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Articles

Oral Exposure to Butter, but Not Fat Replacers Elevates Postprandial Triacylglycerol Concentration in Humans¹

Purdue University, Department of Foods and Nutrition, W. Lafayette, IN 47907-1264

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Oral exposure to dietary fat augments the postprandial triacylglycerol (TAG) concentration. We investigated the TAG response after oral exposure to butter and selected fat replacers. At 2200 h, 17 healthy adults consumed 80 g of almonds and fasted until 0700 h. Safflower oil (50 g in 1-g capsules) was then consumed. Oral stimulation was provided periodically for 2 h as potatoes, potatoes containing butter or one of three fat replacers or no oral stimulation in random order at weekly intervals. Blood was collected at stipulated intervals for 8 h. Oral exposure to butter led to a significantly longer postprandial TAG elevation than the other treatments. The results could not be explained by differential stimulus ingestion, palatability or perceived fat content. There was no significant treatment effect on concentrations of serum oleic acid, apolipoprotein (apo)B-48 or apoB-100, suggesting any oral exposure influence on release of dietary lipid stored in the lacteals or chylomicron and VLDL particle number contributed little to the postprandial TAG rise. In summary, oral exposure to butter elicited a greater postprandial TAG elevation than the tested fat replacers, possibly due to reduced TAG clearance.

KEY WORDS: • fat • oral • lipid • taste • humans

	INTRODUCTION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Numerous studies indicate that the postprandial serum triacylglycerol (TAG)² concentration is an independent risk factor for coronary heart disease (CHD) and myocardial infarction (1 2 3 4 5) . If not directly related, it remains a powerful predictor due to its correlation with other lipid fractions (6) . Nonpharmacologic means to reduce CHD risk involve moderation of fat consumption (7) . Dietary recommendations typically focus on total fat consumption and the proportional intake of saturated, monounsaturated and polyunsaturated fatty acids (PUFA). Less attention has been paid to eating frequency.

The number of eating occasions may be critical because after fat ingestion, the serum TAG concentration is elevated for 2–6 h. Thus, a high meal frequency may result in a continuously high TAG concentration throughout the day. Estimates of eating frequency vary based on the definition of meals and snacks, but generally range from 3.5 to 5.3 times per day for men and 3.4 to 4.9 times per day for females (8 9 10 11) . On the basis of the first National Health and Examination Survey data, a majority of Americans eat five or more times per day (10) . Most eating occasions include 18–30 g of fat (12) and those that contain as little as 0.2 g/kg elicit a significant elevation of serum TAG (13) .

Moderation of total and saturated fat intake can ameliorate the peak postprandial TAG concentration and its duration (13 ,14) . Such advice is a key component of the nonpharmacologic management of CHD risk. One approach to implementing these changes is to substitute fat-modified products for their full-fat counterparts. When this entails consumption of products containing fat replacers, less fat will be ingested, but the sensory impression may closely mimic that experienced with the full-fat version. The implications are uncertain, given evidence that oral exposure to dietary fat significantly increases the postprandial TAG concentration (15) . The effective stimulus (i.e., taste, odor or texture) has not been determined. If it is a chemosensory signal, differences among fat replacers comprised of protein, fat or carbohydrate would be predicted, whereas if texture is the primary cue, well-matched replacers should lead to comparable effects. By contrasting the postprandial TAG stimulating effects of selected, widely used fat replacers with butter, this study sought to gain insights into the effective stimulus and the public health implications of fat replacer use. The present study was not designed to establish the mechanism(s) underlying the effect of oral fat exposure on postprandial TAG concentrations, but initial insights were sought to direct future studies.

	SUBJECTS AND METHODS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
General protocol.

Testing sessions were conducted 1 d/wk for 6 wk. At 2200 h the night before each session, participants were instructed to consume a load of 80 g of almonds and to refrain from all food and beverages until arrival at the laboratory at 0700 h the next morning. The aim was to provide a palatable load with a high concentration of oleic acid. An 80-g portion of almonds contains 28.6 g monounsaturated fatty acid, 8.6 g PUFA and 4.3 g saturated fatty acid (16) . Upon arrival, blood was collected by venipuncture. The subjects then ingested 50 g safflower oil in 1-g capsules with 300 mL of water in 10 min. This load, which was rich in linoleic acid, was provided to determine whether any noted change in postprandial TAG was attributable to release of lipid stored from the previous meal or absorption of the present load. This approach was used successfully in earlier trials (17) . A second blood sample was drawn 20 min later. Oral stimulation was initiated immediately after the second blood draw and occurred at 3-min intervals for 60 min and 15-min intervals for an additional 60 min. Stimulation entailed masticating a given stimulus for 10 s and expectorating. Different stimuli were provided each week in a random order. They included potatoes alone, potatoes containing either butter or one of three fat replacers or no oral stimulation. Additional blood samples were collected 2.5, 4.5, 6.5 and 8.5 h after baseline. After the initial and final exposure to each oral stimulus, ratings were obtained on an array of their sensory attributes. The protocol was approved by the Purdue University Committee on the Use of Human Research Subjects.

