SEARCH

SEARCH BY CITATION

Keywords:

  • food intake;
  • stomach;
  • emptying;
  • volume;
  • satiation

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

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.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

Obesity can be defined as a state of excess body fat or body energy stores in excess of physiological needs. Obesity increases the risk of medical illness and premature death. During the past 25 years, the prevalence of this disorder has increased dramatically throughout the world. Obesity is a common condition in every continent (1).

Despite the greater understanding of the physiological mechanisms regulating body weight and energy balance, the causes of human obesity remain relatively poorly understood. Human obesity seems to result from a combination of genetic, developmental, environmental, and psychological influences (2). Body weight seems to be determined by an interaction among these factors acting through the physiological mediators of energy intake and expenditure. Although genetic differences are very important in determining the development of obesity, the marked rise in the prevalence of obesity in the last 2 decades is best explained by behavioral and environmental changes that have resulted from technological advances. Much of human obesity is multifactorial and usually involves relative overconsumption of food. Thus, the control of food intake, determined by meal size and frequency of meals, is a main factor in the maintenance of weight or the development of obesity (3). Multiple regulatory pathways seem to promote or inhibit feeding and, thus, regulate energy balance. However, these pathways and their interactions remain incompletely understood, and the approved medical and surgical approaches available for treatment of obesity are limited.

Sensory information about food intake and digestion is communicated from the gastrointestinal tract and liver to several areas of the brain and seems to have a strong influence over ingestive behavior and overall energy homeostasis (4,5). Feelings of hunger and satiety have long been associated with gastric motor and sensory functions, and the role of the stomach in the control of food intake has been of interest for at least a century.

Historical Perspectives of Stomach Function in Obesity

Cannon and Washburn (6) described contractions of the stomach, which they believed were the basis for feelings of hunger. Hertz (7) and Boring (8) tested the sensation of the stomach in several human subjects and observed that mechanical distension of the stomach with a balloon could elicit a feeling of fullness. These data suggested that the sensory function of the stomach, conveying information of the state of fullness, may play a key role in the cessation of food ingestion. Thus, the stomach has been considered to be the most important organ in the gastrointestinal tract in the regulation of satiety (9,10,11). However, it is important to realize that the sensation of the stomach is, in part, determined by its motor functions.

Regulation of Gastric Motor and Sensory Functions

Gastric motor and sensory functions are regulated through a complex, interacting network of gut regulatory peptides, hormones, and the autonomic and enteric nervous systems. It has become increasingly clear that these mechanisms have the potential not only to modulate gastric motor and sensory functions but also to participate in the regulation of appetite and satiety and, hence, weight homeostasis. Thus, changes in gastric motor and sensory functions in obesity could reflect disturbances in these regulatory mechanisms and may contribute to the development and maintenance of obesity.

Purpose of Review and Definitions

In this review, we explore how changes in gastric motor and sensory functions may be part of the pathophysiology of obesity. We review the differences in gastric motor and sensory functions between normal-weight and obese persons and the effect of weight loss on these functions.

Because the term satiety has been used to reflect the sensations of fullness or of appetite, this has created some confusion in the literature. For the purpose of clarity, we shall use the term satiation to describe early postprandial fullness and satiety to describe appetite, hunger, or the desire to ingest a subsequent meal after the ingestion of an index meal. Satiety describing hunger is not specifically addressed in this review of gastric function.

Gastric Emptying of Liquids and Solids

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

There are differences in the patterns and the motor mechanisms involved in the gastric emptying of solid and liquid food. Gastric emptying of liquid food is driven mainly by the tone of the gastric fundus, under the control of both vagal (12) and hormonal (13) influences, and the resistance to flow at the level of the pylorus and duodenum. Noncaloric liquids are emptied in an exponential manner, and as the calorie content and viscosity of the liquid food increase, the pattern of emptying becomes more linear rather than exponential and is, therefore, relatively delayed.

Emptying of solid food requires initial grinding or trituration through antral contractions, retropulsive and propulsive actions of the distal stomach, as food is sheared by the mincing action of the antral contractions propelling solids against a closed pylorus (14). During this process, very little gastric emptying occurs initially. After a lag time during which solid food is triturated to small particles of <2-mm diameter (15), the food empties in a manner resembling that of high calorie or viscosity liquid meals, i.e., in a linear fashion.

