Modified Sham Feeding Research Articles

Vagal activation alters prandial bile acid composition and glycemia in patients with hypoglycemia after Roux-en-Y gastric bypass surgery.

Altered prandial glycemic response after Roux-en-Y gastric bypass (RYGB) is exaggerated in patients with post-RYGB hypoglycemia. Increased contribution of glucagon-like peptide 1 (GLP-1) to prandial insulin secretion plays a key role in developing hypoglycemia after RYGB, but the role of nonhormonal gut factors remains unknown. Here, the effect of vagal activation on prandial bile acid (BA) composition in relation to glucose, insulin and gut hormone responses was examined in a small size group of nondiabetic subjects after RYGB with intact gallbladder compared to nonoperated controls. Concentrations of blood glucose, hormones, and BAs were measured in two RYGB subjects with documented hypoglycemia (HGB), three asymptomatic RYGB-treated subjects (AGB), and four nonoperated controls with intact gallbladders during a meal-tolerance test with (MTT-Sham) and without (MTT) preceding modified sham feeding (chew and spit). Meal ingestion raised serum total BAs in RYGB-treated subjects without any effect in nonoperated controls. Modified sham feeding similarly increased meal-induced responses of conjugated BAs (CBAs) in all subjects (p < 0.05 compared to MTT alone), whereas unconjugated BAs (UBAs), mainly deoxycholic and chenodeoxycholic acid, were raised only in the HGB group (p < 0.001 for interaction). Prandial UBAs had an inverse correlation with glucose nadir (r = -0.75, p < 0.05) and were directly associated with ISR and GLP-1 during MTT-Sham. In this small cohort, vagal activation by modified sham feeding increases prandial CBAs in both operated and nonoperated subjects but enhances UBAs only in patients with documented post-RYGB hypoglycemia. Our findings highlight a potential role for nonhormonal gut factors, such as BA and gut microbiome, in glucose abnormalities after RYGB.

Differential effects of nutritive and non-nutritive sweet mouth rinsing on appetite in adults with obesity

BackgroundExcessive added sugar intake has been associated with obesity; however, the effect of dietary sweetness on energy intake (EI) and appetite in adults with and without obesity has not yet been determined. ObjectiveTo assess the effect of mouth rinses with and without energy and sweetness on measures of appetite, and to compare responses between subjects with body mass index (BMI) between 18.5 and 24.9 kg/m2 or ≥30 kg/m2. MethodsIn this randomized, double-blind crossover study, 39 subjects (age 23±5y; 17 male, 22 female; BMI 18.5–24.9 kg/m2: n = 21; ≥30 kg/m2: n = 18) performed modified sham-feeding (MSF) with a mouth rinse containing either sucrose, sucralose, maltodextrin, or water for 2min before expectorating the solution. Blood sampling and subjective appetite assessments occurred at baseline (−5) and 15, 30, 60, and 90min post-MSF. After, EI was assessed at a buffet meal and post-meal appetite ratings were assessed hourly for 3h. ResultsPost-MSF ghrelin increased for water vs. maltodextrin (water: p = 0.03). Post-MSF cholecystokinin increased following maltodextrin-MSF (p = 0.03) and sucralose-MSF (p = 0.005) vs. sucrose for those with BMI:18.5–24.9 kg/m2 only. There was greater post-MSF desire to eat in response to water vs. sucrose (p = 0.03) and reduced fullness with sucralose for those with BMI≥30 vs. 18.5–24.9 kg/m2 (p < 0.001). There was no difference in EI at the buffet meal by mouth rinse (p = 0.98) or by BMI (p = 0.12). However, there was greater post-meal fullness following sucralose-MSF vs. water (p = 0.03) and sucrose (p = 0.004) for those with BMI≥30 vs. 18.5–24.9 kg/m2. ConclusionSucralose rinsing led to greater cephalic phase CCK release in adults with a BMI:18.5–24.9 kg/m2 only; however, ghrelin responses to unsweetened rinses were energy-specific for all adults. As subsequent EI was unaffected, further investigation of cephalic phase appetite is warranted.