Subjects.

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, fasting serum TAG concentration between 0.56 and 2.82 mmol/L and no donation of blood in the preceding 3 mo. A total of 23 individuals were recruited. A complete set of data were obtained for 20 subjects. After a review of baseline TAG concentrations, it was determined that three participants had not adhered to the protocol (i.e., had eaten on one or more test mornings before arrival). The present report is based on the remaining 17 participants (2 men and 15 women). Their mean age (± SEM) was 28.5 ± 1.9 y and mean body mass index (BMI) was 26.1 ± 1.4 kg/m² (2 overweight and 3 obese participants based on cut-off values of 25 and 30 kg/m², respectively).

Oral stimuli.

Mashed potatoes served as the vehicle for delivery of the primary oral stimulants and were tested as one control condition. The potatoes were prepared by adding 12.5 g of Potato Buds (General Mills, Minneapolis, MN) to 50 g of boiling water and stirring until smooth. Imitation butter flavor (10 µL/5 g of prepared potatoes; Durkee, Buffalo, NY) was then added. Samples were prepared to have comparable textural characteristics. The butter stimulus was comprised of the potatoes with 50 g of unsalted butter (Land O Lakes, Arden Hills, MN) added to the water before heating. Three additional stimuli were prepared with fat replacers comprised primarily of different macronutrients. The carbohydrate-based replacer was Passelli (Avebe America, Princeton, NJ). A Passelli gel was made first by adding 30 g of Passelli to 70 g of water, blending for 60 s and refrigerating overnight. To prepare the sample, 41.5 g of the gel was added to the prepared potatoes (16.5 g potato buds and 50 g water). The protein-based replacer was Simplesse (Nutrasweet, San Diego, CA). The sample was made by adding 20 g of potato buds to 50 g of boiling water and adding 45 g of a 30 g/100 g Simplesse solution. Olestra (Procter & Gamble, Cincinnati, OH) served as the fat-based fat replacer. Olestra (20 g) was added to potatoes (prepared as the vehicle alone) and mixed until smooth. The final condition involved no oral stimulation. The macronutrient composition of the oral stimuli are presented in Table 1 . Stimulus portions (5-g portions; n = 23) were prepared fresh the morning of testing, but were served at room temperature. In addition to aliquots of nonmasticated stimuli, all expectorated samples were collected, lyophilized and weighed to determine the amount of unaccounted for (i.e., ingested) stimuli.

The linoleic and oleic acid levels in serum and potato samples (fresh and expectorated) were assayed by gas chromatography. Lipid was extracted from the appropriate samples and transmethylated using 1 mol/L sodium methoxide in methanol/benzene (60:10, v/v) as described by Glass (18) . The analysis of the fatty acid composition was carried out using a Hewlett-Packard gas chromatograph, model 5830A with a 6-ft column of 10% SP-2300 on 80/100 Supelcoport (Supelco, Bellefonte, PA). Apolipoprotein (apo)B-48 and apoB-100 were quantified by enhanced chemiluminesence Western blotting analysis using the methods recommended by the manufacturer (Amersham Pharmacia Biotech., Piscataway, NJ). Briefly, 2-µL plasma samples were separated by electrophoresis on a 6% SDS polyacrylamide gel. The proteins separated were then electrotransferred onto a nitrocellulose membrane. Nonspecific binding sites on the membrane were blocked by incubation overnight in Tris-buffered saline containing 50 g/L nonfat milk powder. The actual incubation with the primary and secondary antibodies and the washes in between the incubation with antibodies were conducted according to the procedure suggested by the manufacturers. Rabbit anti-rat apoB was used because it showed greater specificity than commercially available anti-human apoB serum on the basis of the Western blot. An apoB standard curve was constructed using human apoB isolated from serum LDL; linear regression gave a correlation coefficient of 0.99. The assay is sensitive enough to detect 0.1 µg apoB (samples ranged from <0.15 to >5.4 µg/L) and had an interassay variability of 10%.