Gastric Emptying in Obesity

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

Despite several studies about the relationship between body size and gastric emptying, these studies in obesity have revealed inconclusive data, in part, because of the variety or the lack of standardization of measurements or methods used. Hunt et al. (16) performed classical studies that involved ingesting different meals and emptying the stomach with a large bore tube to withdraw and quantitate gastric contents at different times after ingestion. They suggested that obese patients ate a more energy-dense meal, which accelerated the rate of transfer of calories from the stomach to the duodenum. This accelerated emptying was thought to produce shorter satiety periods, i.e., shorter time to the ingestion of the next meal.

Johansson and Ekelund (17) used a liquid test meal in healthy, nonobese subjects together with a more quantitative multiple-indicator dilution technique and concluded that there was a direct correlation between heavier subjects and energy transfer from the stomach to the intestine.

Lavigne et al. (18) investigated the relationship of body size to rates of gastric emptying of solid food in normal-weight persons and demonstrated an inverse linear relationship between gastric emptying and body size, such that larger or heavier normal persons emptied their gastric content more slowly. This is clearly in contradistinction to the observations by Hunt et al. and Johansson and Ekelund, who observed more rapid emptying of caloric liquids.

Wright et al. (19) studied 46 obese and 31 age-, sex-, and race-matched nonobese individuals; gastric emptying of solids in the obese group was significantly more rapid than that of the nonobese controls, whereas no difference was noted in the gastric emptying of the liquid test meal between the two groups. They suggested that the faster rate of solid gastric emptying in the obese subjects might be a fundamental cause of obesity that does not change after weight loss.

In summary, some studies have suggested more rapid gastric emptying in obesity (19,20,21), whereas others have reported normal (22,23,24,25) or even slow (26,27,28,29) emptying. These conflicting results could be attributed, in part, to differences in the selection of participants, group matching, or standardization of test meals (25), or to confounding factors that may also influence gastric emptying, such as weight stability, previous diet history (30,31), menstrual cycle, or smoking (19,26,27,28) (Table 1). Multicenter studies using standardized methods designed to minimize the effects of the potential confounding factors are needed to determine whether gastric emptying is normal, accelerated, or delayed.

Table 1. . Gastric emptying in obesity
ReferenceNo. of obeseNo. of ControlsBMI (kg/m2) or % overweight in obese groupMealEnergy (kcal)Gastric-emptying solidsGastric-emptying liquidsMethod
  1. S, solid; L, liquid; Scint, scintigraphy; USG, ultrasonogram; Breath, 13 C-octanoic acid breath test.

(19)4631Mean BMI = 37.9S/L212/81RapidNo changeScint
(26)151163% to 182%S/L272/0SlowerNo changeScint
(27)71798% to 161%S/L270/0 or 153SlowerNo changeScint
(20)312132% to 240%S/L410 to 440No changeNot measuredScint
(28)3131Median BMI = 42.4S/L272/61SlowerSlowerScint
(80)79Mean BMI = 39.7L432Not measuredNo changeMultiple marker dilution
(24)87BMI range = 30 to 34.5L73 to 320Not measuredNo changeScint
(81)24825% to 216%S/L504No changeNo changeScint
(32)3023>25%S/L379No changeNo changeScint
(82)1118Mean BMI = 37.4L300Not measuredNo changeScint
(83)1118Mean BMI = 39.0L12Not measuredSlowerUSG
(21)2020BMI range = 45.3 to 58.0S638RapidNot measuredScint
(84)921Mean BMI = 42.3S360RapidNot measuredScint
(25)1912Mean BMI = 38.7S597No changeNot measuredScint
(29)1616Mean BMI = 34.5S478SlowerNot measuredBreath

Effect of Weight Loss on Gastric Emptying in Obesity

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

Few studies have examined the effect of major weight loss on gastric emptying rate (25,32,33,34). Some show no change in gastric emptying in obese individuals and no change with weight loss. Thus, Wright et al. (19) showed no significant change in the gastric emptying rates of solids or liquids in four obese subjects who lost weight and were within 10% of their ideal body weight (19). Hutson et al. (32) reported that gastric emptying of both solids and liquids with a dual radioisotope technique was similar in 30 obese (>125% of ideal body weight) and 23 age- and sex-matched nonobese controls. In eight obese subjects who experienced substantial weight reduction (mean 8.3%), gastric emptying rates were similar before and after the weight loss.

In contrast, Tosetti et al. (21) observed that 20 morbidly obese subjects (BMI 45.3 to 58.0 kg/m2) had accelerated gastric emptying as compared with 20 healthy controls (BMI 20.3 to 24.8 kg/m2). The obese subjects showed slower gastric emptying after significant weight loss following 4 months of dietetic treatment.