Leptin increases hepatic triglyceride export via a vagal mechanism in humans

Recombinant human leptin (metreleptin) reduces hepatic lipid content in patients with lipodystrophy and overweight patients with non-alcoholic fatty liver disease and relative hypoleptinemia independent of its anorexic action. In rodents, leptin signaling in the brain increases very-low-density lipoprotein triglyceride (VLDL-TG) secretion and reduces hepatic lipid content via the vagus nerve. In this randomized, placebo-controlled crossover trial (EudraCT Nr. 2017-003014-22), we tested whether a comparable mechanism regulates hepatic lipid metabolism in humans. A single metreleptin injection stimulated hepatic VLDL-TG secretion (primary outcome) and reduced hepatic lipid content in fasted, lean men (n= 13, age range 20-38 years) but failed to do so in metabolically healthy liver transplant recipients (n= 9, age range 26-62 years) who represent a model for hepatic denervation. In an independent cohort of lean men (n= 10, age range 23-31 years), vagal stimulation by modified sham feeding replicated the effects of metreleptin on VLDL-TG secretion. Therefore, we propose that leptin has anti-steatotic properties that are independent of food intake by stimulating hepatic VLDL-TG export via a brain-vagus-liver axis.

Sham Feeding Induced Gastric Acid Secretion in Patients with Caustic Induced Esophageal Stricture.

Caustic ingestion can lead to structural changes in the upper gastro-intestinal tract. However, there is limited data on the effect of caustic ingestion on gastric secretion. This study was planned to determine changes in gastric acid output after sham feeding in patients with caustic induced esophageal stricture and to compare it with healthy controls. It was a prospective study done at tertiary care center in North India. Consecutive patients with caustic induced esophageal stricture were evaluated for the study. Gastric secretory function was estimated in the basal state and after modified sham feeding. These results were compared withage-matched controls. The mean age of the included patients (n = 18) was 30.11 ± 9.19years and 13 patients were male. 16 (88%) patients had history of acid ingestion. Patients with caustic sequelae had significantly lower basal and stimulated acid secretion compared to controls (n = 10) (5.84 ± 2.44mmol/hr; p < 0.01 and 17.16 ± 7.53mmol/hr; p < 0.01; respectively). Patients with lower esophageal stricture (n = 8) had significantly lower increase in acid output compared to patients with stricture elsewhere in esophagus (0.20 ± 0.3 vs. 2.31 ± 1.74mmol/hr, p < 0.01). Patients with lower esophageal involvement had significantly lower stimulated acid secretion and increase in acid secretion compared to controls (4.74 ± 4.67 vs. 17.16 ± 7.53mmol/hr; p < 0.01 and 20 ± 0.3 vs. 2.09 ± 0.88mmol/hr; p < 0.01; respectively).

Utility of the plasma pancreatic polypeptide response to modified sham feeding in diabetic gastroenteropathy and non-ulcer dyspepsia.

The relationship between cardiovascular and gastrointestinal (ie, plasma pancreatic polypeptide [PP] response to modified sham feeding [MSF]) indices of vagal function is unclear. Hyperglycemia inhibits PP secretion via vagally mediated mechanisms. Our aims were to (a) compare the PP response, (b) its relationship with glycemia, and (c) the relationship between PP response to MSF, gastric emptying (GE) of solids, and symptoms during GE study in healthy controls, patients with diabetic gastroenteropathy (DM), and non-ulcer dyspepsia (NUD). In 24 healthy controls, 40 DM, and 40 NUD patients, we measured plasma PP concentrations during MSF, cardiovagal functions, GE, and symptoms during a GE study. Baseline PP concentrations were higher in DM than in controls and NUD (P=.01), and in type 2 than in type 1 DM patients (P<.01). The PP increment during MSF was normal (≥20pg/mL) in 70% of controls, 54% of DM, and 47% of NUD patients. Overall, the PP response and cardiovagal tests were concordant (P=.01). Among patients with a reduced PP increment with MSF, 7/10 of T1DM and 1/7 of T2DM patients had moderate or severe cardiovagal dysfunctions (P<.05). The PP response to MSF was not associated with GE. Up to 30% of healthy controls have a reduced PP increment during MSF, limiting the utility of this test to detect vagal injury. The PP response is more useful when it is normal than abnormal. A reduced PP response is more likely to be associated with cardiovagal dysfunctions in T1DM than in T2DM.