Sensory testing.

Participants rated 5-g portions of each stimulus in duplicate on 9-point category scales. For taste qualities, end anchors ranged from, "No (sweetness, saltiness, sourness, bitterness) at all" to "Extremely (sweet, sour, salty, bitter)." Fat level and creaminess were rated from "None at all" to "Extremely high"; appearance, flavor, aftertaste and overall opinion were rated between "Extremely unpleasant" and "Extremely pleasant." A water rinse was interspersed between samplings.

Statistical analyses.

The data were used to test two principal hypotheses. The first, based on earlier findings, was that oral stimulation elevates the postprandial TAG concentration. This was tested by comparing TAG responses after exposure to the various oral stimuli with responses measured without oral stimulation. Second, to establish whether fat is the only or the most effective oral stimulus, comparisons were made between TAG responses to butter exposure relative to the other oral stimuli. Repeated measures ANOVA, followed by paired t-tests for post-hoc comparisons, was used to examine oral stimulus effects on serum TAG, fatty acid and lipoprotein concentrations, sensory responses and potato fatty acid concentrations. Indices of TAG status included peak increase after loading, duration of elevation relative to baseline and area under the curve (AUC) determined by the trapizoidal rule. The binomial test was used to determine whether a higher proportion of subjects showed a greater TAG response after butter exposure than after the other treatments. An association between stimulus sensory characteristics and serum TAG response was explored by correlation analysis. The criterion for statistical significance was set at P < 0.05.

	RESULTS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Repeated-measures ANOVA indicated that there was a significant treatment effect (P = 0.024) on TAG during the 8 h after lipid loading and oral stimulation (Fig. 1 ). Only exposure to butter led to a significant postprandial TAG elevation relative to that after no oral stimulation. Further, exposure to the butter sample resulted in a significantly greater AUC than exposure to the samples containing Simplesse or Olestra. Although not significantly different, the AUC after butter exposure were more than double those after exposure to potato only (P = 0.11) or Passelli (P = 0.16). Similar findings were obtained in an analysis based on the percentage of change from baseline. In addition, only the TAG AUC after butter exposure was significantly elevated relative to baseline.

View larger version (24K): [in this window] [in a new window]   Figure 1. Area under the curve triacylglycerol (TAG) concentrations >8 h after lipid loading and oral stimulation with potatoes alone, potatoes with butter, Simplesse, Passelli or Olestra or no oral stimulation. Values are means ± SEM, n = 17. On the basis of a repeated-measures ANOVA, with paired t-tests used for post-hoc comparisons, the value after butter exposure was significantly greater than values after no oral stimulation or stimulation with Simplesse or Olestra (all P < 0.05, marked with an asterisk). The pooled SEM = 14.20. No other treatment differed significantly from no oral stimulation. Only the value after butter exposure was significantly >0.

View larger version (24K): [in this window] [in a new window]   Figure 2. Change of serum triacylglycerol (TAG) from baseline after lipid loading and oral stimulation with potatoes alone, potatoes with butter, Simplesse, Passelli or Olestra or no oral stimulation. Values are means ± SEM, n = 17. Letters indicate time points at which TAG concentrations are significantly (P < 0.05) different from baseline (based on repeated-measures ANOVA with paired t-tests used for post-hoc comparisons). Filled squares along the bottom x-axis indicate the timing of blood draws.

There were no consistently significant effects of baseline TAG concentration or BMI on serum TAG treatment responses. BMI was significantly correlated with TAG response only after oral exposure to Simplesse (r = 0.7, P < 0.01). A lack of association with baseline TAG may reflect the narrow range of concentrations in participants due to study eligibility criteria.

Serum linoleic and oleic acid levels were monitored in four individuals after exposure to all treatments (Fig. 3 ). Two had the largest TAG responses to butter stimulation and the other two had the smallest responses. Although there was a significant time effect (P = 0.032), there was no significant treatment effect or a treatment by time interaction for oleic acid. Thus, oral stimulation did not alter the serum oleic acid concentration at the sampled time points. The time effect was much stronger and significant for linoleic acid (P < 0.001). In addition, there was a significant treatment effect (P = 0.035) in which butter exposure led to a significantly higher concentration relative to Passelli (P = 0.034), Simplesse (P = 0.031) and a trend for a higher level compared with Olestra (P = 0.066). There was only a trend for a treatment by time interaction (P = 0.096).