Gastric emptying of a solid meal was faster in nine obese subjects (BMI 31 ± 4 kg/m2) compared with nine normal-weight controls. Obese patients underwent jejunoileal bypass, and gastric emptying was delayed when measured 9 months after surgery (33).

There are a number of potential pitfalls in the interpretation of these studies comparing pre- and post-weight loss gastric emptying rates. For example, there is an intraindividual coefficient of variation in gastric emptying of ∼13% (34,35), so that the magnitude of the differences in gastric emptying may be statistically significantly different but not clinically relevant. There may be differences in the initial vs. overall rates of gastric emptying that require careful and thorough analysis to be ascertained, but they may reflect important differences in food handling and sensations postprandially. Thus, an initial acceleration of gastric emptying may result in reduced symptoms of fullness arising in the stomach but a greater symptom response or satiation from loading of the proximal small intestine, especially if there is a substantial osmotic load that results in large volume distension of the small bowel. Moreover, many studies (21,32,33) do not include a period of weight maintenance before the reexamination of gastric emptying to distinguish the effect of weight loss per se from the effect of the energy restriction that induced the weight loss.

A carefully performed study by Verdich et al. (25) compared gastric emptying in 19 obese (mean BMI = 38.7 kg/m2) and 12 lean (mean BMI = 23.1 kg/m2) men matched for age and height. Before weight loss, there were no differences in the overall 3-hour emptying rate, and there was a higher percentage of gastric emptying during the initial 30 minutes in the obese participants. It is conceivable that this was associated with reduced postprandial fullness (36) and, hence, reduced satiation. After the obese subjects achieved a mean weight loss of 18.8 kg by 16 weeks of dietary intervention and a further 8 weeks of weight stabilization, there was a reduction in gastric emptying during the initial 30 minutes, whereas the overall 3-hour emptying rate was not affected. The data suggested that the initial gastric emptying of a solid meal is increased in obese men and was normalized after major, sustained weight reduction. Because the result was documented after weight maintenance, it is unlikely that the actual weight loss caused the change in initial gastric emptying but, rather, that the energy restriction contributed to the change in gastric emptying.

Another pitfall in the interpretation of the effects of weight loss on gastric emptying in obesity is illustrated by the observations in patients undergoing jejunoileal bypass. Clearly, the delivery of fat and complex carbohydrate to the terminal ileum stimulates the ileal brake mechanisms (37,38) that result in retardation of gastric emptying. This mechanism is not activated in obesity preoperatively, so the slowing of gastric emptying after weight loss is related to the activation of mechanisms that are independent of the weight loss per se.

In summary, the reports about gastric emptying rate in obese subjects have shown inconsistent results, with many confounding factors that prevent unequivocal interpretation of the effect of obesity. It is not clear from these studies whether the abnormal emptying pattern is intrinsic to obesity itself or secondary to weight gain. Further studies are needed to clarify whether or not development and maintenance of obesity can be attributed to the changes in gastric emptying rate. Other factors may influence food intake and need to be carefully evaluated. These factors include gastric volumes, as discussed below.

Gastric Volumes in Obesity

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

Gastric distention during and after food ingestion contributes to the feeling of fullness or satiation. The mechanism resulting in this symptom is unclear, but distending the stomach stimulates gastric stretch receptors, triggering vagal discharges that activate hypothalamic neurons (39) and inducing the feeling of satiety (11). A relatively small study on healthy nonobese humans showed that gastric distention volumes of 800 to 900 mL regularly induced epigastric fullness, pain, nausea, and occasionally retching (40).

Autopsy studies in obese subjects have shown that some intraabdominal organs, such as the liver, small intestine, and pancreas, are heavier than in normal-weight individuals (41). However, other studies have shown wide variation of stomach size with no significant relationship to body weight (42). Obese subjects have been shown to choose more food and to consume more food per minute than nonobese subjects (43). This may indicate that obese subjects simply have a greater appetite; alternatively, some data suggest that obese individuals have larger gastric capacity or a tendency to more rapid gastric emptying than nonobese subjects. There have been two classes of studies, intubated and imaging studies, which have investigated the difference in gastric capacity between normal-weight and obese subjects. In intubated studies using an intragastric balloon to measure gastric capacity, two kinds of methods will be discussed separately. There are several methodological differences between water-filled intragastric latex balloons and air-filled intragastric, barostatically controlled polyethylene balloons. Latex balloons are less compliant than polyethylene balloons, and the method of distension also differs in the studies reported using different balloons. Thus, a volume-controlled distension of water in the gastric fundus is performed with latex balloons, whereas a pressure (barostatically)-controlled air distension is used with polyethylene balloons. Moreover, the flow of air or water volume into the balloon is different between the two methods. Hence, it is necessary to separate the review and interpretations of published data using such diverse methods.

