Effect of orosensory stimulation on postprandial thermogenesis in humans

Physiology & Behavior 75 (2002) 71 – 81

Effect of orosensory stimulation on postprandial thermogenesis in humans Thomas J. Tittelbach*, Richard D. Mattes Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907, USA Received 23 May 2001; received in revised form 8 August 2001; accepted 17 September 2001

Abstract This study assessed the effects of orosensory stimulation by equipalatable stimuli that differed in macronutrient content (lipid and carbohydrate) on postprandial thermogenesis. Sixteen healthy, normal-weight adults (eight males, eight females) participated in six test sessions conducted weekly. The test sessions were administered randomly after overnight fasts and included: ingestion of 50 g of butter in capsules (to avoid oral stimulation with lipids) and 500 ml of water in 15 min followed by no oral stimulation or oral stimulation with a cracker or one of the following foods on a cracker—butter, unsaturated fatty acid (UFA) margarine, jelly, UFA margarine + jelly. Sensory stimulation entailed masticating and expectorating
5.0 g samples of each stimulus every 3 min for 110 min. Blood was drawn immediately after preload ingestion and at minutes 35, 85, 200, 320, and 440 postloading and was analyzed for insulin, glucagon, and glucose. No significant treatment differences were observed for thermogenesis or oxidation of carbohydrate or lipid. Insulin, glucagon, and glucose concentrations were not different between treatments. These data suggest that orosensory stimulation with stimuli differing in lipid and carbohydrate content, but rated similarly in palatability, does not elicit an increased or differential diet-induced thermogenic response. D 2002 Elsevier Science Inc. All rights reserved. Keywords: Cephalic phase; Thermogenesis; Postprandial; Thermic effect of food; Diet-induced thermogenesis; Energy expenditure; Human

1. Introduction Diet-induced thermogenesis (DIT) can be partitioned into two phases. The first phase, cephalic phase thermogenesis (CPT), refers to the loss of metabolizable energy as heat due to cognitive, olfactory, and gustatory stimulation provided by feeding [1]. It is estimated to account for 30 –53% of DIT [2]. CPT has been documented in animal [3– 5] and human [2,6,7] studies. The second phase, termed gastrointestinal phase thermogenesis, is defined as the energy required for digestion, absorption, metabolism, and storage of nutrients [8]. Several diet-related effectors of thermogenesis have been investigated, including carbohydrates [9– 12], proteins [13 – 15], lipids [16 – 18], and dietary fibers [19,20], as well as properties associated with meal size [21], food consistency * Corresponding author. University of Maryland Baltimore, Baltimore VAMHCS, 10 North Greene Street (BT/GR/18), Baltimore, MD 212011524, USA. E-mail address: [email protected] (T.J. Tittelbach).

[22], and palatability [23 – 26]. However, the specific sensory properties of foods that may elicit DIT are not well characterized. Meal palatability has been shown by some authors [14,25,27] to increase DIT, whereas others have not observed an effect [26,28]. The taste of monosodium glutamate, proposed to signal the presence of proteins [29], elicits a small, but measurable, increase in DIT when added to a meal [15]. Sweet taste has not been reported to effect DIT, but discrepancies in thermogenesis between aspartame (a high-intensity/low-energy sweetener) and sucrose suggest a substrate effect [30]. Oral chemical irritation may also elicit DIT, as ingestion of a meal containing capsaicin increases thermogenesis [31]. The objective of this study was to assess the effects of orosensory stimulation by equipalatable stimuli that differed in macronutrient content (lipid and carbohydrate) on DIT in normal-weight, young adults. Investigation into the possible role that macronutrients have on orosensory-induced thermogenesis is warranted as even small changes in energy expenditure, over time, can lead to positive energy balance and increased body weight.

