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Oral Stimulation Influences Postprandial Triacylglycerol Concentrations in Humans: Nutrient Specificity

Purdue University, West Lafayette, Indiana

Address reprint requests to: Thomas J. Tittelbach, Ph.D., Baltimore Veterans Affairs Medical Center, Geriatrics (18), 10 N. Greene Street, Baltimore, MD 21201-1524. E-mail: ttittelb{at}grecc.umaryland.edu.

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Objective: To determined whether the nature of the lipid in an oral stimulus modifies postprandial triacylglycerolemia.

Methods: Sixteen healthy adults (eight male, eight female) participated in six test sessions conducted weekly. The test sessions were administered randomly after overnight fasts and included: ingestion of 50 grams of butter in capsules (to avoid oral stimulation with lipids) and 500 mL of water in 15 minutes followed by oral stimulation with one of the following foods on a cracker: butter, unsaturated fatty acid (UFA) margarine, jelly, UFA margarine + jelly, cracker alone or no oral stimulation. Sensory stimulation entailed masticating and expectorating 5.0 g samples of each stimulus every three minutes for 110 minutes. Blood was drawn immediately after preload ingestion and at minutes 35, 85, 200, 320, and 440 post loading and analyzed for serum triacylglycerol (TAG), insulin and glucose concentrations.

Results: Only the oral samples containing the UFA margarine led to significant elevations of serum TAG concentration compared to baseline (p < 0.05). Maximum change of TAG concentrations were greater following orosensory stimulation with UFA margarine compared to orosensory stimulation with butter, jelly or UFA margarine + jelly. No differences were observed relative to vehicle alone or no orosensory stimulation, but this is due to lower nadir values for these treatments. Insulin and glucose concentrations were not different between treatments.

Conclusion: Oral exposure specifically to an unsaturated dietary lipid augments the postprandial rise of TAG, compared to baseline.

Key words: oral stimulation, triacylglycerol, dietary fat, postprandial period, human

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Electrophysiological studies demonstrate that long-chain cis-polyunsaturated fatty acids (PUFA) are effective taste stimuli in rats [1]. Behavioral studies suggest that rats select long-chain fatty acids based, in part, on olfactory and/or gustatory cues associated with the number and position of double bonds [2]. Saturated fatty acids (SFA) are not effective stimuli. The presence of a fatty acid transporter messenger RNA exclusively expressed in lingual tissue provides further support for a gustatory mechanism for lipid detection in rats [3].

In humans, consumption of low or high fat meals subsequent to the ingestion of a high fat meal elicits a significant augmentation of postprandial peak triacylglycerol (TAG) concentration [4,5]. Accumulating evidence suggests this may be initiated by a sensory property of the foods [6,7,8]. Sham feeding (which provides sensory stimulation without ingestion) a palatable meal several hours after ingestion of an retinal ester oil emulsion leads to an immediate increase in plasma retinal ester concentration suggesting an orosensory influence on lipid absorption [9]. More recent work indicates the sensory cue is a dietary fat. Oral exposure to lipid following ingestion of 50 grams of safflower oil in capsules leads to significantly higher peak TAG concentrations and a more prolonged TAG elevation compared to exposure with fat-replacers (e.g. passelli, simplesse and olestra) or primarily carbohydrate (CHO) based foods (e.g., potatoes, cracker) [6,7,8]. Whether oral stimulation with UFA or SFA differentially modulates postprandial TAG concentrations has not been determined in humans. Previous human studies have used primarily SFA as the oral stimulus. This study assessed whether the postprandial elevation in TAG concentration is influenced by the nature of the lipid in the oral cavity.

The mechanism by which oral lipid exposure influences postprandial TAG concentration is not known but likely involves an influence on lipid absorption. Oral stimulation without lipid loading does not elevate postprandial TAG concentration [8]. While there is evidence that this effect is differentially influenced by specific fatty acids in the oral cavity, the importance of the nature of the lipids in the gut has not been assessed. Previous controlled trials have used lipid composed of primarily PUFA. It is well known that saturation level modifies fatty acid absorption, but not whether oral stimulation influences the process. This trial tested responses with a primarily SFA gastrointestinal (GI) load. Further, questions about the importance of the interaction between the types of fatty acids used at both sites (i.e., oral and GI) have not been addressed. It may be hypothesized that, based on the specificity in responses to a given food throughout the GI tract, a greater TAG response would occur for matched oral and GI stimuli than mismatched samples. This study addressed this question by matching a GI load of primarily SFA rich lipid with oral stimuli composed of items rich in SFA, unsaturated fatty acid (UFA) and/or CHO.