Observations Using Intragastric Latex Balloons

Granstrom and Backman (44) measured distension of the stomach with a balloon system in 16 extremely obese and 11 normal-weight subjects and reported that the mean maximal tolerated volume was significantly greater in the obese group (1763 ± 70 vs. 1000 ± 67 mL). Geliebter (45) studied four obese and four lean subjects, using a water-filled latex balloon, which was passed through the oral route into the stomach. The balloon was filled with 0, 200, 400, 600, and 800 mL of water in a random sequence on different days. Intrabag volumes > 400 mL reduced subsequent intake of a liquid meal in both obese and lean subjects, and differences between obese and lean subjects were not significant. In the second study, the balloon was gradually filled at the rate of 100 mL/min with 30-second pauses. The subjects rated their discomfort on a scale of 1 (no discomfort) to 10 (extreme discomfort). The volume filled at a rating of 10, which is extreme discomfort, was used as an index for stomach capacity. Obese subjects had a significantly larger stomach capacity than lean subjects (1925 ± 175 vs. 1100 ± 185 mL). However, although the obese participants had a larger capacity, they did not ingest more liquid meal than the lean subjects when the balloon volume was 0. This questions whether capacity (as measured by this method that uses sensation to indicate highest volume tolerated) and meal intake on a separate occasion are truly correlated. In fact, three other studies have attempted to determine the relationship between maximum tolerated volume and independently measured gastric volume. Tack et al. (46,47) suggested that the maximum tolerated volume was significantly predictive of gastric volume measured by barostat. In contrast, Boeckxstaens et al. (48) were unable to confirm such a significant association with barostat measured gastric volumes, and Gonenne et al. (49) showed that maximum tolerated volume accounted for <25% of the variance in gastric volumes measured by single-photon emission computed tomography (SPECT).1

After some reports (44,45) suggested that gastric capacity was significantly larger in obese than in lean subjects, Geliebter et al. (43) studied 23 obese subjects using a water-filled balloon to assess the change in gastric capacity of obese subjects consuming a hypoenergetic diet for 4 weeks. They reported that subjects in the diet group, who lost a mean of 9.1 kg, showed a significant reduction in gastric capacity. Because gastric capacity can be reduced by dieting in obese subjects, the authors concluded that increased gastric capacity was a consequence of obesity. An alternative explanation of these observations is that obese individuals have reduced gastric sensation or increased gastric compliance. The latter was not measured with the latex balloon, which has an intrinsic compliance that precludes assessment of compliance. A barostatic measurement of compliance with a polyethylene, infinitely compliant balloon would be required to differentiate an effect of dieting on gastric intrinsic properties vs. reduced intake because of changes in appetite after weight loss.

A stomach with a large capacity may require a bigger meal to trigger early postprandial fullness (51). Geliebter et al. (52) compared the stomach capacity of three groups of women (10 normal, 11 obese, and 10 with bulimia) using a gastric balloon and identified a gradation in the gastric volumes from normal-weight to obese to bulimic patients. The capacity of the binge-eating obese patients was similar to that of bulimics, whereas the gastric capacity of the non-binge-eating subset was similar to that of normals. They concluded that gastric capacity seems to be influenced more by binge eating behavior than by body weight.

Observations with Intragastric, Barostatically Controlled Polyethylene Balloons

Klatt et al. (53) studied 31 obese patients and 20 healthy volunteers using a polyethylene balloon linked to an electronic barostat to investigate whether severe obesity is related to gastric dysfunctions or to abnormal perception in response to distension. This study showed that basal gastric tone, gastric accommodation postprandially, and perceptions in response to distension were not altered in obese patients. This result was different from the two studies (44,45) in which a water-filled balloon was used, but the methods are very different. Thus, Klatt et al. (44,45,53) used an electronic device to control intrabag pressure constantly and performed pressure- rather than volume-controlled distensions of the gastric fundus rather than the whole stomach. The flow of air rather than water into the balloon was also different. These factors and the differences in intrinsic compliance of the balloon itself can affect the determination of gastric compliance (54).