Exacting Responses: Lack of Endocrine Cephalic Phase Responses Upon Oro-Sensory Exposure.

Oro-sensory exposure (OSE) to food plays an important role in the regulation of food intake. One proposed underlying mechanism is the occurrence of cephalic phase responses (CPRs). CPRs include the pre-digestive endocrine responses induced by food-related sensory input. Yet, whether OSE duration or sweetness intensity affects CPRs is unknown. The objective of this study was to determine the independent and interactive effects of oro-sensory duration (chewing) and stimulation intensity (sweetness) on endocrine CPRs and satiation. Eighteen males (22 ± 2 years, BMI 22 ± 2 kg/m2) participated in a 2 × 2 randomized study with a control condition. Each session participants performed modified sham feeding (MSF) with one of the four gel-based model foods. During the control session no MSF was performed. Model foods differed in chewing duration (hard or soft texture) and sweetness (low or high intensity). During each session, eight blood samples were collected up till 25 min after MSF onset. Subsequently, food intake from an ad libitum lunch was measured. No typical CPR was found for insulin, pancreatic polypeptide (PP), and ghrelin. However, the overall PP response was 1.1 times greater for the hard sweet MSF condition compared to control (p = 0.02). Overall ghrelin responses were 1.1 times greater for the hard model food compared to the soft model food conditions (p = 0.003). These differences in endocrine response were not associated with differences in food intake at the subsequent meal. Exploratory sub-analysis of the responsive insulin curves showed that after 2.5 min of MSF the hard texture model foods insulin concentrations were 1.2 greater compared to the soft texture. These findings indicate that texture hardness and sweetness increase the overall PP response and that MSF on hard texture increases the overall ghrelin response compared to soft texture model foods. However, MSF on model foods does not lead to a typical CPR. This study, among others, shows that there are major dissimilarities in the endocrine responses to food stimulation between individuals. This emphasizes the importance of considering cephalic responders and non-responders. More research is needed to understand CPRs in relation to food texture and taste properties.

Salivary endocannabinoids and N-acylethanolamines upon mastication of a semisolid food: implications in fat taste, appetite and food liking.

This study aimed to evaluate whether salivary endocannabinoid (EC) and N-acylethanolamine (NAE) concentrations upon mastication of a semisolid food were involved in the sensory perception of fat taste, food liking and appetite in humans. A fat-enriched (FEP) and a low-fat control (CP) pudding were developed and used in a randomized cross-over study with 19 healthy volunteers. The study protocol combined a Modified Sham-Feeding (MSF) with a multiple-spoon Temporal Dominance of Sensations method. Subjects masticated and expectorated 10 spoons of the pudding and selected the dominant sensations among a list of attributes. Saliva samples, appetite and food liking scores were collected at baseline, immediately after the MSF of the pudding and every 5 min until 20 min after MSF. Salivary concentrations of all monitored ECs and NAEs increased during pudding mastication compared to baseline (except for palmitoylethanolamide with FEP). The raise was lower with FEP than with CP for all compounds except for 2-arachidonoylglycerol whose increase was higher than the other compounds and independent of pudding type. Salivary N-arachidonoylethanolamine, linoleoylethanolamide and palmitoylethanolamide were significantly lower at 10 and 20 min after MSF of FEP than CP. Fatty taste at the 2nd spoon and creaminess at the 5th spoon were perceived as dominant with FEP whereas only wateriness was dominant with CP at the 2nd spoon. No difference between puddings for individual appetite or food liking over the 20 min of the protocol was recorded. During mastication of a semisolid fat-enriched food, the fatty taste and the creaminess were perceived as dominant. Salivary ECs and NAEs were not associated with the individual perception of fatty taste, pudding liking and appetite sensations.

