutrition, Purdue University, W. Lafayette, IN 47907-1264
2To whom correspondence should be addressed. Email: mattesr{at}cfs.purdue.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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0700 h. After placement of a catheter in a hand vein and 4 blood draws at 10-min intervals, 50 1-g safflower oil (high linoleic acid content) capsules were consumed. After another blood draw, modified sham feeding was initiated with a cracker only or cracker with cream cheese in random order with 1 wk between trials. Oral exposures occurred at 5-min intervals for 60 min then at 15-min intervals from min 60 to 120. Additional blood draws occurred at 2, 4, 6, 8, 10, 12, 14, 30, 60, 120, 240, 360 and 480 min. Oral stimulation, especially by fat, prompted the rapid (mean 23 min) release of lipid stored from the previous meal (almonds) in all participants. This resulted in multimodal postprandial triacylglycerol (TAG) peaks generally occurring at 0–30 min, 60–120 min and 240–480 min after loading and initiation of oral stimulation. TAG magnitudes during these times were correlated (r = 0.40–0.89, P < 0.001–P = 0.053). It is proposed that the sensory-enhanced release of lipid from the residual pool initiates an early TAG rise, which augments the peak attributable to absorption of meal lipid; this in turn supplements a later peak associated with release of endogenously synthesized TAG because lipid from all three sources competed for a common clearance mechanism. If substantiated, additional understanding of the behavioral factors (e.g., eating patterns) that initiate this cascade will be warranted.
KEY WORDS: • fat • oral • lipid • taste • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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–4
), a more complete understanding of the factors that influence its time course and magnitude is warranted. Typically, a unimodal elevation is reported with a lag time of 1–2 h, a concentration peak at 4–6 h and a return to baseline 6–9 h after meal initiation. However, this pattern may be, in large measure, a function of infrequent blood sampling, which limits resolution power and the reporting of mean group responses that mask individual variability. More rigorous fat challenge studies have revealed bi- or, less commonly, triphasic postprandial serum TAG concentration peaks (5
–12
). When observed, an initial sharp peak generally occurs 60 min after ingestion with a broader second peak appearing 2–4 h later. The third peak may occur 6–7 h postloading. Considerable data indicate that the peak occurring 1–2 h after lipid ingestion is comprised primarily of chylomicrons derived from the recently ingested lipid and that the next peak is rich in VLDL (3
,5
,13
–16
). However, this is not absolute; VLDL have been identified in the first peak and chylomicrons are present in the later peak (14
,16
). Less well established is a third source of lipid that reportedly is comprised of residual TAG from the previous meal, which may be rapidly mobilized from the enterocyte or lymphatics (9
,17
,18
). Verification of this "residual pool," characterization of the mechanisms that prompt its release and establishment of its health implications are incomplete.
One approach to demonstrate the source of lipid in the residual pool entails feeding known, but different types of fatty acids in successive meals while monitoring the fatty acid profile of absorbed lipid. This has been used successfully with a first meal rich in linoleic acid and second containing oleic acid (9
). However, because of inherent differences in fatty acid absorption (19
) and clearance (11
), this observation requires verification with the reverse sequence or a different pair of fatty acids. This was one aim of the present study.
The mechanisms regulating the release of lipid from the residual pool have received little systematic study. Studies identifying the pool have used infrequent blood sampling (i.e., 20- to 30-min intervals) relative to the time frame of its reported activation (i.e., within h 1). Thus, its timing remains poorly characterized and this characterization was a second aim of this study.
As a possible release mechanism, simple displacement of stored lipid by recently ingested lipid seems unlikely given that release occurs after ingestion of a low fat meal (20
). However, such a manipulation could provide an adequate stimulus for release by a cephalic phase response in which oral fat exposure generates a neural signal that modifies absorption processes. Modified sham-feeding with a mixed meal after vitamin A administration rapidly enhances plasma vitamin A, and necessarily, the lipid concentration in humans (17
). The response is delayed by administration of atropine, suggesting that it is mediated by parasympathetic stimulation. Studies in rats (21
) and humans (22
–24
) indicate that oral exposure to dietary fat, as opposed to other macronutrients, may be the most effective oral stimulus for raising TAG postprandially. One recent study reported no effect on serum TAG of modified sham feeding with low or high fat meals (25
). However, participants were tested in a fasted state and the augmented TAG concentration associated with oral stimulation by fat requires the presence of fat in the gut (23
) as would occur under customary eating conditions. Another aim of this study was to document the effect of oral stimulation on release of lipid stored in the residual pool.