Potential Pitfalls of Intubated Studies to Measure Gastric Capacity

Although the majority and classical observations in the literature, to date, have used such methods, there are potential pitfalls that might influence some of the observations. Such studies of gastric capacity performed to date have required insertion of a gastric balloon or tube into the stomach, and the maximum latex water-filled balloon volume has been used as an indirect index of gastric capacity. Such balloons filled to maximum sensation are assumed to fill the entire stomach. In contrast, the objective with the barostat is to keep the balloon in apposition with the gastric internal lining, but under typical barostatically controlled low pressure, the balloon does not conform to the inner wall of the entire stomach. It is also possible that intubation and placement of the balloon into the stomach may evoke reflex relaxation of the stomach in these studies (55). It is unclear whether obese individuals have a more pronounced reflex relaxation in response to intubation or inflation with an artificial stimulus, which is a balloon, in contrast to the ingestion of a meal.

Using the sensation as the guide to determining gastric capacity by the volume of water infused into the latex balloon needed to produce discomfort on a 10-point sensation scale or to increase intragastric pressure above a specific threshold provides an additional source of variation that is unrelated to capacity. It is important to note that this method was not validated to be a reliable measurement of gastric capacity or pressure. The use of a latex balloon (which itself has an intrinsic compliance) and volume-based distentions introduces several potential errors in the estimation of gastric capacity. For example, this estimation ignores the resistance or compliance of the balloon itself, fails to correct for gastric relaxation in response to deglutition and distention, and cannot exclude individual differences in gastric sensation.

With repeat studies before and after weight loss, there are also potential effects of the differences in the abdominal wall pannus on the volume required to reach the threshold of intragastric pressures that trigger sensation and are used to define gastric capacity. Given these pitfalls, it seems that noninvasive methods that can avoid reflex relaxation and more closely reflect physiological reactions are required. The literature now presents three imaging-based methods to appraise gastric volumes: three-dimensional ultrasound (56), magnetic resonance imaging (57), and SPECT imaging (58,59,60,61,62,64), which is discussed below.

Observations on Gastric Volumes Using Imaging

Given the potential pitfalls associated with intubated methods, noninvasive methods have been developed to measure capacity in response to physiological distension with a meal. Kuiken et al. (58) developed an approach using 99mTc-pertechnetate with SPECT imaging of the gastric mucosa followed by image processing and analysis using AnalyzeAVW software (Figure 1). This method is noninvasive (58), has been validated in healthy subjects in comparison with an intragastric barostat balloon (58,59), and has been applied to measure stomach volumes and response to feeding a standard meal in patients who have dyspepsia (60) or diseases including diabetes, postgastric surgery, and rumination that are associated with upper gastrointestinal symptoms (61).

image

Figure 1. SPECT assessment of gastric volume. Images of the stomach were acquired by SPECT from a healthy subject. The reconstructed images of the stomach and its volume by using AVW 3.0 image-processing libraries during fasting (left) and 10 minutes after ingestion of 300 mL of Ensure (right). Note that the volumes and shape do not reflect the intragastric content but rather the volume and shape of the viscus (from ref. (64) with permission).

Download figure to PowerPoint

Kim et al. (62) studied 13 asymptomatic obese (mean BMI, 37.0 ± 4.9 kg/m2) and 19 nonobese control subjects (mean BMI, 26.2 ± 2.9 kg/m2) using the 99mTc-SPECT method (58) to measure fasting and postprandial gastric volumes. They showed that fasting and postprandial gastric volumes were not different in the two groups of subjects. These results do not support previous reports (44,45,50) that the gastric volume is larger in patients with obesity. Kim et al. (62) observed that the fasting volume of the distal stomach was greater in obese than in control subjects, and this was also reported by Chiloiro et al. (63) using an ultrasound study in obese children. This change in distal gastric volume in children seems to be associated with obesity itself because it was not significant after correcting for BMI.

Another approach has been used to evaluate the separate influences of gastric volume and BMI on satiation. Delgado-Aros et al. (64) measured gastric volume during fasting and after 300 mL of Ensure using SPECT imaging in 134 participants (81 women and 53 men, BMI range 17 to 48 kg/m2). Increased body mass was not associated with larger fasting gastric volumes. Conversely, increased BMI was weakly associated with reduced postprandial gastric volume. The clinical significance of reduced postprandial volume to a standardized small volume liquid nutrient meal is unclear. The relationship among gastric volume, BMI, and satiation was more formally tested by means of a nutrient drink stress test as described below.