0031-9384/02/$ – see front matter D 2002 Elsevier Science Inc. All rights reserved. PII: S 0 0 3 1 - 9 3 8 4 ( 0 1 ) 0 0 6 4 4 - 8

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2. Materials and methods 2.1. Subjects Sixteen (eight men and eight women) nonsmoking, healthy, adults aged 18 – 35 years were recruited through public advertisements. They were required to have a body mass index (BMI) of 19 – 28 kg/m2, to exercise  3 days per week, and not use medication except oral contraceptives. Subject characteristics are presented in Table 1. Study procedures were approved by the Purdue University Committee on the Use of Human Research Subjects. 2.2. General protocol The study consisted of six randomized test sessions differing only in the composition of the oral stimulus and were separated by at least 1 week (Fig. 1). On the day preceding each treatment session, participants were instructed to maintain their customary diet, but abstain from alcohol, caffeinated beverages/foods, and exercise. Each experimental session included measurement of resting respiratory gas exchange, ingestion of 50 g of powdered butter (1661.5 kJ, 15.3 g of protein, 7.4 g of carbohydrate, and 35.7 g of lipid; determined by package label) in 0.8 g capsules (to avoid oral stimulation with lipid) and 500 ml of water within
15 min, followed by a 110-min period of intermittent oral stimulation. Oral stimulation occurred at 3-min intervals during a 110-min period for a total of 26 individual oral exposures. An oral exposure consisted of one oral sample that was masticated for 10 s and expectorated. The oral samples were prepared fresh in the morning of testing and were served at room temperature. Subsequent to the oral stimulation period, subjects rested in a semisupine position for an additional 330 min, during which respiratory gas exchange measurements and blood samples were collected. 2.3. Oral samples The weight and nutrient composition of the oral samples are presented in Table 2. Each oral stimulus consisted of 0.7 g of a cracker (Premium Fat Free Saltine Crackers; Nabisco, 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, Arden Hills, MN), primarily unsaturated fatty acid margarine (UFA) (Lee Iacocca’s Olivio Vegetable Oil Spread; Nicola, Boston, MA), grape jelly, a sweet carbohydrate source Table 1 Subject characteristics Subject

Age (years)

Height (cm)

Weight (kg)

BMI (kg/m2)

Fat mass (%)

Male (n = 8) 23.4 ± 1.6a 184.4 ± 2.4 76.7 ± 4.4 22.4 ± 0.9 16.3 ± 1.5 Female (n = 8) 21.6 ± 0.8 164.7 ± 2.3 58.1 ± 1.7 21.5 ± 0.7 29.4 ± 1.6 a

Mean ± S.E.M.

Fig. 1. Study protocol: PQ, palatability questionnaire; Blood, blood draw; HQ, hunger questionnaire; EE, measurement of energy expenditure and substrate utilization; OS, period of oral stimulation; Load, ingestion of butter capsules.

(CHO; Welch’s, Concord, MA), or primarily UFA margarine plus jelly (UFA + CHO). Additional conditions included vehicle alone (Veh) and no oral stimulation (NO). All samples were preweighed, and expectorated samples were collected. In addition to aliquots of nonmasticated stimuli, all expectorated samples were lyophilized to determine the amount of unaccounted (i.e., ingested and plate residual) stimuli. In a pilot study (n = 7), the oral samples were rated similarly in palatability. 2.4. Respiratory gas exchange measurement Subjects arrived in the laboratory between 0600 and 0700 h immediately upon waking after a 12-h fast. Resting energy expenditure (REE) and substrate utilization were assessed in the supine position for 45 min using an indirect, open circuit calorimeter (Sensor Medics Vmax 229 n; Sensor Medics, Yorba Linda, CA). Respiratory gas exchange (oxygen consumption and carbon dioxide production) was continuously measured using a transparent semielliptical respiratory canopy. The analyzers were calibrated with fresh atmospheric air and standard calibration gas mixtures (4% CO2, 24% O2, 72% N2; 0% CO2, 26% O2, 74% N2). Raw data were continuously recorded on-line in 30-s intervals. The values for oxygen consumption, carbon dioxide production, and respiratory quotient (RQ; VCO2/VO2) were calculated using Vmax software (version 03-1). The last 10 min of steady state data were used to determine REE. During the 110-min period of intermittent oral stimulation, respiratory gas exchange was measured from minutes 25 – 35 and 60 –70 and averaged. Upon termination of the oral stimulation period, respiratory gas exchange was measured continuously for an additional 5.5 h. For the duration of this postoral stimulation period (110 –440 min), subjects remained in a semisupine position and were allowed to watch movies or read. A bathroom break was allowed one time during the postoral stimulus period, but was permissible only immediately following a measurement period. For analysis, oxygen consumption and carbon dioxide production were averaged over 10-min intervals at times 30,