Finally, previous work demonstrated significant associations between the magnitude of the 1–2 h and 4–6 h TAG peaks. Should these be causally related, due to increased competition for clearance of VLDL by chylomicrons, the influence of lipid released from the residual pool would also be important to quantify. It too would increase the load to be cleared and provide additional substrate for de novo hepatic VLDL synthesis. An improved understanding of the contribution of the residual pool to postprandial TAG levels could hold important public health and therapeutic implications because activation of this pool may be largely under behavioral control. Assessment of contributions from this pool to later TAG levels was another aim of this work.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Two testing sessions were conducted 1 wk apart. Figure 1
presents a time line of activities conducted at each session. At 2200 h the night before each session, participants ingested 80 g of almonds and refrained from all food and beverages until arrival at the laboratory at 0700 h the following morning. The almond meal contained 53% of energy as oleic acid, and 14% as linoleic acid (26
). Upon arrival, arterialized blood was collected through an indwelling catheter in a hand vein at 10-min intervals for 40 min. Participants then ingested 50 g of safflower oil in 1-g capsules with 500 mL of water in 10 min. This load contained 13% of energy as oleic acid and 77% as linoleic acid. Subjects tolerated the load well. Immediately after lipid loading, another blood sample was drawn followed by mastication of either 3 g of cracker (Premium Fat-Free Nabisco, East Hanover, NJ) or 3 g cracker plus 5 g of cream cheese (Philadelphia Brand, Kraft foods, Northfield, IL) for 10 s. The sample was then expectorated. The cream cheese contained 0.06% oleic acid and undetectable amounts of linoleic acid. Oral stimulation with the same stimulus was repeated every 5 min for 60 min and every 15 min for another 60 min. Blood samples were drawn every 2min for 14min and again at 30, 60, 90, 120, 240, 360 and 480 min. The stimuli were presented in random order. The protocol was approved by the Purdue University Committee on the Use of Human Research Subjects.
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Participants were recruited by public advertisement. Eligibility included good health, no regular use of medications except oral contraceptives (if used throughout the study period), 18–50 y of age, normal lipid status and no donation of blood in the preceding 3 mo. Twenty-five (13 men, 12 women) individuals completed testing. Their age was 28.0 ± 2.1 y and their body mass index (BMI) was 24.8 ± 0.8 kg/m2 (mean ± SEM). Serum metabolite concentrations in fasting subjects were: total cholesterol, 3.77 ± 0.13 mmol/L; LDL serum cholesterol, 2.06 ± 0.09 mmol/L; triacylglycerol, 0.97 ± .08 mmol/L; glucose 4.67 ± 0.10 mmol/L; and insulin 89.5 ± 10.3 pmol/L.
Laboratory analyses.
Serum TAG concentrations were measured in duplicate with a Cobas Mira Clinical Analyzer (Roche Diagnostics, Indianapolis, IN). The linoleic and oleic acid levels in serum were assayed by gas chromatography. Sample lipid was extracted and transmethylated using one part tetramethylguanidine in 4 parts methanol (v/v). Fatty acid analyses were conducted with a Varian gas chromatograph, model 3900 with a Varian fused silica 30 m x 0.32 mm column with a coating of CP wax 52 CB DF = 0.25 µm (Varian Analytical Instruments, Walnut Creek, CA).
Statistical analyses.
A TAG peak was defined as a concentration rise of 
15% relative to the concentration at a preceding inflection point from a flat or negative curve segment. Treatment effects on TAG concentration peaks as well as oleic and linoleic acid concentrations and the oleic acid/linoleic acid ratio were assessed by repeated-measures ANOVA with type of stimulation (cream cheese plus cracker, cracker alone) as a within-subject factor. Paired-sample t tests were used for post-hoc analyses. Pearson correlation coefficients were computed to assess the association between the first and subsequent TAG peaks. The criterion for statistical significance was P < 0.05 and all tests were two-tailed. Values in the text are means ± SEM.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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. Although it was not possible to obtain complete sample collections for all participants during the initial 30-min period after lipid loading, all participants had an early peak on at least one trial. Twenty-four individuals exhibited an early TAG peak after oral stimulation with cracker plus cream cheese. Two participants (O and R) had 2 peaks in this time period. Twenty-three participants had an early peak after exposure to cracker alone with three (F,N,T) exhibiting two peaks in the first 30-min time period. The other 3 trials yielded peaks with increments of 11, 14 and 14%, which did not meet the minimal criterion of a 15% rise. To facilitate response magnitude comparisons across individuals, data from all participants (except X and Y, who had markedly higher resting and stimulated values) are plotted on the same ordinate. This hampers visual identification of some peaks for individuals with low resting values, but 6 participants (panels C,H,I,J,P and Q in Fig. 2
) had a peak in the 60- to 120-min period after cracker plus cream cheese and five participants (panels C,J,K,W and X in Fig. 2
) had a peak during this time after cracker alone. Twenty participants had peaks in the 240- to 480-min time period after each treatment.