In summary, the studies estimating gastric volume by the barostat (53) or SPECT techniques (62,64) reported no differences in gastric volume or in gastric compliance between obese and lean subjects. In contrast, several (44,45) studies of stomach capacity using an intragastric latex balloon filled with water to assess a sensory endpoint showed that gastric capacity was larger in moderate and severe obesity. Well-controlled studies assessing gastric volumes and accommodation in obese patients are necessary to determine whether gastric capacity is changed in obesity or not.

Satiation and Postprandial Symptoms in Obesity

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

Under standardized laboratory conditions, no differences in food intake behavior have been shown between obese and nonobese subjects (65,66). Hence, environmental influences in everyday activities are currently believed to be the main factors responsible for the increased food intake usually associated with obesity (67,68,69,70). However, there are data that suggest that satiation feedback signals that induce meal termination may be impaired in obese subjects (71,72,73,74).

Our group (64) has studied the associations of body mass and gastric volumes (fasting and postprandial) with satiation and postprandial symptoms among 134 participants (81 women and 53 men, BMI range 17 to 48 kg/m2) using SPECT measurements (53,58) and a nutrient drink test (46,75,76). In this study, increased body mass was associated with delayed satiation (higher maximum tolerated volume), and overweight and obese subjects ingested, on average, 225 ± 57 more kcal at maximum satiation compared with normal-weight individuals. Increased fasting gastric volume was significantly associated with delayed satiation, and this effect was independent of BMI (Figure 2). Increased BMI was associated with lower fullness and higher bloating and pain scores 30 minutes after a meal. Thus, greater BMI and fasting gastric volume were associated with delayed satiation in a controlled, laboratory-based environment with a constant rate of liquid calorie ingestion. These data strongly suggest that mechanisms that alter the fasting gastric volume may influence satiation. It is possible that fasting gastric volume is a surrogate for the sensitivity of the stomach to distension; the sensation of the stomach and other levels of the gut is altered by volume or tension mechanoreceptors (77,78,79). There is a paucity of literature in this area, and we believe it deserves further investigation. Specifically, the neurohormonal modulation of gastric volume in obesity is still poorly understood. Understanding the mechanisms of the decreased satiation responses and gastric volume will require further study that may also lead to novel approaches to controlling food intake and obesity.

image

Figure 2. (A) Effect of fasting gastric volume on time to satiation. Kaplan-Meier curves with the proportion of participants who reported maximum satiation while drinking at a constant rate, grouped by fasting gastric volume [below and above the median (211 mL) of the sample]. Note that those with a lower fasting volume presented maximum satiation sooner (median time, 40 minutes) than those with a higher fasting gastric volume (median time, 55 minutes); p = 0.007 by the log-rank test. (B) Effects of BMI and fasting gastric volume on caloric intake to achieve satiation. This bidimensional plot depicts the independent effects of BMI and fasting gastric volume on caloric intake to reach maximum satiation. Note that caloric intake increases with a different slope with BMI and with fasting gastric volume (from ref. (64) with permission).

Download figure to PowerPoint

Conclusions

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References

Gastric motor and sensory functions in obesity have been investigated in many studies to assess the potential role of the stomach in developing and maintaining obesity, but the results are not yet conclusive. Subject inclusion criteria and methodological differences are, in part, responsible for the inconsistent results. The changes in gastric sensory or motor functions in obese persons compared with those of normal-weight persons could be regarded as either part of the pathophysiology or a consequence of overeating and might be related to alterations of mechanisms that alter gastric function, including orexigenic and anorexigenic gut peptides. Our overall assessment is that the rate of gastric emptying (slow, resulting in gastric symptoms, or fast, resulting in intestinal distension) alters the postprandial sensations including satiation. Recent observations also suggest that fasting gastric volume may be an important determinant of sensations after meals. Further well-controlled, validated studies are needed to clarify a potential role of changing the motor functions of the stomach in obesity.

Footnotes
  • 1

    Nonstandard abbreviation: SPECT, single-photon emission computed tomography.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Gastric Emptying of Liquids and Solids
  5. Gastric Emptying in Obesity
  6. Effect of Weight Loss on Gastric Emptying in Obesity
  7. Gastric Volumes in Obesity
  8. Satiation and Postprandial Symptoms in Obesity
  9. Conclusions
  10. Acknowledgement
  11. References