Effects of Oral Exposure Duration and Gastric Energy Content on Appetite Ratings and Energy Intake in Lean Men.

Studies show that longer oral exposure to food leads to earlier satiation and lowers energy intake. Moreover, higher energy content of food has been shown to lead to higher satiety. Up to now, it has not been studied systematically how oral exposure duration and gastric energy content interact in satiety regulation. Thirty-seven men (22 ± 4 years, 22 ± 2 kg/m2) participated in a randomized cross-over trial, in which we independently manipulated: (1) oral exposure duration by modified sham feeding (MSF) for 1 or 8 min; and (2) energy content of gastric load (GL) by a nasogastric tube: 100 kcal/500 mL or 700 kcal/500 mL. Outcome measures were appetite ratings and subsequent energy intake from an ad libitum meal. Energy intake was 35% lower after the GLs with 700 kcal than with 100kcal (p < 0.0001). All appetite ratings were lower in the 700 kcal than in the 100 kcal treatments (area under the curve (AUC); p-values ≤ 0.002); fullness was higher and prospective consumption was lower in the 8 min than in the 1 min MSF treatments (AUC; p-values ≤ 0.02). In conclusion, the current showed that a GL of 700 kcal/500 mL vs. 100 kcal/500 mL increased satiety and lowered energy intake. No additional effects of oral exposure duration could be observed, presumably due to the high contrast in energy between the manipulations. Future research should also focus on the role of oral exposure as such and not only the duration.

Food Liking Enhances the Plasma Response of 2-Arachidonoylglycerol and of Pancreatic Polypeptide upon Modified Sham Feeding in Humans1–3

Background: Food palatability increases food intake and may lead to overeating. The mechanisms behind this observation are still largely unknown.Objectives: The aims of this study were the following: 1) to elucidate the plasma responses of endocannabinoids, N-acylethanolamines, and gastrointestinal peptides to a palatable (sweet), unpalatable (bitter), and sensory-acceptable (tasteless control) food, and 2) to verify whether some of these bioactive compounds can serve as plasma biomarkers of food liking in humans.Methods: Three puddings providing 60 kcal (35% from proteins, 62% from carbohydrates, and 3% from fats) but with different taste were developed. Twenty healthy subjects (11 women and 9 men; mean age 28 y and BMI 22.7 kg/m2), selected because they liked the puddings in the order sweet > control > bitter, participated in a randomized crossover study based on a modified sham feeding (MSF) protocol. Blood samples at baseline and every 5 min up to 20 min after the MSF were analyzed for gastrointestinal peptides, endocannabinoids, and N-acylethanolamines. Thirty minutes after the MSF, energy intake at an ad libitum breakfast was measured.Results: After the MSF, no response was observed in 7 of 9 gastrointestinal peptides measured. The plasma ghrelin concentration at 20 min after the sweet and bitter puddings was 25% lower than after the control pudding (P = 0.04), and the pancreatic polypeptide response after the sweet pudding was 23% greater than after the bitter pudding (P = 0.02). The plasma response of 2-arachidonoylglycerol after the sweet pudding was 37% and 15% higher than after the bitter (P < 0.001) and control (P = 0.03) puddings, respectively. Trends for greater responses of anandamide (P = 0.06), linoleoylethanolamide (P = 0.07), palmitoylethanolamide (P = 0.06), and oleoylethanolamide (P = 0.09) were found after the sweet pudding than after the bitter pudding. No differences in subsequent energy intake were recorded.Conclusions: The data demonstrated that food palatability influenced some plasma endocannabinoid and N-acylethanolamine concentrations during the cephalic phase response and indicated that 2-arachidonoylglycerol and pancreatic polypeptide can be used as biomarkers of food liking in humans.