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Without imposing a constraint for whether TAG peaks occurred in a specified time period, the lag times to the first, second and third peaks when oral stimulation with cracker and cream cheese was provided were 22.6 ± 1.4 min (n = 24), 221.8 ± 24.5 min (n = 23) and 384.0 ± 44.9 (n = 5) min, respectively. The times to peaks 1, 2 and 3 in trials involving oral stimulation with cracker alone were 24.4 ± 1.1 min (n = 22), 217.1 ± 22.4 min (n = 23) and 360.0 ± 69.3 min (n = 4), respectively. When we limited analyses to only those participants with three TAG peaks, the lag times were 18.0 ± 3.2 min, 45.0 ± 8.7 min and 360.0 ± 49.0 min when crackers plus cream cheese were provided. The lag times after intake of cracker alone were 18.5 ± 2.8 min, 60.0 ± 21.2 min and 360.0 ± 69.3 min. For the full sample (for which adequate statistical power was available), the time courses were not affected by the different forms of oral stimulation. In addition, resting TAG concentrations were not correlated with the timing of peak TAG occurrences, and the time course and magnitude of TAG peaks did not differ between men and women. TAG peaks also were not related to age or BMI; thus, all data were pooled for subsequent analyses.
Table 1
presents the correlations between mean TAG concentrations at four time points [baseline, 0–30 min (time 1), 60–120 min (time 2) and 240–480 min (time 3)] after initiation of oral stimulation with cracker alone or cracker plus cream cheese. Strong correlations were observed between baseline TAG concentrations and concentrations during each of the time periods. With the exception of the marginal association between time 1 and 3 concentrations after oral stimulation with cracker plus cream cheese, significant correlations were also observed between TAG concentrations at the three times after oral stimulation with both treatments. Correction for baseline TAG concentrations did not affect the associations. Analyses of only individuals with peaks during each of the three time periods were hampered by limited sample size. Nevertheless, the data suggested meaningful associations. After oral stimulation with cracker plus cream cheese, correlations between peaks 1 and 2, 2 and 3 and 1 and 3 were 0.60 (n = 6, P = 0.21) and 0.83 (n = 6, P < 0.05) and 0.41 (n = 17, P = 0.10) respectively. The values after oral stimulation with cracker alone were 0.98 (n = 4, P < 0.05) and 0.99 (n = 4, P < 0.01) and 0.71 (n = 19, P = 0.001).
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). Repeated-measures ANOVA revealed a significant difference across peaks [F (3
,21
) = 17.7, P < 0.001] in which the ratio was lower (P = 0.007) at baseline compared with peak 1 and peak 2 (P = 0.029). The ratio in peak 3 was lower than in peaks 1 and 2 (both P < 0.005). Peak 3 also had a lower (P = 0.0021) ratio than baseline, likely due to the extended fast and exhaustion of a source of oleic acid.