CHO added to an oral lipid load amplifies the excursion of postprandial TAG [10,11,12,13,14]. Possible explanations for this response include differential rates of gastric emptying, stimulation of endogenous TAG synthesis or inhibition of TAG clearance. Test meal palatability also may contribute to discrepancies in postprandial triacylglycerolemia [15]. The role of orosensory stimulation with CHO on postprandial triacylglycerolemia was assessed in this study by contrasting the effects of oral stimuli matched for palatability but varying in sweetness and macronutrient composition.

Study of these issues is important because elevated postprandial TAG concentration is associated with a preponderance of potentially atherogenic, small, dense low-density lipoprotein-cholesterol and decreased high density lipoprotein-cholesterol particles [16,17,18,19,20]. Elevated postprandial TAG concentration is an independent risk factor for coronary artery disease [21,22,23]. The potential health impact is great because consumption of a typical Western diet leads to a sustained postprandial state [15] that may be enhanced by its orosensory characteristics.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
Subjects
Eight men and eight women were recruited through public advertisements. They were required to be in good health, 18 to 35 years of age, not using medication except oral contraceptives, exercising 3 days per week, body mass index (BMI) 19 to 28 kg/m² and non-smokers. Their mean ± SEM age was 23 ± 0.7 years and BMI was 22.2 ± 0.4 kg/m². Study procedures were approved by the Purdue University Committee on the Use of Human Research Subjects.

General Protocol
The study consisted of six randomized test sessions, identical in design but differing in the composition of the oral stimulus. Each treatment session was separated by at least one week. Subjects arrived in the laboratory between 0600 and 0700 hours after a 12-hour fast. On the day prior to each testing session, subjects were instructed to maintain their customary diet but abstain from alcohol and caffeinated beverages and exercise. Each treatment session included measurement of resting respiratory gas exchange (presented elsewhere), ingestion of 50 g powdered butter in 0.8 g capsules (to avoid oral stimulation with lipid) and 500 mL of water within 15 minutes, followed by a 110 minute period of intermittent oral stimulation. Subsequent to the oral stimulation period, subjects rested in a semi-supine position for an additional 330 minutes during which continuous gas exchange measurements and blood samples were collected.

Oral Stimuli
Oral stimulation was initiated at three minute intervals for 110 minutes. Stimulation entailed masticating the oral stimulus for 10 seconds and expectorating. Each oral stimulus consisted of 0.7 g of a cracker (Premium Fat Free Saltine Crackers, Nabisco, Inc., East Hanover, NJ), as a vehicle, with one of the following: butter, a rich source of saturated fatty acids (SFA; Sweet Cream Salted Butter, Land O’Lakes, Inc., Arden Hills, MN), unsaturated margarine (UFA; Lee Iacocca’s Olivio Vegetable Oil Spread, Nicola Corporation, Boston, MA), grape jelly, a carbohydrate source (CHO; Welch’s, Concord, MA) or unsaturated margarine plus jelly (UFA + CHO). Control conditions included vehicle alone (Veh) and no oral stimulation (NO). Twenty-six stimulus portions were prepared fresh the morning of testing and were served at room temperature. All samples were pre-weighed and expectorated samples were collected and weighted. In addition to aliquots of non-masticated stimuli, all expectorated samples were lyophilized to determine the amount of unaccounted (i.e. ingested and plate residual) stimuli. The weight and nutrient composition of the oral stimuli are presented in Table 1.

Sensory Testing
Subjects rated selected sensory properties of the oral stimuli after the first and last stimulus presentation on 9-point category scales. Overall opinion, appearance, creaminess, and flavor were rated on scales with end anchors of "extremely unpleasant" and "extremely pleasant." Taste qualities (sweetness, sourness, bitterness, saltiness), fat level, and aftertaste were rated on scales ranging from "extremely low" to "extremely high."