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Table 2 Oral stimuli characteristics Treatmenta

Weight

Carbohydrateb

Protein

Total lipid

Saturated FA (g/sample)

Unsaturatedc FA

Monounsaturated FA

Polyunsaturated FA

Energy (kJ/sample)

SFA UFA CHO UFA + CHO Veh NO

5.2 5.2 4.7 4.7 0.7 –

0.0 0.6 3.2 1.9 0.6 –

0.0 0.0 0.0 0.0 0.0 –

3.7 2.6 0.0 1.1 0.0 –

2.3 0.3 0.0 0.1 0.0 –

1.2 2.1 0.0 0.9 0.0 –

1.1 1.4 0.0 0.6 0.0 –

0.1 0.6 0.0 0.3 0.0 –

146.4 131.8 53.6 80.3 11.7 –

a

Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle alone, NO = no oral stimulus, FA = fatty acids. b Energy and macronutrient composition obtained from package label. c Unsaturated lipid values were obtained from the USDA nutrient database for standard reference, Release 13 [63], except for UFA for which the values used came from the package label.

65, 115, 135, 195, 255, 315, 375, and 435 min. Nitrogen (N) values were determined assuming protein oxidation accounted for 12.5% of REE [32,33] and were used to calculate the nonprotein respiratory quotient (NPRQ) during

the test. The oxidation of carbohydrate and lipid was calculated from nonprotein oxygen consumption (NPVO2), their relative oxidative proportions as indicated by the NPRQ, and the amount of oxygen consumed per gram of

Fig. 2. Thermic effect of orosensory stimulation. All values are expressed as mean changes from baseline relative to no oral stimulation. The inner figure represents the mean ± S.E.M. change in energy expenditure for the no-oral-stimulation treatment. Oral stimulation occurred from 0 to 110 min (gray bar). Oral stimuli: SFA = butter, UFA = highly unsaturated margarine, CHO = jelly, UFA + CHO = highly unsaturated margarine + jelly, Veh = vehicle alone. * Significantly different from baseline ( P < .05).

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substrate oxidized. The calculations were performed as follows [34]: carbohydrate oxidation ðg=minÞ ¼ 4:113VCO2  2:907VO2  0:375 protein

fat oxidation ðg=minÞ ¼ 1:689VO2  1:689VCO2  0:324 protein

DIT was calculated as the postprandial increment in energy expenditure above fasting baseline. In order to determine the thermic effect of orosensory stimulation (TEOS), the DIT values obtained in the no-oral-stimulation treatment (NO) were subtracted from the DIT values obtained during each treatment (i.e., the response due to the GI load is removed). Similarly, changes in carbohydrate and lipid oxidation values were determined by subtracting the changes from baseline values during the no-oral-stimulus treatment (NO) to determine the effect of orosensory stimulation alone.

Energy expenditure (EE) was calculated using the following equation [32]:

2.5. Body composition

EE ðkcal=minÞ ¼ 3:941VO2 þ 1:106VCO2  2:17 g N

Fat mass was estimated using bioelectrical impedance analysis (BIA, model TBF-105; Tanita of America, Skokie, IL) at the start of each treatment session. Fat-free mass

ðkcal was converted to kJ by multiplying by 4:184Þ

Fig. 3. Effect of orosensory stimulation on carbohydrate oxidation. All values are expressed as mean changes from baseline relative to no oral stimulation. Oral stimulation occurred from 0 to 110 min (gray bar). The inner figure represents the mean ± S.E.M. change in carbohydrate oxidation for the no-oralstimulation treatment. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle alone. * Significantly different from baseline ( P < .05).