View larger version (24K): [in this window] [in a new window]   Figure 3. Serum linoleic and oleic acid concentrations after lipid loading and oral stimulation with potatoes alone, potatoes with butter, Simplesse, Passelli or Olestra or no oral stimulation. Values are means ± SEM, n = 4. The pooled SEM for the linoleic and oleic acid data were 13.26 and 11.02, respectively. On the basis of a repeated-measures ANOVA, with paired t-tests used for post-hoc comparisons, butter exposure led to a significantly higher concentration relative to Passelli (P = 0.034), Simplesse (P = 0.031) and a trend for a higher level compared with Olestra (P = 0.066).

Only a small amount of each stimulus was not recovered in the expectorated samples. It is presumed that this amount may have been ingested, although some loss was due to the residual left on the spoon and serving plate. Dry weights were 7.4 ± 1.8 g, butter; 4.8 ± 0.9 g, potatoes only; 4.3 ± 1.6 g, Olestra; 1.0 ± 1.1 g, Passelli; and 4.8 ± 1.2 g, Simplesse. Repeated-measures ANOVA indicated there was a treatment difference (P = 0.014) in which the loss was lower for Passelli than butter, Simplesse or Olestra. Butter was not significantly different from the others.

The concentrations of linoleic acid and oleic acid in the expectorated stimuli from the full study sample are presented in Figure 4 . The butter sample contained significantly more linoleic acid than the samples containing Passelli or Simplesse (P = 0.015) and significantly more oleic acid than any of the other samples (P < 0.001). With the exception of Passelli vs. Simplesse for oleic acid, the other samples did not differ significantly from each other.

View larger version (48K): [in this window] [in a new window]   Figure 4. Linoleic and oleic acid concentrations in expectorated stimuli samples after lipid loading and oral stimulation with potatoes alone, potatoes with butter, Simplesse, Passelli or Olestra or no oral stimulation. On the basis of a repeated-measures ANOVA, with paired t-tests used for post-hoc comparisons, fatty acid concentrations marked with an asterisk are significantly (P < 0.05) different from concentrations after butter exposure. Values are means ± SEM, n = 17.

View larger version (28K): [in this window] [in a new window]   Figure 5. Ratings of perceived fat content of the orosensory stimuli obtained after the initial and final exposure during a test session. Values are means ± SEM, n = 17. On the basis of a repeated-measures ANOVA, with paired t-tests used for post-hoc comparisons, the samples containing butter and Olestra were rated as significantly (P < 0.001) higher in fat than the other samples and did not differ from one another.

	DISCUSSION

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

The results cannot be ascribed to differential ingestion of the various stimuli. Analysis of the expectorated samples indicated very little of any stimulus was lost (i.e., swallowed) during exposure. The samples were rated as comparably pleasant; thus palatability was not a factor. The butter and Olestra samples were rated as higher in fat content, but they led to the most divergent TAG responses. All other sensory ratings were comparable across stimuli after both the initial and final exposures. Cognitive effects were minimized because participants were not informed of the true purpose of the study or nature of any sample. In addition, no influence of baseline TAG concentration (within the narrow range studied) or BMI was detected.

The present work was not designed to elucidate the mechanisms underlying an effect of oral fat exposure on TAG concentration, but preliminary insights may be gleaned from the literature and our data. The first issue concerns the sensory attributes of dietary fat that serve as the effective initial stimulus. Data were collected pertaining to the taste of the fat, but olfactory and tactile properties are other possible candidates. A linoleic acid concentration of 10 µmol/L is sufficient for taste receptor cell depolarization in rats (23) . The linoleic acid concentration of the expectorated samples from our participants, which presumably reflect concentrations in the mouth, were highest for butter, but were >200 µmol/L for all stimuli. Thus, if the sensitivity of humans and rats are comparable, this would not explain the observed differential TAG responses. The oleic acid concentration of expectorated samples was markedly higher after butter stimulation relative to the other stimuli. This fatty acid does not depolarize taste receptor cells in rats at 10 µmol/L (23) but is detectable by some orosensory cue at 35 µmol/L (24) . Again, if rats are a good model for human sensitivity, all stimuli led to suprathreshold oleic acid concentrations, and this would not explain the differential TAG responses. However, if humans have a detection or effect threshold between 250 µmol/L and 1 mmol/L, this fatty acid could serve as an initiating signal. Additional testing will be required to determine whether humans possess an oral chemosensory detection system for oleic acid.