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. Oral stimulation with the cracker plus cream cheese resulted in a greater proportion of oleic acid in peak 1 compared with baseline (P = 0.02) or peak 3 (P < 0.001). The peak 1 oleic acid composition after oral stimulation with cream cheese was also greater than the composition after oral stimulation with cracker alone (P = 0.002). The two forms of oral stimulation did not result in different oleic acid composition in peaks 2 or 3. The linoleic acid composition after the two forms of oral stimulation did not differ at baseline or in any peak. The linoleic acid composition in peak 1 was lower than the composition at baseline (P < 0.001; P = 0.025) or in peak 2 (both P < 0.001) after oral stimulation with cracker alone or cracker plus cream cheese.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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) and averaging responses would mask individual oscillations. However, in studies in which sample collection timing permits greater resolution of the TAG pattern after lipid loading and/or individual response patterns are explored, bi- and triphasic concentration peaks have been noted. In the present study, biphasic responses were observed by 21 (80%) and 20 (84%) participants after cracker plus cream cheese or cracker alone, respectively. Five and four individuals exhibited three peaks under the two conditions. Although our data and those of others (6
) indicate that individual responses are reliable, marked individual differences have been reported across studies. For example, Olefsky et al. (5
) observed a biphasic pattern in 34 of 41 participants, whereas Cohn et al. (6
) noted single, double and triple peaks occurring in 5/22, 11/22 and 6/22 participants, respectively. We observed a predominance of biphasic responses, but our sampling protocol focused on early events and may not have been the best approach for capturing later peaks. Most earlier studies exploring postprandial TAG patterns sampled hourly and had limited ability to detect an early TAG response. The present results reveal a clear, robust, but transient peak within 1 h after loading, typically 18–30 min postloading (mean 23min). It was observed in all study participants in trials after cracker stimulation alone and in all but one participant after cracker plus cream cheese stimulation. These data indicate that multimodal responses are probably the rule rather than the exception and call for a more complete understanding of the underlying mechanisms and health implications of different patterns.
Combined with other published evidence, the present findings suggest that there are three contributory lipid sources that may provide sequential surges leading to multiple peaks. The first peak, typically occurring within 30 min of loading, likely arises from the release of lipid presumably stored in the enterocytes or lymph from the prior meal. This is supported by the elevated oleic acid/linoleic acid ratio noted here in which the prior meal was rich in oleic acid. Other studies have lacked the resolution to isolate this first peak, but using varied approaches, have indicated that lipid from the residual pool is also present in peaks occurring 60–120 min postloading. First, using the reverse sequence of fatty acids employed here, Fielding et al. (9
) demonstrated that the TAG peak at 1 h postloading was rich in the species consumed in the prior meal. The findings from this study and from Fielding et al. (9
) combined confirm the validity of this approach. However, the residual pool may also contain endogenously synthesized lipid. Studies in rats demonstrate that ingestion of olive oil reliably results in lymph TAG concentrations greater (121%) than the original load, suggesting transport of endogenous sources to this pool (19
,27
). Others have shown that a portion of TAG absorbed from this pool is of endogenous origin (14
,28
). Further, Peel et al. (18
) noted an elevation of TAG that did not contain retinal palmitate when this vitamin had been added to a lipid test meal. Finally, a recent isotopic tracer study (12
) reported a peak of labeled TAG within 1 h after ingestion of a second, unlabeled, meal (provided 5 h after the first meal that contained the label). Another rapid, postmeal rise occurred after ingestion of an additional unlabeled meal 5 h later and it also contained unlabeled TAG. Thus, each meal appears to effectively displace residual TAG from the previous meal.
Prior work indicates that the TAG peak, occurring 1–2 h postloading is comprised predominantly of fatty acids provided in the test meal. This has been confirmed by studies demonstrating the predominance of selected fatty acids present in the test meal (9
) as well as high levels of apolipoprotein B-48 (18
), a marker for intestinally derived lipid, in the peak. This peak also contains endogenous TAG (14
,16
). Sources may include preformed VLDL released from the intestine or lymph as well as newly synthesized VLDL. Once absorbed, TAG may be repackaged in the liver and released within 30–40 min (29
).
Subsequent peaks also contain TAG carried in chylomicrons, but there is a predominance of VLDL (5
,13
–15
). As much as 80% of the lipid in these peaks is derived from a surge contributed by the liver once substrate is available for de novo lipid synthesis. This component may be the most variable among individuals (30
). The composition of this peak also reflects the preferential clearance of chylomicron TAG over VLDL (31
). The relatively small, later TAG peak observed here may have occurred because the participants were provided a pure lipid load. The addition of a carbohydrate sweetener to the load, as is often used in fat challenge tests and present in mixed meals, augments the later peak (10
).