Hunger was assessed immediately before and after ingestion of the capsules, after the oral stimulation period and at the end of treatment using a 10 cm visual analog scale. The questions "how hungry do you feel right now?" "how full does your stomach feel right now?" and "how nauseous are you right now?" were anchored by "not (hungry, full, nauseous) at all" to "as (hungry, full, nauseous) as I’ve ever felt."

Statistical Analysis
All results presented are expressed as mean ± SEM. The effects of oral stimulation on TAG concentration, insulin and glucose concentration were assessed by repeated measures analysis of variance (ANOVA). The within-subject factors were the composition of the oral stimulus and time. To test if the responses were robust, rank-order tests were conducted. Maximum change of TAG concentration was determined by measuring the nadir to peak TAG response. Area under the curve (AUC) for changes in TAG concentration were computed by the trapezoidal method. One-sample and paired-samples t tests were conducted for post hoc comparisons where appropriate. The two hedonic ratings, given after the first and last oral stimulus presentation, were not significantly different from each other and were averaged to provide a mean hedonic rating during the oral stimulus period. The 9-point hedonic rating scale yields ordinal level data so a Friedman test was used to determine significant differences in hedonic ratings between treatments. A Wilcoxon rank-order test was used for post hoc comparisons. Bonferroni corrections were made when applicable. Statistical procedures were performed with the SPSS software package release 10.0.5 (SPSS Inc., Chicago, IL). The criterion for statistical significance was set at p < 0.05.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
The range of baseline TAG concentrations was 0.58–2.20 mmol/L. No significant difference in serum TAG concentration was observed immediately following lipid ingestion (used as baseline) across treatments. The change of serum TAG concentration over time associated with each study treatment condition is shown in Fig. 1. For all treatment conditions, except the UFA, a significant decrease in TAG concentration occurred at minute 35. At 85 minutes, exposure to SFA and NO produced TAG concentrations that remained significantly lower than baseline. Following oral exposure to the UFA and the UFA + CHO stimulus, serum TAG concentrations were significantly elevated over their baseline values at the 320 minute time point. UFA, CHO and NO conditions produced TAG concentrations that were significantly lower than baseline at the 440 minute time point. Thus, only the stimuli that contained UFA produced postprandial TAG concentrations significantly greater than their baseline. Rank-order tests indicated that differences were robust: 13 of 16 subjects for the UFA condition (p < 0.01) and 11 of 16 subjects for the UFA + CHO condition, with one tie (p < 0.05) had serum TAG concentrations greater than baseline at 320 minutes. Pooled standard error of the mean for change of postprandial TAG concentration was 16.2 mmol/L. Differences were not observed between the conditions containing UFA and vehicle alone or no orosensory stimulation.

View larger version (22K): [in this window] [in a new window]   Fig. 1. Mean change of serum TAG concentration from baseline. Letters indicate time points where TAG concentrations are significantly different from baseline. The gastrointestinal lipid load was given immediately prior to the first blood collection (minute 0). Oral stimulation occurred from minute 0 to 110. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle and NO = no oral stimulus.

View larger version (21K): [in this window] [in a new window]   Fig. 2. Mean ± SEM maximum change of postprandial triacylglycerol concentration. Significant differences across treatments are indicated by dissimilar letters at each time point.

View larger version (22K): [in this window] [in a new window]   Fig. 3. Mean change of serum insulin concentration from baseline. Letters indicate time points where insulin concentrations are significantly different from baseline. The gastrointestinal lipid load was given immediately prior to the first blood collection (minute 0). Oral stimulation occurred from minute 0 to 110. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle, and NO = no oral stimulus.

Ingestion of the capsules was well tolerated by the subjects. Ratings for nausea were not significantly different between treatments with a inter-treatment mean ± SEM of 1.3 ± 3.2, 1.9 ± 0.4, 0.9 ± 0.3 and 0.9 ± 0.3 cm on a 10 cm scale for nausea ratings before capsule ingestion (-15 min), after capsule ingestion (0 min), after orosensory stimulation (110 min) and at the end of the session (440 min), respectively. No significant differences were observed between treatments for hunger ratings at baseline. Hunger increased significantly over time (F(7,91) = 21.8, p = 0.000) after capsule ingestion in a similar pattern for all treatments, Fig. 4.

