Retrograde Gastric Electrical Stimulation Reduces Food Intake and Weight in Obese Rats

Objective: To investigate the therapeutic potential of retrograde gastric electrical stimulation (RGES) for obesity in a rodent model of obesity. Research Methods and Procedures: The study was performed in 12 obese Zucker rats implanted with two pairs of gastric serosal electrodes, one pair for stimulation and the other for recording intrinsic gastric myoelectrical activity. It was composed of an acute study in three sessions to study the effect of RGES on intrinsic gastric myoelectrical activity and acute food intake and a chronic phase to study the short‐term effect of RGES on weight. RGES was performed through the distal stomach using long pulses at a frequency of tachygastria (known to induce gastric hypomotility). Results: RGES completely entrained intrinsic gastric myoelectrical activity and turned it into tachygastria at a certain strength. RGES reduced acute food intake compared with the control (p < 0.01). A 2‐week treatment of RGES resulted in a significant reduction in food intake (p = 0.002) and a significantly greater weight loss than sham stimulation (p = 0.004). Discussion: RGES at a tachygastrial frequency reduces food intake and results in weight loss in obese Zucker rats, and its effect is probably attributed to the introduction of tachygastria in the stomach.     

Chronic tachygastrial electrical stimulation reduces food intake in dogs

Objective: Tachygastria is known to be associated with gastric hypomotility. This study investigated the effect of tachygastrial electrical stimulation (TES) on food intake and its effects on gastric motility. Research Methods and Procedures: Five experiments were performed to study the effects of TES on gastric slow waves, gastric tone, accommodation, and antral contractions, gastric emptying, acute food intake, and chronic food intake in dogs. Results: TES at tachygastrial frequencies induced tachygastria and reduced normal slow waves. TES significantly reduced gastric tone or induced gastric distention, impaired gastric accommodation, and inhibited antral contractions. TES significantly delayed gastric emptying. Acute TES reduced food intake but did not induce any noticeable symptoms. Chronic TES resulted in a 20% reduction in food intake, and the effect of TES was found to be related to specific parameters. Discussion: TES at the distal antrum results in a significant reduction in food intake in dogs, and this inhibitory effect is probably attributed to TES‐induced reduction in proximal gastric tone, gastric accommodation, antral contractility, and gastric emptying. These data suggest a therapeutic potential of the specific method of TES for obesity.     

Gastric Electrical Stimulation for Obesity: The Need for a New Device Using Wider Pulses

Gastric electrical stimulation (GES) has been proposed as a therapeutic option for obesity. However, its clinical efficacy is not proven, and its mechanisms remain largely unknown. To compare the peripheral and central neural and behavioral effects in rats of GES with a pulse width currently used in clinical trials (GES‐A: 6 mA, 0.3 ms, 40 Hz, 2 s on, 3 s off) and GES with a wider pulse (GES‐B: same as GES‐A, except that the pulse width is 3 ms). Experiment 1: assessing gastric volume changes as a result of GES. Experiment 2: recording the extracellular potentials of a single neuron in the paraventricular nucleus (PVN) with GES. Experiment 3: determining the effects of GES on oxytocin‐immunoreactive (OT‐IR) neuron expression in the hypothalamus. Experiment 4: determining the effects of GES on food intake and body weight. GES‐B, but not GES‐A, significantly increased gastric volume. GES‐B activated a higher percentage of gastric distention‐responsive neurons in the PVN (93% vs. 81%, P = 0.021) and elicited more intensive neuronal responses than GES‐A. The number of OT‐IR neurons was significantly increased in the PVN and supraoptic nucleus with both methods of GES compared with control groups. The increase in OT‐IR neurons in the PVN was higher with GES‐B than with GES‐A. A 1‐week GES treatment significantly reduced daily food intake and body weight. GES‐B was more potent than GES‐A in producing weight loss (P < 0.001). The effects of GES depend on the stimulation pulse width. GES with a wider pulse is more effective both peripherally and centrally and more potent in reducing body weight in rats.     