The degree to which the different input sources result in discernible peaks is likely determined by a host of methodological, behavioral and physiologic factors. Methodologically, failure to control load size and form (liquid or solid meals, fatty acid composition), time of load administration, temporal proximity of eating occasions as well as the frequency and duration of blood lipid sampling will likely obscure peaks (5
,11
,32
–35
). It is also noteworthy that in an earlier study (7
), a biphasic TAG response was observed in the afternoon when the time between meals was short, but was absent in the morning after an overnight fast. Questions have been raised concerning whether intervals > 5h may be too long to observe multimodal responses (25
). However, we observed such a pattern in participants after an overnight fast. The more frequent sampling times and longer duration of testing used here may have enabled detection of multiple peaks even after an overnight fast. This indicates that residual fat may be stored for substantial periods of time. Customary diet [e.g., fat content, proportion of energy from fat, fatty acid composition, carbohydrate form and content (35
–42
) and activity patterns (43
–45
)] may also influence the efficiency of lipid digestion, absorption, clearance and rerelease. Although postprandial TAG concentrations are higher in men than in women, the elderly compared with the young. and hypertriglycemic compared with normal individuals (6
,46
–49
), age, gender, BMI and resting TAG concentration were not predictive of the TAG pattern in this or previous studies (6
,50
,51
).
Significant correlations have been reported between resting TAG concentration and lag time to the first peak detected with hourly blood sampling (5
). It is possible that we did not detect this association due to the uniformity of resting TAG concentrations because low concentrations were an eligibility criterion. A novel, but potentially important determinant of the TAG pattern identified in this study concerns the sensory properties of the load.
Mendeloff (17
) demonstrated that modified sham feeding a mixed meal promoted release of lipid consumed 2 h previously. The response was delayed when atropine was administered 20 min before oral stimulation, confirming its neural basis. Jackson et al. (25
) did not find an influence of sensory stimulation on the postprandial TAG concentration, but their work differed from the present study and the Mendeloff study in that a lipid load was not administered close to the time of the sensory exposure. We also did not observe an augmentation of postprandial TAG concentration after oral exposure to dietary fat when lipid loading was not provided (23
). The present findings show that oral stimulation, specifically with a high fat food, augments the release of stored lipid. Studies in rats also indicate that oral fat exposure is an especially effective stimulus for enhancing the postprandial TAG response (21
). Further, duodenal infusion of long-chain triglyceride oil, which bypasses oral stimulation, does not prompt a biphasic response (46
). Neither water (20
) nor carbohydrate loads, as shown here and elsewhere (22
–24
) are effective. It may be that processes associated with lipid digestion that are activated by orosensory stimulation with fat are necessary for promoting the release of stored lipid. Candidate processes include effects on gastric motility and lipase secretion because both are modified by sensory stimulation (52
,53
). Whether the magnitude of the response to sensory stimulation would be greater after a more recent meal is not known. The effects of altering the timing and duration of oral fat exposure must also be explored to determine the relevance of this work under "normal" eating conditions.
The ecological importance of a fat-specific sensory influence on lipid metabolism is not clear. One hypothesis is that it may be a system to ensure efficient absorption of essential fatty acids (EFA). Enterally administered EFA maintain plasma EFA better than parenterally delivered EFA (54
). Some evidence indicates that only EFA are effective taste stimuli (55
), and fats with higher levels of EFA exert stronger effects on TAG metabolism (56
). Alternatively, it may be a more generalized response in which the early sensory event promotes clearance of residual fat from a previous meal so that digestion and absorption of incoming lipid can be optimized. This issue remains unresolved.
The importance of clarifying postprandial TAG patterns is underscored by evidence that the postprandial TAG concentration is an independent risk factor for coronary heart disease (1
–4
). Causation cannot be established through correlational analyses, but we hypothesize that the strong association between peak magnitudes shown here and by others (5
) may reflect a causal association. Because TAG clearance is largely dependent on a single saturable mechanism (lipoprotein lipase) (31
,57
,58
), the release of stored lipid (peak 1) by sensory stimulation would create competition for clearance of lipid absorbed from a fat-containing meal, thereby augmenting peak 2. Absorption of stored and recently ingested lipid would competitively reduce VLDL clearance and provide substrate for VLDL synthesis, resulting in a larger third peak. A portion of this VLDL is then transported to the lymph where it is available for release upon initiation of the subsequent eating occasion, especially one containing fat. Given this proposed sequence, additional attention to early events, such as meal timing, frequency and orosensory stimulation by fat may be warranted. Although only 33% of eating occasions contain >20 g of fat (59
), oral exposure to even small amounts may be adequate to promote or sustain an elevated serum TAG concentration.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: BMI, body mass index; EFA, essential fatty acid; TAG, triacylglycerol.
Manuscript received 10 June 2002. Initial review completed 5 July 2002. Revision accepted 5 September 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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