View larger version (16K): [in this window] [in a new window]   Fig. 4. Hunger ratings were assessed using a 10 cm visual analog scale at -15 (before capsule ingestion), 0 (after capsule ingestion), 110 (after orosensory stimulation) and at 440 (end of session) minutes. Subjects were asked "how hungry do you feel right now?". Oral stimulation occurred from minute 0 to 110. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle and NO = no oral stimulus.

	DISCUSSION

 
A significant increase of postprandial TAG concentrations occurred only when the oral stimulus contained the UFA, when compared to baseline. The predominantly SFA stimulus (butter), CHO stimuli (jelly and cracker) and the no oral stimulus control did not promote increased TAG concentrations at any time postprandially. The oral stimuli were not ingested, suggesting the UFA effect was attributable to its orosensory stimulation. The UFA and UFA + CHO oral stimuli contained a six- and threefold greater quantity, respectively, of PUFA compared to SFA, CHO, Veh and NO conditions. The most parsimonious explanation for the observed differential responses is provided by rat studies that indicate selected lipids are detected in the oral cavity via a gustatory mechanism [1,24,2]. Gilbertson et al. [1] have shown that long-chain cis-PUFA inhibit delayed-rectifying K⁺ channels in taste receptor cells. SFA have no significant effect in rats. Although not significantly different, Gilbertson et al. [1] reported a trend for an indirect relationship between free fatty acid saturation and the rapidity and potency of effect on the K⁺ current. Tsuruta et al. [2] found that rats select long-chain PUFA (including mono-UFA) from gustatory and/or olfactory cues. Whether these mechanisms for lipid detection occur in humans has yet to be determined, but preliminary evidence from prior work and this study support a gustatory component for dietary lipids [8]. The present finding of a significant rise only with the UFA stimuli is consistent with the reported fatty acid specificity noted in rats [1].

Although the relative increase in postprandial TAG concentration was small (0.29 and 0.16 mmol/L 320 minutes post-loading compared to baseline for UFA and UFA + CHO, respectively), it cannot be dismissed as inconsequential. Dubois et al. [25] have shown that relatively small changes in postprandial triacylglycerolemia (0.21 mmol/L) are capable of altering the composition and concentration of high-density lipoproteins and low-density lipoproteins. The peak and duration of the postprandial TAG response between oral stimuli were not significantly different, due in large part to the large inter-individual variation which is characteristic of human postprandial responses [26]. TAG concentrations expressed as maximum change were significantly greater during UFA compared to SFA, CHO and UFA + CHO conditions, but were similar to Veh and NO conditions. Maximum TAG concentrations are determined by taking the mean difference from nadir to peak TAG concentration. The similarity in maximum change of TAG concentration values for UFA and control conditions occurred because the nadir TAG concentrations were lower for the Veh (-0.33 mmol/L) and NO (-0.34 mmol/L) conditions relative to the SFA, CHO and UFA + CHO conditions (-0.27, -0.29, and -0.29 mmol/L, respectively). This produced a larger maximum change of TAG concentration for the Veh and NO conditions, even though their peak TAG concentrations were only 0.11 and 0.05 mmol/L, respectively, compared to the UFA peak TAG concentration of 0.29 mmol/L.

Textural properties of dietary lipids are regarded as the primary cue for their discrimination [27]. Electrophysiological tests in rhesus macaques indicate that texture alone is a sufficient stimulus as paraffin and silicone (chemically different from dietary lipids, but with similar textural properties) are effective stimuli [28]. However, it is unlikely the response observed here is attributable to the textural properties of the oral lipid stimuli since discrepant TAG concentrations were observed between oral stimuli comparable in texture (SFA and UFA). Other studies have also failed to note differential responses to stimuli closely matched on texture [6,7]. Further support for a non-textural oral cue is provided by Mela et al. [29], who demonstrated that solutions of PUFA are rated higher in fat compared to SFA solutions when matched for texture. In the present study, palatability can not account for these differences as subjects rated the oral stimuli equally palatable. Cognitive influences can not be ruled out as subjects discriminated between the oral stimuli, and cognitive cues have been shown to influence several cephalic phase responses in humans [30,31]. However, a previous human study using fat-free and fat-containing versions of the same food, closely matched on sensory properties, led to discrepant TAG responses [6]. Thus a cognitive influence is not necessary for the effect.