Nesfatin-1对大鼠摄食、胃酸分泌、胃运动及胃排空的影响

目的:观察Nesfatin-1对大鼠摄食、胃酸分泌、胃运动及胃排空的影响并探究其可能机制。方法:将大鼠随机分为摄食实验组、胃酸实验组、胃运动实验组以及胃排空实验组。大鼠经腹内侧核置管后给予nasfatin-1,检测大鼠摄食量,使用Na OH滴定法测定大鼠胃酸分泌,记录清醒大鼠胃运动,以比色法测定大鼠胃排空。结果:低剂量和高剂量nesfatin-1均减少2小时累积食物摄入量;高剂量组4小时累积食物摄入量仍显著低于NS对照组。Nesfatin-1能够抑制2-DG对胃酸分泌的促进作用。SHU9119能够部分阻断nesfatin-1对2-DG的抑制作用。Nesfatin-1能够抑制胃运动及胃排空,SHU9119可部分阻断nesfatin-1对胃运动及胃排空的抑制作用。结论:Nesfatin-1能够调控大鼠摄食、胃酸分泌、胃运动及胃排空,黑皮质素信号通路可能也参与该调控过程。     

Effect of Alginate on Satiation,Appetite, Gastric Function,and Selected Gut Satiety Hormones in Overweight and Obesity

Lack of control of food intake, excess size, and frequency of meals are critical to the development of obesity. The stomach signals satiation postprandially and may play an important role in control of calorie intake. Sodium alginate (based on brown seaweed Laminaria digitata) is currently marketed as a weight loss supplement, but its effects on gastric motor functions and satiation are unknown. We evaluated effects of 10 days treatment with alginate or placebo on gastric functions, satiation, appetite, and gut hormones associated with satiety in overweight or obese adults. We conducted a randomized, 1:1, placebo‐controlled, allocation‐concealed study in 48 overweight or obese participants with excluded psychiatric comorbidity and binge eating disorder. All underwent measurements of gastric emptying (GE), fasting, and postprandial gastric volumes (GVs), postprandial satiation, calorie intake at a free choice meal and selected gut hormones after 1 week of alginate (three capsules vs. matching placebo per day, ingested 30 min before the main meal). Six capsules were ingested with water 30 min before the GE, GV, and satiation tests on days 8–10. There were no treatment group effects on GE or volumes, gut hormones (ghrelin, cholecystokinin (CCK), glucagon‐like peptide‐1 (GLP‐1), peptide YY (PYY)), satiation, total and macronutrient calorie intake at a free choice meal. There was no difference detected in results between obese and overweight patients. Alginate treatment for a period of 10 days showed no effect on gastric motor functions, satiation, appetite, or gut hormones. These results question the use of short‐term alginate treatment for weight loss.     

Gastric Pacing for Morbid Obesity: Plasma Levels of Gastrointestinal Peptides and Leptin

Objective: A gastric pacemaker has been developed to treat morbid obesity. Patients experience increased satiety, the ability to reduce food intake, and a resultant weight loss. However, the mechanism behind the changed eating behavior in paced patients is still under investigation. Research Methods and Procedures: This study was performed on 11 morbidly obese patients (mean BMI, 46.0 kg/m²) treated with gastric pacing. The peripheral blood levels of satiety signals of cholecystokinin (CCK), somatostatin, glucagon‐like peptide‐1 (GLP‐1), and leptin were studied 1 month before gastric pacer implantation, 1 month after implantation, and 6 months after activation of electrical stimulation. Blood samples were drawn 12 hours after fasting and in response to a hypocaloric meal (270 kcal). Patients were followed monthly for vital signs and weight level. Results: Gastric pacing resulted in a significant weight loss of a mean of 10.4 kg (4.4 BMI units). No negative side effects or complications were observed during the treatment. After activation of the pacemaker, meal‐related response of CCK and somatostatin and basal levels of GLP‐1 and leptin were significantly reduced (p < 0.05) compared with the tests before gastric pacing. The weight loss correlated significantly with a decrease of leptin levels (R = 0.79, p < 0.01). Discussion: Gastric pacing is a novel and promising therapy for morbid obesity. Activation of the gastric pacer was associated with a decrease in plasma levels of CCK, somatostatin, GLP‐1, and leptin. More studies are necessary to elucidate the correlations between satiety, weight loss, and digestive neuro‐hormone changes.     