It has been posited that oral stimulation reduces gastric emptying, thereby facilitating more efficient lipid digestion (20) . Consistent with this view, recent evidence in humans documents slower gastric emptying during oral stimulation with fat (25) , and modified sham-feeding stimulates gastric lipase secretion and activity (26 ,27) . However, absorption of safflower oil is nearly complete (28) ; thus, these actions likely influence only chylomicron packing and the kinetics of fat absorption. The similarity in apoB-48 concentrations after butter and Olestra exposure suggests that they did not lead to discrepant chylomicron particle numbers. Stored fat in the lacteals may be released and add to the load entering the blood, but fat from this source is cleared within 2 h (17) and the maximal effect noted here occurred 6 h poststimulation. The timing of blood sampling in the present protocol precluded identification of the first peak in TAG concentration, but confirmed that release of preformed chylomicrons does not contribute substantially to the TAG rise 2–8 h postprandially. There was no differential treatment effect on serum oleic acid levels, and participants had consumed 80 g of almonds, a rich source of this fatty acid, in the meal before testing. Together, these observations suggest that an oral exposure influence on absorption alone does not account for the present findings.

Hepatic TAG synthesis and release as VLDL may contribute to the rise. A cephalic phase release of pancreatic polypeptide (PP) has been demonstrated in humans (29 30 31) and is positively related to the fat content of an oral stimulus (29) . In vitro studies with rats indicate that PP enhances hepatic TAG synthesis and release (32) . The absence of a marked rise in apoB-100 concentration after oral stimulation with butter or a differential response relative to Olestra stimulation suggests that an increase in VLDL particle number was not a factor in the present study. Secretion of more lipid-rich VLDL may have occurred and would not have been detected using apoB-100 as a marker. After fat loading, the greatest increment in VLDL occurs in the subcellular fraction 60–400 apoB-100 fraction (33) . Further, studies in rats suggest that acute dietary challenges that promote postprandial lipemia do so by increased VLDL mass, whereas chronic manipulations result in greater particle number (34) . Assessment of VLDL mass may prove revealing in future human studies of this issue.

The fact that the divergence of serum TAG concentrations was greatest 6 h postloading suggests that orosensory stimulation with fat may influence TAG clearance. A reduction of adipose tissue lipoprotein lipase (ALPL) activity seems unlikely. Indeed, oral stimulation with fat elicits a cephalic phase insulin response in humans (35) and, in rats, this prompts a proportional activation of ALPL (36) . Current studies are exploring this mechanism in humans. Additionally, given the strong correlation between LPL activity and 18:2 free fatty acid concentration (37) , our data on serum18:2 free fatty acid indicate that oral exposure to butter did not suppress ALPL activity, nor did Olestra raise it. Alternatively, the late TAG elevation could be attributable to less efficient clearance due to alterations of TAG-rich particles. In rats, lipid loading after food deprivation results in large chylomicron particles with little effect on particle number (38) . This could be promoted by a sensory influence on gastric lipolysis and emptying as noted above. With a relatively constant particle number, these large particles would be cleared more slowly (39) .

In summary, the present findings provide further evidence that oral fat exposure augments the postprandial TAG concentration. This was not true of the fat replacers tested. Thus, in addition to aiding with moderation of fat and energy intake when replacing dietary fat, these products may have favorable effects on postprandial lipid metabolism. The nature of the chemosensory signal that initiates processes leading to an augmented postprandial TAG concentration and its site and mode of action remain uncertain. We hypothesize that an orosensory cue from dietary fat promotes formation of large chylomicron and VLDL particles that are cleared more slowly. With accumulating evidence that the postprandial TAG concentration is an independent risk factor for coronary heart disease (3 ,40) , further study of this issue is warranted.

	ACKNOWLEDGMENTS

 
The author would like to thank Leslie Bormann and Carrie Thunberg for their assistance in the conduct of this study and Patrick Tso for free fatty acid and apoB analyses as well as thoughtful insights. The author would also like to thank Avebe America for donating the Passelli, Nutrasweet for donating the Simplesse and Procter & Gamble for donating the Olestra.

	FOOTNOTES

 
¹ Supported by grant DK45294 from the U.S. Public Health Service.

² Abbreviations used: ALPL, adipose tissue lipoprotein lipase; apo, apolipoprotein; AUC, area under the curve; BMI, body mass index; CHD, coronary heart disease; PP, pancreatic polypeptide; PUFA, polyunsaturated fatty acids; TAG, triacylglycerol.

Manuscript received December 1, 2000. Initial review completed January 4, 2001. Revision accepted February 26, 2001.

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