Longer Oral Exposure with Modified Sham Feeding Does Not Slow Down Gastric Emptying of Low- and High-Energy-Dense Gastric Loads in Healthy Young Men1–3

Background: A long oral exposure to food and a high-energy density of food have been shown to increase satiety feelings. The effect of energy density is predominantly caused by an inhibition of gastric emptying. It is hypothesized that prolonging oral exposure may have an additional effect on this inhibition of gastric emptying. However, little human data are available to support this hypothesis.Objective: The objective was to assess the effect of the duration of oral exposure to food on gastric emptying rate of gastric loads (GLs) low and high in energy density and on satiety feelings.Methods: Twenty-six healthy men [mean ± SD age: 22 ± 3 y; BMI (in kg/m2): 23 ± 1] participated in a randomized crossover trial with 4 treatments and a control. Treatments consisted of either 1- or 8-min modified sham feeding (MSF) of cake, and a GL of either 100 or 700 kcal infused in the stomach via a nasogastric tube (500 mL, 62.5 mL/min). The control consisted of no MSF and a GL of 500 mL of water. Gastric emptying rate was assessed with a 13C breath test. Breath samples and satiety feelings were collected at fixed time points until 90 min after start of the treatment.Results: Gastric emptying rate and satiety feelings were not affected by duration of MSF (P ≥ 0.27). However, the 700-kcal GL treatments slowed gastric emptying [41% lower area under the curve (AUC)] and increased satiety feelings (22–31% higher AUC) compared with the 100-kcal GL treatments (P < 0.001). No interaction between MSF duration and energy density of GL was found (P ≥ 0.44).Conclusions: Higher gastric energy density inhibited gastric emptying and increased satiety feelings in healthy young men. However, prolonging oral exposure to food did not have an additional effect. This study provides more insight in satiety regulation. This trial was registered at trialregister.nl as NTR3601.

Moderate alcohol consumption stimulates food intake and food reward of savoury foods

The aim of this study was to investigate whether food reward plays a role in the stimulating effect of moderate alcohol consumption on subsequent food intake. In addition, we explored the role of oral and gut sensory pathways in alcohol's effect on food reward by modified sham feeding (MSF) or consumption of a preload after alcohol intake.In a single-blind crossover design, 24 healthy men were randomly assigned to either consumption of vodka/orange juice (20 g alcohol) or orange juice only, followed by consumption of cake, MSF of cake or no cake. Food reward was evaluated by actual food intake measured by an ad libitum lunch 45 min after alcohol ingestion and by behavioural indices of wanting and liking of four food categories (high fat, low fat, sweet and savoury).Moderate alcohol consumption increased food intake during the ad libitum lunch by 11% (+338 kJ, P = 0.004). Alcohol specifically increased intake (+127 kJ, P < 0.001) and explicit liking (P = 0.019) of high-fat savoury foods. Moreover, moderate alcohol consumption increased implicit wanting for savoury (P = 0.013) and decreased implicit wanting for sweet (P = 0.017) before the meal. Explicit wanting of low-fat savoury foods only was higher after alcohol followed by no cake as compared to after alcohol followed by cake MSF (P = 0.009), but not as compared to alcohol followed by cake consumption (P = 0.082). Both cake MSF and cake consumption had no overall effect on behavioural indices of food reward.To conclude, moderate alcohol consumption increased subsequent food intake, specifically of high-fat savoury foods. This effect was related to the higher food reward experienced for savoury foods. The importance of oral and gut sensory signalling in alcohol's effect on food reward remains largely unclear.

The impact of the cephalic phase on postprandial blood glucose and satiety

Summary Background and aims The impact of cephalic phase on postprandial insulin response is well documented however its effects on postprandial blood glucose remain inconsistent. The purpose of the current study was to assess the impact of cephalic phase on postprandial blood glucose and satiety. Methods Twelve participants were recruited and tested on two different occasions (i) with modified sham feeding (MSF) (ii) without MSF (Control) followed by white bread (50 g available carbohydrate) consumption. Finger-prick blood samples were taken at regular interval for 120 min to measure blood glucose. Measurements of satiety (hunger, fullness, desire to eat and prospective eating) were taken using 100 mm visual analogue scales (VAS). Results Blood glucose changes did not differ between the two occasions after 30, 60 and 120 min. Similarly, there were no differences in satiety between the MSF test compared with the control. Conclusion These findings suggest that the cephalic phase do not affect either postprandial blood glucose or satiety.