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(FFM) was estimated by subtracting fat mass from total body mass. 2.6. Blood collection and analysis Immediately after ingestion of the butter capsules, but before the initiation of oral stimulation, an indwelling cannula was inserted into an antecubital vein and the first blood sample was drawn (time 0). The blood glucose concentration was assessed immediately (SureStep; Lifescan, Milpitas, CA) and confirmed that participants had complied with the overnight fast (blood glucose concentration between 3.9 and 6.1 mmol/l). Subsequent blood samples were drawn at minutes 35, 85, 200, 320, and 440, all immediately after respiratory gas exchange sampling. Serum samples were analyzed for insulin and glucagon by radioimmunoassay (Linco Research, St. Louis, MO). To determine the effect of orosensory stimulation alone on insulin and glucagon concentrations, changes in these hormone

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concentrations were expressed relative to the no-oral-stimulus treatment (NO). This was determined by subtracting the change of insulin or glucagon values during the NO from the change of insulin or glucagon values during each treatment providing orosensory stimulation (SFA, UFA, CHO, UFA + CHO, Veh). Serum glucose was analyzed spectrophotometrically using an automated sample analyzer (Cobas Mira Plus; Roche Diagnostic Systems, Branchburg, NJ). 2.7. Sensory testing Subjects rated selected sensory properties of the oral samples after the first and last stimulus presentation on ninepoint category scales. Overall opinion, appearance, creaminess, flavor, and aftertaste 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.

Fig. 4. Effect of orosensory stimulation on lipid oxidation. All values are expressed as mean changes from baseline relative to no oral stimulation. Oral stimulation occurred from 0 to 110 min (gray bar). The inner figure represents the mean ± S.E.M. change in lipid oxidation for the no-oral-stimulation treatment. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle alone.

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Hunger was assessed immediately before and after ingestion of the capsules, during the oral stimulation period, and every hour for 6 h following the onset of orosensory stimulation using a 10-cm visual analog scale (Fig. 1). 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. 2.8. Statistical analysis All results presented are expressed as mean ± S.E.M. The effects of oral stimulation on DIT, substrate utilization, insulin, glucagon, and glucose were assessed by repeated measures analysis of variance (ANOVA). One-sample and paired-sample t tests were conducted for post hoc comparisons, where appropriate. The hedonic and intensity ratings given after the first and last stimulus presentations were not significantly different from each other and were averaged to provide a mean hedonic and intensity rating during the oral stimulation period. The nine-point hedonic and intensity

scale yields ordinal level data so a Friedman test was used to determine significant differences between treatments. A Wilcoxon rank-order test was used for post hoc comparisons. Associations between hedonic ratings and area under the curve (AUC) for TEOS were determined using Spearman correlation coefficients. Bonferroni corrections were made when applicable. Statistical procedures were performed with the SPSS software package release 10.0.5 (SPSS, Chicago, IL). The criterion for statistical significance was set at P < .05.

3. Results REE was not significantly different between treatments. The mean was 4.8 ± 0.2 kJ kg ffm  1 min  1 with a mean coefficient of variation of 6.2%. Postprandial thermogenesis increased significantly for all treatments compared to baseline and remained significantly elevated during the entire 440-min period except for NO at minutes 195, 375, 435 and UFA, CHO, and UFA + CHO at minute 435.

Fig. 5. Effect of orosensory simulation on insulin concentrations. All values are expressed as mean changes from baseline relative to no oral simulation. Oral stimulation occurred from 0 to 110 min (gray bar). The inner figure represents the mean ± S.E.M. change in insulin concentrations for the no-oralstimulation treatment. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle alone. * Significantly different from baseline ( P < .05).

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No significant differences in DIT were observed between treatments. Mean DIT over the 440-min measurement period for all treatments was 12.6 ± 0.29%, expressed as a percent of energy ingested. TEOS and changes of carbohydrate and lipid oxidation are presented in Figs. 2, 3, and 4, respectively. Calculated over the first 115- and entire 440-min measurement periods, the relative percentage of TEOS to DIT was 57.6 ± 5.2% and 23.7 ± 4.52%, respectively. Baseline values for carbohydrate and lipid oxidation were 0.15 ± 0.04 and 0.05 ± 0.01 g/min, respectively, and were not significantly different between treatments. There were no significant differences in TEOS or carbohydrate and lipid oxidation. Substrate oxidation expressed relative to FFM was not significantly different between treatments. Mean baseline insulin values ranged from 50.4 ± 5.5 to 75.2 ± 9.1 pmol/l and were not significantly different between treatments. Expressed as changes of insulin concentration from baseline relative to NO, no significant differences between treatments were present (Fig. 5). Mean baseline glucagon concentrations were not significantly