Potential of intestinal electrical stimulation for obesity: a preliminary canine study

Objective: The aims of this study were to investigate the therapeutic potential of intestinal electrical stimulation (IES) for obesity. Experiments were performed to investigate the effects of IES on food intake, gastric tone, gastric accommodation, and its possible pathway. Research Methods and Procedures: Ten normal dogs and six dogs with truncal vagotomy were used in this study. Each dog was equipped with a gastric cannula for the measurement of gastric tone and accommodation by barostat and one pair of duodenal serosal electrodes for IES. The experiment on food intake was composed of both control session without IES and IES session after a 28‐hour fast. The experiment on gastric tone and accommodation was performed in the fasting and fed states and composed of three sessions: control, IES, and IES with N^G‐nitro‐l ‐arginine. Results: IES significantly reduced food intake in the normal dogs (459.0 vs. 312.6 grams, p < 0.001). The food intake was negatively correlated with the fasting gastric volume during IES. IES significantly decreased fasting gastric tone in the normal dogs reflected as a decrease in gastric volume (89.1 vs. 261.3 mL, p < 0.01), which was abolished by vagotomy and N^G‐nitro‐l ‐arginine. Discussion: IES reduces food intake and inhibits gastric tone in the fasting state. The inhibitory effect of IES on gastric tone is mediated by both vagal and nitrergic pathway.     

Duodenum electrical stimulation delays gastric emptying, reduces food intake and accelerates small bowel transit in pigs

Duodenum electrical stimulation (DES) has been shown to delay gastric emptying and reduce food intake in dogs. The aim of this study was to investigate the effects of DES on gastric emptying, small bowel transit and food intake in pigs, a large animal model of obesity. The study consisted of three experiments (gastric emptying, small bowel transit, and food intake) in pigs implanted with internal duodenal electrodes for DES and one or two duodenal cannulas for gastric emptying and small bowel transit. We found that (i) gastric emptying was dose-dependently delayed by DES of different stimulation parameters; (ii) small bowel transit was significantly accelerated with continuous DES in proximal intestine but not with intermittent DES; (iii) DES significantly reduced body weight gain with 100% duty cycle (DC), but not with DES with 40% DC. A marginal difference was noted in food intake among 100% DC session, 40% DC session, and control session. DES with long pulses energy-dependently inhibits gastric emptying in pigs. DES with appropriate parameters accelerates proximal small bowel transit in pigs. DES reduces body weight gain in obese pigs, and this therapeutic effect on obesity is mediated by inhibiting gastric emptying and food intake, and may also possibly by accelerating intestinal transit. DES may have a potential application to treat patients with obesity.     

Gastric Motor and Sensory Functions in Obesity

In the vast majority of affected individuals, obesity involves overconsumption of food relative to calorie requirements. The sensory function of the stomach may play a key role in the cessation of food ingestion. This sensation of the stomach is, in part, determined by its motor functions, such as tone and compliance and the rate of emptying. However, studies of gastric emptying in normal‐weight and obese persons have shown inconsistent results. Gastric capacity was larger in obese persons when tested with an intragastric latex balloon filled with water. In contrast, other studies using the barostat or imaging (single‐photon emission computed tomography) techniques reported no differences in gastric volume or compliance between obese and lean subjects. On the other hand, increased body mass and fasting gastric volume are independently associated with delayed satiation under standard laboratory conditions of food ingestion. These data suggest that changes in gastric motor and sensory functions in obesity may present useful targets to prevent and treat obesity. Further well‐controlled, validated studies are needed to clarify the potential role of altering the stomach's function as a means of controlling food intake in obesity.     

Preproghrelin-derived peptide, obestatin, fails to influence food intake in lean or obese rodents

Objectives: Obestatin has been initially characterized as a new peptide derived from the ghrelin precursor, which suppresses food intake and inhibits the orexigenic and prokinetic actions of ghrelin when injected peripherally or centrally in lean mice. However, reproducing these data remains controversial. Reasons for the disparity may be the use of different doses, routes, and animal models. We aimed to investigate the effects of peripheral and intracisternal (IC) injection of obestatin on feeding, gastric motility, and blood glucose in rats as well as in diet‐induced obese (DIO) mice. Research Methods and Procedures: Food intake and gastric emptying of a semi‐liquid caloric meal were measured after intraperitoneal (IP) injection of obestatin in rats and DIO mice. Gastric phasic motility and blood glucose were monitored in urethane‐anesthetized rats after IC or intravenous (IV) injection of obestatin. Results: Obestatin injected intraperitoneally at doses ranging from 0.1 to 3 mg/kg influenced neither acute food intake nor gastric emptying in rats. Obestatin injected intravenously at 0.3 or 3 mg/kg and IC at 7.5 or 30 µg/rat modified neither fasted gastric phasic motility nor blood glucose levels, while ghrelin (30 µg/kg, IV) increased and vagotomy suppressed gastric motility, and an oligosomatostatin analog (3 µg/rat, IC) decreased blood glucose. Obestatin, injected intraperitoneally (0.3 mg/kg) in DIO mice, did not alter feeding response to a fast, while urocortin 1 (10 µg/kg, IP) induced a 73.3% inhibition at 2 hours. Discussion: Our data demonstrate that peripheral administration of obestatin did not modify food intake in rats or obese mice or gastric motor function in rats.     