Modified sham feeding of foods with different macronutrient compositions differentially influences cephalic change of insulin, ghrelin, and NMR-based metabolomic profiles

Little is known about the effect of the macronutrient composition of foods on cephalic phase response of gastrointestinal hormones. In addition, the metabolomics of cephalic phase response has not been studied before. The objective of the present study was to assess cephalic phase endocrinological and metabolomic responses following modified sham feeding (MSF) of foods with different macronutrient compositions. Ten healthy males attended four separate test sessions after overnight fasting, for a 3-min MSF of water, high-fat, high-carbohydrate or high-protein food, respectively, in a randomized order. Blood samples were collected at baseline and at regular time points for 10min following the completion of MSF and assayed for plasma glucose, insulin, ghrelin and glucose-dependent insulinotropic peptide. 1H nuclear magnetic resonance was used to acquire metabolomic profiles of the plasma samples. Plasma glucose increased after MSF of all test foods, but there were no differences due to the macronutrient composition of the test foods. MSF of the high-carbohydrate food elicited significantly higher insulin, and the high-protein food resulted in higher ghrelin compared to other test sessions. No significant change in glucose-dependent insulinotropic peptide was found. Analysis of plasma metabolomic profiles revealed concentrations of lipids were lower after MSF while plasma glucose increased after MSF. There was also a macronutrient-dependent change in certain amino acids. In conclusion, short-term oral exposure to foods with different macronutrient compositions can induce a macronutrient-specific cephalic change in insulin and ghrelin, as well as metabolomic profiles.

Mechanisms and effects of “fat taste” in humans

Evidence supporting a "taste" cue from fat in the oral cavity continues to accrue. The proposed stimuli for fat taste, non-esterified fatty acids (NEFA), are released from food through hydrolytic rancidity and lipase activity derived from foods or saliva. NEFA must then be released from the food matrix, negotiate the aqueous environment to reach taste cell surfaces, and interact with receptors such as CD36 and GPR120 or diffuse across cell membranes to initiate a taste signal. Knowledge of these processes in non-gustatory tissues should inform understanding of taste responses to NEFA. Additionally, downstream effects of oral triglyceride exposure have been observed in numerous studies. Data specific to effects of NEFA versus triglyceride are scarce, but modified sham feeding trials with triglyceride document cephalic phase responses including elevations in serum lipids and insulin as well as potential, but debated, effects on gut peptides, appetite, and thermogenesis. In this review, we highlight the mechanisms by which NEFA migrate to and interact with taste cells, and then we examine physiological responses to oral fat exposure.

Influence of the tolerability of vinegar as an oral source of short-chain fatty acids on appetite control and food intake

Vinegar is promoted as a natural appetite suppressant, based on previous reports that vinegar ingestion significantly increases subsequent satiety. However there are concerns about the appropriateness and safety of this advice, and it is unclear if poor product palatability may explain previously published effects on appetite. To investigate if vinegar palatability and tolerability have a role in suppressing appetite and food intake in two sequential and related acute human feeding studies. Healthy, young, normal weight unrestrained eaters were recruited to Study 1 (n=16), an acute feeding study supplying vinegar within both palatable and unpalatable drinks alongside a mixed breakfast in comparison to a non-vinegar control; and to Study 2 (n=14), a modified sham feeding study (taste only without ingestion) comparing vinegar to a non-vinegar control following a milkshake preload. Both studies were a randomized crossover balanced design for the assessment of appetite, energy intake and glycaemic response. In Study 1, ingestion of vinegar significantly reduced quantitative and subjective measures of appetite, which were accompanied by significantly higher nausea ratings, with unpalatable treatment having the greatest effect. Significant correlations between palatability ratings and appetite measures were found. In Study 2, orosensory stimulation with vinegar did not influence subsequent subjective or quantitative measures of appetite compared with control. These studies indicate that vinegar ingestion enhances satiety whereas orosensory stimulation alone does not, and that these effects are largely due to poor tolerability following ingestion invoking feelings of nausea. On this basis the promotion of vinegar as a natural appetite suppressant does not seem appropriate.