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different, ranging from 51.6 ± 4.8 to 60.6 ± 2.9 ng/l. At minute 35, UFA (  13.2 ng/l) and CHO (  15.6 ng/l) were significantly lower than Veh, relative to the change for NO (Fig. 6). Mean glucose concentrations at baseline were not significantly different, ranging from 4.4 ± 0.1 to 4.6 ± 0.1 mmol/l. Changes of glucose concentration relative to NO were not significantly different. Hedonic and intensity ratings are presented in Table 3. No significant differences were observed between treatments for hedonic ratings. Within-treatment associations between hedonic ratings to the oral samples and TEOS AUC values were not significantly different when TEOS AUC values were calculated during the entire treatment period (0 – 440 min; overall opinion: SFA r = .11, UFA r = .32, UFA + CHO r =  .21, CHO r = .26, and Veh r =  .37) or only during orosensory stimulation (0– 110 min; overall opinion: SFA r = .04, UFA r = .05, UFA + CHO r =  .14, CHO r =  .06, and Veh r =  .50). No significant differences were observed between treatments for intensity ratings except for the expected difference for sweetness and fat level. Correlations between the TEOS

Fig. 6. Effect of orosensory simulation on glucagon concentrations. All values are expressed as mean changes from baseline relative to no oral simulation. Grey bar represents period of orosensory stimulation. The inner figure represents the mean ± S.E.M. change in glucagon concentrations for the no-oralstimulation treatment. Oral stimuli: SFA = butter, UFA = unsaturated margarine, CHO = jelly, UFA + CHO = unsaturated margarine + jelly, Veh = vehicle alone. * Significantly different from baseline ( P < .05).

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Table 3 Hedonic and intensity ratings Treatment

Overall opinion Appearance Creaminess Flavor Sweetness Sourness Bitterness Saltiness Fat level Aftertaste a b c d e f g

SFA

UFA

CHO

UFA + CHO

Veh

5.3 ± 0.6a (1 – 9)b 4.8 ± 0.5 (1 – 9) 5.2 ± 0.5 (1 – 9) 5.3 ± 0.5 (1 – 9) 3.8 ± 0.5c,d (1 – 7) 3.5 ± 0.5 (1 – 6) 3.6 ± 0.5 (1 – 6) 5.5 ± 0.3 (4 – 8) 6.5 ± 0.4c,g (4 – 9) 5.3 ± 0.6 (1 – 9)

4.8 ± 0.5 (1 – 8) 4.5 ± 0.4 (1 – 7) 4.9 ± 0.5 (1 – 8) 5.0 ± 0.5 (1 – 8) 4.3 ± 0.5c (1 – 5) 2.9 ± 0.4 (1 – 5) 2.6 ± 0.4 (1 – 5) 5.5 ± 0.4 (2 – 8) 6.4 ± 0.4c,g (3 – 9) 4.8 ± 0.4 (1 – 8)

6.1 ± 0.3 (5 – 8) 5.9 ± 0.3 (4 – 7) 5.0 ± 0.2 (4 – 8) 6.0 ± 0.3 (4 – 8) 6.4 ± 0.3e,f,g (6 – 8) 3.6 ± 0.5 (1 – 6) 3.0 ± 0.5 (1 – 6) 3.9 ± 0.4g (1 – 6) 3.6 ± 0.4d,e,f,g (1 – 5) 5.8 ± 0.3 (4 – 8)

5.2 ± 0.5 (2 – 8) 5.0 ± 0.4 (2 – 8) 4.9 ± 0.5 (1 – 8) 5.3 ± 0.5 (2 – 9) 6.0 ± 0.3e,g (4 – 8) 3.6 ± 0.4 (1 – 5) 3.4 ± 0.4 (1 – 6) 5.1 ± 0.3 (4 – 8) 5.8 ± 0.3c,g (3 – 8) 4.9 ± 0.4 (1 – 8)

5.7 ± 0.4 (3 – 9) 5.3 ± 0.3 (3 – 8) 4.2 ± 0.5 (1 – 8) 5.8 ± 0.3 (3 – 9) 2.6 ± 0.4c,d (1 – 5) 3.0 ± 0.5 (1 – 5) 3.1 ± 0.5 (1 – 6) 6.0 ± 0.3c (4 – 8) 2.8 ± 0.4c,d,e,f (1 – 6) 5.5 ± 0.3 (3 – 8)

Mean ± S.E.M. Response range. Significantly different from CHO. Significantly different from UFA + CHO. Significantly different from SFA. Significantly different from UFA. Significantly different from Veh.