Short‐Term Effects of Gastric Bypass Surgery on Circulating Ghrelin Levels

Objective: To prospectively evaluate the short‐term effects of Roux‐en‐Y gastric bypass (RYGBP) on ghrelin secretion and its relevance on food intake and body weight changes. Research Methods and Procedures: Ghrelin response to a standardized test meal was evaluated in eight obese patients (BMI, 43.5 to 59.1 kg/m²) before and 6 weeks after RYGBP. Ghrelin response was compared with that of an age‐matched group of six normal weight individuals (BMI, 19.6 to 24.9 kg/m²). Results: Fasting serum ghrelin levels were lower in obese subjects compared with controls (p < 0.05). Meal ingestion significantly suppressed ghrelin concentration in controls (p < 0.05) and obese subjects (p < 0.05), albeit to a lesser degree in the latter group (p < 0.05). Despite a 10.3 ± 1.5% weight loss, fasting serum ghrelin levels were paradoxically further decreased in obese subjects 6 weeks after RYGBP (p < 0.05). Moreover, at this time‐point, food intake did not elicit a significant ghrelin suppression. The changes in ghrelin secretion after RYGBP correlated with changes in insulin sensitivity (p < 0.05) and caloric intake (p < 0.05). Discussion: This study showed that the adaptive response of ghrelin to body weight loss was already impaired 6 weeks after RYGBP. Our study provides circumstantial evidence for the potential role of ghrelin in the negative energy balance in RYGBP‐operated patients.     

Inhibitory effects of intestinal electrical stimulation on food intake, weight loss and gastric emptying in rats

The aim was to investigate the effects of intestinal electrical stimulation (IES) on food intake, body weight, and gastric emptying in rats. An experiment on food intake and weight change was performed in 22 rats on a control diet and 10 diet-induced obese (DIO) rats for 4 wk with IES or sham IES. The effect of IES on gastric emptying was performed in another 20 rats in the control group. We found that 1) in control rats, 4-wk IES resulted in a reduction of 18.2% in the total amount of food intake compared with sham-IES (P = 0.02); the rats treated with IES had a weight change of -1 +/- 7.8g (P = 0.03), which was equivalent to a weight loss of 6.2% due to IES when adjusted for normal growing. 2) Acute IES delayed gastric emptying by 20% in the control rats (P < 0.01). 3) In the DIO rats, 1-wk IES with the same parameters as those used in the control rats resulted in a significant reduction in the total amount of food intake (126.6 +/- 6.3 g vs. 116.9 +/- 3.2 g, P < 0.01). More reduction in food intake was noted, and a significant weight change was also observed when stimulation energy was increased. 4) No adverse events were observed in any of the experiments. In conclusion, IES delays gastric emptying, reduces food intake, and decreases weight gain in control growing rats. These data suggest that it is worthy to explore therapeutic potentials of IES for obesity.     

Gastric electrical stimulation parameter dependently alters ventral medial hypothalamic activity and feeding in obese rats

Gastric electrical stimulation (GES) has been used to treat obesity with unclear mechanisms and limited parameter ranges. This study explores effects of GES parameters on ventral medial hypothalamic (VMH) activity, feeding, and body weight in diet-induced obese (DIO) rats. For experiment 1, discharge rates were recorded in 39 gastric distension-responsive (GD-R) neurons in 12 DIO rats. Basal rates were compared with rates under GES using varied pulse amplitudes, widths, frequencies, and train-on times. For experiment 2, a crossover experiment in 16 DIO rats measured food intake and weight effects of GES pulse width, the parameter with the steepest neuronal response gradient in experiment 1. Treatments were sham and 0.5-, 2.0-, and 5.0-ms pulse GES. In experiment 1, 11 of 13 GES parameter sets tested produced significantly (P < 0.05) altered discharge rates of GD-R neurons. Increases in pulse amplitude (P < 0.05) and width (P < 0.0001) produced significant upward linear trends in response over the range tested, with the trend being strongest for pulse width. In experiment 2, over 4 days of 0.5-, 2.0-, and 5.0-ms GES treatment, food intake was 9.6% (P < 0.05), 21.0% (P < 0.0001), and 47.3% (P < 0.0001) lower than under sham-GES, whereas body weight changes were 0.7 (P = 0.48), 2.2 (P < 0.05), and 3.5 (P < 0.002) percentage points lower, respectively. We concluded that GES pulse width increases had the largest effect on VMH neuronal activity, and these effects were paralleled by pulse width-dependent reductions in food intake and body weight. Lengthening pulse width beyond the range used in prior clinical studies may be critical to making GES a viable obesity treatment.     