Effects of Oral and Gastric Stimulation on Appetite and Energy Intake

Appetite is regulated by many factors, including oro-sensory and gastric signals. There are many studies on contributions of and possible interaction between sensory and gastric stimulation, but there are few studies in humans using simultaneous oral and gastric stimulation. We investigated the effect of simultaneous, but independently manipulated, oral and gastric stimulation on appetite ratings and energy intake. We hypothesized that compared with no stimulation, oral and gastric stimulation would equally and additively decrease appetite ratings and energy intake. Healthy men (n = 26, 21 ± 2 years, BMI 22 ± 3 kg/m(2)) participated in a randomized crossover trial with four experimental conditions and a control condition. Experimental conditions consisted of oral stimulation, with either 1 or 8 min modified sham feeding (MSF), and gastric stimulation, with either 100 or 800 ml intragastrically infused liquid (isocaloric, 99 kcal, 100 ml/min). The control condition consisted of no oral or gastric stimulation. Outcome measures were energy intake 30 min after the treatment and appetite ratings. Compared with the control condition, energy intake decreased significantly after the 8 min/100 ml (19% lower, P = 0.001) and 8 min/800 ml conditions (15% lower, P = 0.02), but not after the 1 min/100 ml (14% lower, P = 0.06) and 1 min/800 ml conditions (10% lower, P = 0.39). There was no interaction of oral and gastric stimulation on energy intake. Hunger and fullness differed across all conditions (P ≤ 0.01). In conclusion, duration of oral exposure was at least as important in decreasing energy intake as gastric filling volume. Oral and gastric stimulation did not additively decrease energy intake. Longer oro-sensory stimulation, therefore, may be an important contributor to a lower energy intake.

Impaired gastric response to modified sham feeding in patients with postprandial distress syndrome

Impaired vagal function has been reported to be important in some patients with functional dyspepsia (FD). However, the pathophysiologic mechanisms influencing the cephalic phase of vagal activity in FD are incompletely understood. The aim of this study was to investigate the gastric response to modified sham feeding (MSF) on ultrasound and cardiovascular autonomic function in FD patients. Nineteen patients with postprandial distress syndrome (PDS, 11 men and eight women; mean age: 48.2 years) and 26 healthy subjects (HS, 13 men and 13 women; mean age: 45.0 years) were studied prospectively. Firstly, cardiovascular autonomic function was assessed by spectral analysis of RR interval variability. Antral contraction was then evaluated by ultrasonography after MSF was performed to stimulate the cephalic phase of vagal activity. Spectral analysis of RR interval variability showed that the high-frequency component was significantly smaller in the patients than in the HS (P<0.01). The frequency of antral contraction in response to MSF over 15 min was also significantly lower in the PDS patients than in the HS. The 15-min integrated antral contractile response (area under the contraction vs time curve) was significantly smaller in the PDS patients than in the HS (P<0.01). Univariate analysis revealed a modest correlation between the high-frequency component of RR interval variability and the area under the contraction vs time curve (n=46, r=0.49, P<0.01). Autonomic abnormalities affecting the cephalic phase of vagal activity may be important in the pathogenesis of FD.