AUC values and the response to sweetness and fat level were not significantly different when TEOS AUC values were calculated for the entire treatment period (r =  .06 and  .13, respectively) or only during the orosensory stimulation period (r =  .24 and  .34, respectively). No significant differences were observed between treatments for hunger ratings at baseline. Hunger increased significantly over time [ F(7,91) = 21.8, P < .001] in a similar pattern for all treatments. Greater sample loss occurred during the UFA + CHO condition compared to the SFA, UFA, and Veh conditions [ F(4,60) = 8.6, P < .005]. However, the amount of unrecovered sample was small. Values for sample losses were 0.3 ± 2.1 g SFA,  0.5 ± 1.6 g UFA, 5.1 ± 2.6 g CHO, 10.4 ± 1.9 g UFA + CHO, and 3.7 ± 0.8 g Veh. Factoring in residue left on the serving plates, the amount possibly ingested equaled 5.4% (112.7 kJ) of the total energy value for the UFA + CHO condition.

4. Discussion The results of the present study are consistent with others noting that DIT represents approximately 10% of an ingested load composed primarily of lipid [18,35]. All treatments, with or without oral stimulation, lead to a significant increase in postprandial thermogenesis. However, discrepancies between oral samples were not observed. Whether the sensory component, inherent to the macronutrient composition of the meal, contributes to a meal’s thermogenic effect is unknown. This could occur through a response following detection of the stimulus (gustatory and/ or olfactory) or its hedonic impression. The reported DIT of individual macronutrients is 20– 30% for protein, 5 – 15% for carbohydrate, and 0– 3% for lipid [34,36]. Acute feeding studies indicate that high-carbohydrate meals produce a

significantly greater thermogenic effect than high-lipid meals [18,37,38]. The magnitude of response is related to macronutrient content. For example, a 30% increase in DIT was measured following a meal containing 68% carbohydrate, 20% lipid, and 12% protein relative to an isocaloric meal containing 40% carbohydrate, 48% lipid, and 12% protein [37]. In another study [38], consumption of a meal containing 85% carbohydrate and 15% protein compared to an isocaloric meal with 85% lipid and 15% protein produced a 50% greater thermogenic response in normalweight subjects. However, where macronutrient influences on DIT were explored, the hedonic properties of the stimuli were not adequately controlled [18,37,38] and palatability ratings were not obtained. The present study controlled for the potential effect of palatability on orosensory stimulation-induced thermogenesis by maintaining similar hedonic properties among oral samples. The oral samples contained either primarily lipid (74% or 50% for SFA and UFA, respectively), carbohydrate (sweet or nonsweet), or a combination of both lipid and carbohydrate. Our data suggest that nonhedonic sensory properties of oral stimuli, composed primarily of carbohydrate or lipid, do not contribute significantly to macronutrient differences in DIT. The influence that meal palatability has on DIT is controversial. Some studies report that palatability modulates DIT [13,20,25,27] and other do not [26,28]. In this study, mean hedonic properties between the oral samples were rated similarly. However, mean values often mask interindividual differences within a treatment. Indeed, hedonic ratings for the SFA stimulus ranged from 1 to 9. To determine whether a hedonic influence was present in our data, hedonic ratings were correlated with TEOS within treatments. No significant associations were observed. Thus, our results are in agreement with evidence suggesting that hedonic properties are not effective elicitors of thermogenesis [26,28].