Gastric emptying rate in Pleuronectes platessa L.

X-ray studies of gastric emptying of Pleuronectes platessa force-fed a moist, artificial diet give the relationship:
where GET is gastric emptying time (h), S is meal size (g), W is body weight (g) and T is temperature (°C).
The corresponding gastric emptying curve is predicted to be:
where stomach contents (g net weight) are S ₀ at start and S_t at time th. Direct observations of residual stomach contents using serial slaughter are in close agreement with the predicted curve, save for small plaice (below 50 g body weight) which empty at only 50–60% of the rate found in larger fish.
The small effects of body weight on gastric emptying rate may reflect the relatively small role of the stomach [Volume (ml) = 0.024 body weight (g)] in digestion when compared with other flatfish.
The emptying curve established here can be used in field studies to estimate feeding rate on natural food items, provided fish greater than 50 g body weight are used and the energy density of the food is greater than 0.5 kcal/g wet weight. Smaller fish will have emptying rates which are only 30–60% of those found in larger fish; the change appears to be abrupt and corresponds to the size at which young plaice move offshore from their nursery grounds.     

Ghrelin Does Not Influence Gastric Emptying in Obese Subjects

Objective: To evaluate the relationship between fasting plasma concentrations of ghrelin and gastric emptying in obese individuals compared with lean subjects. Research Methods and Procedures: We included 20 obese patients (9 men and 11 women, BMI > 30 kg/m²) and 16 nonobese control subjects (7 men and 9 women, BMI ≤ 25 kg/m²). Gastric emptying of solids (egg sandwich labeled with radionuclide) was measured at 120 minutes with (99m)Tc‐single photon emission computed tomography imaging. Ghrelin and leptin were analyzed by radioimmunoassay and ELISA methods, respectively. Results: The gastric half‐emptying time was similar in obese men and women (67.8 ± 14.79 vs. 66.6 ± 13.56 minutes) but significantly shorter (p < 0.001) than in the control population (men: 88.09 ± 11.72 minutes; women: 97.25 ± 10.31 minutes). Ghrelin levels were significantly lower in obese subjects (131.37 ± 47.67 vs. 306.3 ± 45.52 pg/mL; p < 0.0001 in men and 162.13 ± 32.95 vs. 272.8 ± 47.77 pg/mL; p < 0.0001 in women). A negative correlation between gastric emptying and fasting ghrelin levels was observed only in lean subjects (y = ?0.2391x + 157.9; R² = 0.95). Also, in the lean group, ghrelin was the only significant independent determinant of gastric emptying, explaining 98% of the variance (adjusted R²) in a multiple regression analysis. Discussion: This report shows that, in humans, gastric emptying is faster in obese subjects than in lean controls and that, whereas ghrelin is the best determinant of gastric kinetics in healthy controls, this action is lost in obesity.     

副溶血性弧菌在动态体外人胃仿生原位消化系统中的存活情况研究

副溶血性弧菌(Vibrio parahaemolyticus)是一种经口摄入感染的食源性致病菌,广泛存在于水产品中,然而其进入人胃后的存活情况尚属研究空白。本研究将浓度为10~7 cfu/g的副溶血性弧菌接种于三文鱼和南美白对虾中,运用体外人胃仿生原位消化系统进行消化模拟,经过120 min后,测定食物排空率、胃部pH值变化及幽门排出食糜中副溶血性弧菌的存活情况。结果显示三文鱼的胃排空滞后时间为60 min,南美白对虾为90 min,模拟消化120 min时,两种食糜均未完全排空。胃部pH值为(1.6±0.1),在食物摄入10 min后大幅上升,随着胃酸的不断分泌及食物的消化分解,其pH值开始下降,并保持在5.41左右。在食品消化120 min进入肠道后,副溶血性弧菌并没有完全被胃酸杀灭,对虾中该菌的存活率为(0.119±0.025)%,而三文鱼中存活率为(0.007±0.005)%。综上所述,副溶血性弧菌可随食物基质的消化分解通过胃排空进入肠道,从而躲避胃酸的杀灭并导致人体患病。     