Previous human studies investigating the effect of oral lipid stimulation on postprandial TAG have used an oral stimulus and GI load that were not matched for nutrient composition [32,6,7,8]. In particular, the effective oral stimulus in previous studies was butter or cream cheese (sources of primarily SFA), while the GI load contained capsules composed entirely of safflower oil (source of primarily PUFA) [6,7,8]. The present study used butter as the oral stimulus and capsules of butter for the GI load. Based on a hypothesis of specificity in responses to a given food throughout the gastrointestinal tract, a greater TAG response was expected for matched oral and GI stimuli than mismatched samples. However, the postprandial TAG concentrations to matched stimuli were no different from NO stimulation or Veh treatments and were lower than responses to the mismatched pair of UFA (oral) and SFA (GI). Given the stronger effect of UFA oral stimuli, the possibility of a greater postprandial TAG response for a UFA oral and GI pairing warrants evaluation.

The smaller postprandial TAG response observed here compared to previous studies [6,7,8] may be due to differences in the GI load used. The gastric load used in previous studies contained primarily PUFA (safflower oil is approximately 70% linoleic acid and 10% linolenic acid). This study used capsules of powdered butter which contained approximately 62% saturated fatty acid [33]. ¹³C-labelled fatty acid tracer studies have determined that absorption of saturated fatty acids are poor (78%) in comparison to the almost complete absorption of unsaturated fatty acids (99.9%) [34,35,36]. Butterfat contains primarily long-chain SFA (myristic, palmitic and stearic acids) [37]. In rats, butterfat absorption is 55% lower than safflower oil [38]. Thus, the lower absolute level of response between this study and previous work in humans may be due to poor absorption of the GI load. In fact, the change of TAG concentration was significantly lower than baseline at 35 minutes in this study using butter as the GI load compared to similar studies using safflower oil, where the 35 minute TAG concentration was not different from baseline [7,8]. It is also plausible that the differences are due to varying rates of TAG clearance, as the degree of saturation and fatty acid chain length may affect lipoprotein lipase activity [39,40].

There was no effect of oral stimulation with the CHO stimuli on the postprandial TAG concentration. This lack of response is in agreement with a previous study, indicating that sweetness alone is not responsible for the elevation in postprandial triacylglycerolemia in humans [41]. An effect of oral stimulation with the UFA + CHO condition on postprandial TAG concentration was observed. However, the response is likely due to the effects imparted by the UFA margarine rather than the jelly as the oral stimulus containing only jelly had no effect.

We did not measure TAG-rich lipoprotein fractions. Abia et al. [42] has shown that two oils similar in mono-UFA composition produced equal TAG plasma concentrations, but different TAG-rich lipoprotein responses, during the postprandial period, suggesting that determination of postprandial total TAG concentrations can be misleading when assessing the health implications of postprandial triacylglycerolemia. Thus, the health implications of this phenomenon warrant further characterization.

	CONCLUSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
These data add to a growing body of evidence indicating that lipid is detected in the oral cavity and alters postprandial triacylglycerolemia. Consistent with electrophysiological data in rats, these finding indicate UFA may be especially effective oral stimuli. The effect of oral stimulation on postprandial TAG concentration may be greatest if the oral stimulus and GI lipid load are both UFA, possibly due to its stronger gustatory effect and more efficient absorption. Given the association between postprandial TAG concentration and atherogenesis, continued study of this issue is warranted.

	ACKNOWLEDGMENTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 
The authors would like to thank Dana Wislocki for her assistance in the conduct of this study.

Received March 19, 2001. Accepted August 9, 2001.

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TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS CONCLUSION ACKNOWLEDGMENTS REFERENCES

 

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