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The discrepancies in reports regarding a hedonic influence on DIT may be related to differences in degree of palatability variation between meals. A review of the literature reveals a number of meal-related characteristics reported to influence DIT. These include meal size [21,39], meal consistency [22,40,41], meal familiarity [42], duration of sensory stimulation [43], and possibly meal-induced psychological stress [28]. Variations in subject characteristics across studies may also contribute to the differences observed between meal palatability and DIT. For example, insulin resistance [44], percent body fat [45], and age [46] are negatively associated with DIT. In a previous study investigating the effects of sweet taste on DIT, researchers demonstrated that consumption of isocaloric, isovolumic, macronutrient-matched, soft, white cheeses containing maltodextrins (a nonsweet carbohydrate) or maltodextrins + aspartame (a high-intensity/low-energy sweetener) produced similar thermogenic responses [30]. They concluded that variations in sweet taste do not effect DIT. Our results support this conclusion as subjects rated the oral samples containing jelly (CHO and UFA + CHO treatments) significantly sweeter than the high-fat stimuli and the TEOS values with the sweet and nonsweet stimuli were not different. The effect of orosensory stimulation on postprandial substrate oxidation is also unclear. RQs have been reported to remain unchanged during sham feeding (orosensory stimulation alone) [24] while meal ingestion (orosensory stimulation including direct gastro-intestinal stimulation) or tube feeding (gastro-intestinal stimulation only) causes a comparable, significant increase [7]. One study actually reported that RQs were greater with tube feeding compared to meal ingestion [7]. These studies suggest that orosensory stimulation does not influence substrate oxidation. Conversely, higher RQs have been observed after meal ingestion compared to tube feeding using a palatable oral stimulus [1]. Our results are in agreement with studies noting no effect of sensory stimulation on carbohydrate and lipid oxidation rates as oxidation rates were similar with or without oral stimulation. Cognitive influences have been demonstrated for a number of cephalic phase responses in humans [47,48] and cannot be ruled out as a possible explanation for observing a similar thermogenic response between oral stimuli. It is possible that the subjects’ knowledge that they would not be ingesting the oral samples overrides the orosensory influence that a particular nutrient might have on DIT. Additionally, the use of the modified sham-feeding paradigm does not involve swallowing, a potent elicitor of cephalic phase responses [49]. However, a number of human studies using the modified sham-feeding technique have observed significant increases in thermogenesis compared to tube feeding or actual meal ingestion [7,24,43], suggesting that modified sham feeding provides sufficient stimulation to elicit DIT. Cephalic phase insulin and glucagon responses have been observed in humans and other animals [4,50 – 52].

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Both hormones are suggested to contribute to postprandial thermogenesis [4,53 – 55], and both may be stimulated differentially by the macronutrient composition of the meal [56,57]. Insulin is proposed to stimulate thermogenesis by activation of the sympathetic nervous system via hypothalamic insulin-sensitive neurons [53], which in turn stimulate adrenal catecholamine secretion [27,58]. Indeed, blockage of the sympathetic nervous system with b-adrenergic receptor antagonists inhibits the increase in thermogenesis elicited by insulin infusion in humans [8]. In dogs, glucagon activity may account for
20% of total heat production postprandially [54], likely through simultaneous synthesis and breakdown of glycogen (futile cycling) [59]. We monitored insulin and glucagon concentrations to provide insights into a potential macronutrient-related sensory influence on release of these hormones. However, no treatmentrelated changes of circulating insulin and glucagon were observed. Our study design did not allow for a temporal blood sampling pattern capable of directly measuring a cephalic phase insulin or glucagon response [51,52]. However, cephalic phase and postprandial insulin responses are correlated (r=.62) [60] and glucagon elevations lasting several hours have been demonstrated following cephalic phase stimulation [52]. Consequently, the lack of differences in circulating insulin, glucagon, and glucose across treatments postabortively suggests that macronutrientinduced cephalic phase insulin and glucagon response may not have occurred. Our data suggest that sensory stimulation with equipalatable foods comprised of carbohydrate or lipid does not contribute to an increase or differential DIT response. Continued research is needed, as the effects of other sensory characteristics of foods, including their tactile, thermal, irritative, and olfactory properties on thermogenesis, have not been thoroughly investigated. The incidence of obesity has increased worldwide [61]. Although DIT accounts for a relatively small proportion of total energy expenditure (3 –10%) [62], it may play an important role in the development and/or maintenance of obesity, as small differences in DIT, over time, can lead to positive energy balance and increased body weight.

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

References [1] LeBlanc J, Cabanac M, Samson P. Reduced postprandial heat production with gavage as compared with meal feeding in human subjects. Am J Physiol 1984;246:E95 – E101. [2] Garrel DR, de Jonge L. Intragastric vs oral feeding: effect on the thermogenic response to feeding in lean and obese subjects. Am J Clin Nutr 1994;59:971 – 4.

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