Dynamics of Fat Absorption and Effect of Sham Feeding on Postprandial Lipema

Given the importance of postprandial hyperlipidemia to increase risk for atherosclerosis, in the present study, stable isotope-labeled meals were fed to healthy subjects (7 males and 3 females) to investigate the kinetics chylomicron synthesis and the effect of sensory exposure to lipid on metabolism. Subjects performed two, 24-hour inpatient studies that entailed consumption of a liquid formula evening meal containing 30 g of oil (+ (13)C(2) triolein) on day 1. Breakfast (day 2) consisted of triacylglycerols (TAGs) fed as capsules (30 g oil + (13)C(7) triolein) to avoid activation of mouth taste receptors. Next, modified sham feeding of cream cheese occurred over 2 hours. In the 2 trials, the stimulus was either higher fat (HF) or lower fat (LF) cream cheese. A liquid meal was consumed at lunch. Blood sampling occurred intermittently, and chylomicron particles S(f) >400 TAGs were analyzed by gas chromatography-mass spectrometry. (13)C(2)-Label was found in fasting-state lipoproteins, and persons with higher body fat percentages showed greater dilution of meal TAGs from endogenous sources. For both trials, 13% ± 4% of lipoprotein TAGs oleic acid was derived from the previous evening meal. Incremental area under the curve for TAGs during HF was ∼2.5 times higher than after LF exposure (46 ± 15 vs 17 ± 5 μmol/L/h; P = .04). The greater HF morning lipemia occurred with elevated glucose, insulin, and nonesterified fatty acids peak after lunch. These data support a connection between enteral lipid metabolism and oral fat exposure, resulting in elevated postprandial lipemia. The results suggest that the intestine may participate in a mechanism coordinating oral fat signaling with control of subsequent macronutrient disposal in the body.

Short-term oral exposure to white wine transiently lowers serum free fatty acids

In humans little is known as to whether oral sensory stimulation with alcohol elicits cephalic phase responses. This study sought to determine whether oral alcohol exposure, in the form of white wine, provokes cephalic phase responses in normal-weight and overweight women. In a semi-randomized, crossover trial, eleven normal-weight and eleven overweight women sham-fed, after an overnight fast under three separate conditions 4 weeks apart, cake (750kJ), 25cL white wine (750kJ; ∼26g alcohol) and 25cL water. Blood was drawn prior to and for 30min after two 3-min episodes of modified sham-feeding (MSF). Blood samples were analyzed for free fatty acid (FFA), triglyceride, glucose, pancreatic polypeptide (PP), insulin and alcohol concentrations. Incremental area under the curves (IAUC) of FFA concentrations differed significantly between the three treatments but not between BMI categories. After MSF with wine, FFA concentrations dropped to a minimum of 77±3% of baseline concentrations at t=12±2min after baseline and returned to baseline after ∼30min, whereas after MSF with cake and water, FFA concentrations gradually increased. In conclusion, short-term oral white wine exposure substantially and temporarily decreases FFA concentrations suggesting a cephalic phase response of alcohol. This effect occurred regardless of BMI.

Modified sham feeding of sweet solutions in women with anorexia nervosa

Anorexia Nervosa (AN) is a disorder of self-starvation characterized by decreased meal size and food intake. While it is possible that reduced food intake in AN reflects an excess of inhibitory factors, e.g., cognitive inhibition related to fear of weight gain or abnormal postingestive negative feedback, it is also possible that decreased intake reflects diminished orosensory stimulation of food intake. This has been difficult to test directly because the amount of food ingested during a test meal by patients with AN reflects an integration of orosensory excitatory, and cognitive, learned, and postingestive inhibitory controls of eating. To begin to dissociate these controls, we adapted the modified sham feeding technique (MSF) to measure the intake of a series of sweetened solutions in the absence of postingestive stimulation. Subjects with AN ( n = 24) and normal controls (NC, n = 10) were randomly presented with cherry Kool Aid® solutions sweetened with five concentrations of aspartame (0, 0.01, 0.03, 0.08 and 0.28%) in a closed opaque container fitted with a straw. They were instructed to sip as much as they wanted of the solution during 15 1-minute trials and to spit the fluid out into another opaque container. Subjects with AN sipped less unsweetened solution than NC ( p < 0.05). Because this difference appeared to account completely for the smaller intakes of sweetened solutions by AN, responsiveness of intake to sweet taste per se was not different in AN and NC. Since MSF eliminated postingestive and presumably cognitive inhibitory controls, and the orosensory response to sweet taste was not different in AN than NC, we conclude that decreased intake by AN subjects under these conditions reflects the increased inhibition characteristic of this disorder that is presumably learned, with a possible contribution of decreased potency of orosensory stimulation by the sipped solutions.