Clinical Management of Patients Presenting with Non-Adjustable Gastric Band (NAGB) Complications

Background: A number of bariatric surgical procedures have been developed to manage morbid obesity and related co-morbidities. The non-adjustable gastric band (NAGB) was one such procedure that created restriction to food intake by gastric segmentation. Benefits of the procedure included a low risk of perioperative complications and substantial early weight loss. Unfortunately, the long term results of NAGB include a high incidence of complications and failure to maintain weight loss. The purpose of this study was to examine the presentation, workup, and treatment of patients presenting with complications following NAGB placement.Methods: A retrospective review of the diagnosis and management of 11 patients who presented with complications related to NAGB placement.Results: All patients presented with some degree of proximal gastric outlet obstruction. The majority of patients (8/11) presented with vomiting as the main complaint. Other complaints included intolerance to solids, liquids, and reflux. Only 2/11 patients presented with weight loss since undergoing NAGB placement, while the remainder had weight regain to their pre-NAGB level and above. Depending on clinical presentation, desire for additional weight loss and co-morbid conditions, patients underwent a variety of treatments. This included NAGB removal (endoscopic, laparo-endoscopic, and laparoscopic) as well as conversion to another bariatric procedure (sleeve gastrectomy, Roux-en-Y gastric bypass).Conclusion: Patients with NAGB complications present with symptoms related to a proximal gastric outlet obstruction, related to constriction imposed by the band. This may result in severe food and liquid intolerance and subsequent weight loss, but more likely results in maladaptive eating and subsequent weight gain. Optimal therapy involves removal of the NAGB. Laparoscopic conversion to another bariatric procedure, optimally a Roux-en-Y gastric bypass, is warranted to treat morbid obesity and associated co-morbidities.     

The TRPA1 Agonist,Methyl Syringate Suppresses Food Intake and Gastric Emptying

Transient receptor potential channel ankryn 1 (TRPA1) expressed in the gastrointestinal tract is associated with gastric motility, gastric emptying, and food intake. In this study, we investigated the effects of methyl syringate, a specific and selective TRPA1 agonist, on food intake, gastric emptying, and gut hormone levels in imprinting control region (ICR) mice. The administration of methyl syringate suppressed cumulative food intake and gastric emptying. In addition, treatment with ruthenium red (RR), a general cation channel blocker, and HC-030031, a selective TRPA1 antagonist, inhibited methyl syringate-induced reduction of food intake and delayed gastric emptying in ICR mice. Methyl syringate also increased plasma peptide YY (PYY) levels, but not glucagon-like peptide-1 (GLP-1) levels. The elevation in PYY was blocked by treatment with RR and HC-030031. The present findings indicate that methyl syringate regulates food intake and gastric emptying through a TRPA1-mediated pathway and, by extension, can contribute to weight suppression.     

Peripheral mechanisms of sibutramine involving proximal gastric motility in dogs

Objective: Sibutramine, a serotonin‐norepinephrine uptake inhibitor, has been used for treating obesity. However, its possible mechanisms involving gastric motility have not been reported. The aim of this study was to evaluate the effects of sibutramine on gastric accommodation and antral motility. Research Methods and Procedures: The study was performed in seven dogs with a stomach cannula and composed of two separate experiments: antral contractions and gastric tone. Each experiment included two sessions on 2 separate days in a randomized order: a control session and a treatment session with sibutramine (5 mg/kg per os) administrated 2 hours before the study. Results: Sibutramine significantly increased fasting gastric tone; the gastric volume in the fasting state at baseline was 103.8 ± 12.3 mL and significantly decreased to 35.3 ± 16.0 mL with sibutramine (p = 0.0075). Sibutramine also impaired gastric accommodation. The average postprandial gastric volume was 472.1 ± 16.7 mL in the control session and reduced to 302.2 ± 53.6 mL with sibutramine (p = 0.013). The average postprandial increase in gastric volume during the 60‐minute postprandial period with sibutramine was significantly lower than the corresponding values in the control session: 266.8 ± 46.1 vs. 393.9 ± 15.3 mL (p = 0.03). Sibutramine had no effects on postprandial antral contractions. Discussion: Sibutramine increases gastric tone and impairs gastric accommodation to an orally ingested meal. The inhibitory effect of sibutramine on gastric accommodation may partially explain the reduced food intake with sibutramine in patients with obesity.