A disturbance of gastric function in bulimia nervosa

Walsh, B. Timothy; Zimmerli, Ellen; Devlin, Michael J.; Guss, Janet L.; Kissileff, Harry R.

doi:10.1016/s0006-3223(03)00176-8

Cited by 38 publications

(25 citation statements)

References 25 publications

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“…For intake at the hunger quartiles (intake at minimum hunger, 25 were not significant. Similar to the pattern observed with intake at the fullness quartiles, most of the significant differences were observed between BED patients and normalweight controls, but differences were also observed with obese controls at the higher quartiles in the binge meal (see Fig.…”

Section: Intake At Hunger and Fullness Quartilesmentioning

confidence: 78%

“…Some physical processes underlying the perception and hunger and fullness appear to be disturbed among patients with BN, including gastric emptying, [17][18][19][20][21][22] release of the hormone cholecystokinin (CCK 18,23,24 ), gastric capacity, 19 and gastric relaxation. 25 One preliminary study investigating similar processes among patients with BED found that gastric capacity in patients with BED was larger than that of nonbinge eating overweight participants, but there was no evidence that gastric emptying was slowed or that release of the hormone CCK was altered among patients with BED. 26 Although this study provides some evidence for a disturbance in one physiological processes contributing to the development of satiety among patients with BED, 26 additional studies are needed to better understand the role of these physical processes in the maintenance of binge eating.…”

Section: Resultsmentioning

confidence: 99%

“…The value for the ratings range was then divided by four, which established hunger or fullness quartiles (e.g., 25, 50, and 75% of maximum fullness or hunger). Since the hunger and fullness quartiles were interpolated from the ratings range, they did not necessarily correspond to a rating made by the patient during a meal.…”

Section: Discussionmentioning

confidence: 99%

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Satiety and test meal intake among women with binge eating disorder

Sysko

Devlin

Walsh

et al. 2007

Intl J Eating Disorders

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Section: Intake At Hunger and Fullness Quartilesmentioning

confidence: 78%

Section: Resultsmentioning

confidence: 99%

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Satiety and test meal intake among women with binge eating disorder

Sysko

Devlin

Walsh

et al. 2007

Intl J Eating Disorders

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“…Within the BN literature, these studies examine stomach distention and capacity with balloons and barostats, medical devices used to maintain constant pressure in a closed chamber. The barostat is also the gold standard used to evaluate the stomach’s volume, filling and emptying (Geliebter et al, 1992; Geliebter and Hashim, 2001; Walsh et al, 2003; Zimmerli et al, 2006) and is frequently used in distention procedures.…”

Section: Resultsmentioning

confidence: 99%

An interoceptive model of bulimia nervosa: A neurobiological systematic review

Klabunde

Collado

Bohon

2017

Journal of Psychiatric Research

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The objective of our study was to examine the neurobiological support for an interoceptive sensory processing model of bulimia nervosa (BN). To do so, we conducted a systematic review of interoceptive sensory processing in BN, using the PRISMA guidelines. We searched PsychInfo, Pubmed, and Web of Knowledge databases to identify biological and behavioral studies that examine interoceptive detection in BN. After screening 390 articles for inclusion and conducting a quality assessment of articles that met inclusion criteria, we reviewed 41 articles. We found that global interoceptive sensory processing deficits may be present in BN. Specifically there is evidence of abnormal brain function, structure and connectivity in the interoceptive neural network, in addition to gastric and pain processing disturbances. These results suggest that there may be a neurobiological basis for global interoceptive sensory processing deficits in BN that remain after recovery. Data from taste and heart beat detection studies were inconclusive, yet some studies suggest interoceptive disturbances in these sensory domains. Discrepancies in findings appear to be due to methodological differences. In conclusion, interoceptive sensory processing deficits may directly contribute to and explain a variety of symptoms present in those with BN. Further examination of interoceptive sensory deficits could inform the development of treatments for those with BN.

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“…As we learn more about this and other mechanisms promoting satiation, the information gained could have important health-related applications. Disruptions of gastrointestinal satiety mechanisms are thought to contribute substantially to obesity (3) and also to eating disorders, such as bulimia nervosa (9,10,12,33). While the central nervous system remains a hotbed for research in energy balance, we must also continue to elucidate the peripheral mechanisms of feeding control.…”

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confidence: 99%

Serotonin-3 receptors in gastric mechanisms of cholecystokinin-induced satiety

Aja

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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OUR UNDERSTANDING OF THE CONTROLS of food intake has increased substantially during the last 30 years. Important in this has been the recognition of the meal as a controlled, physiologically relevant unit of energy intake. During a meal, ingested nutrients accumulate in the stomach and gradually pass to the small intestine. The gastrointestinal presence of nutrients stimulates the release of peptides and neurotransmitters that coordinate gastrointestinal secretion and motility to facilitate digestion. These events can individually, and in concert, produce signals to the brain that lead to meal termination or satiety (28) and thus determine individual meal size. The gut-brain peptide cholecystokinin (CCK) and the monoamine serotonin (5-HT) are two long-recognized agents of satiation. In this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Hayes et al. (16) present important new information about how CCK and 5-HT systems interact to promote peripheral mechanisms of satiety.Since the original demonstration (14) that systemic administration of CCK inhibits food intake in rats by reducing meal size and duration, CCK has become the best-characterized satiety factor (24). CCK is released from enteroendocrine cells in the proximal small intestine in response to fat and protein. CCK binds to CCK-1 receptors (also known as CCK-A receptors) to promote meal termination (2). CCK activates CCK-1 receptors on mechanoreceptive vagal afferents from the stomach and duodenum, as well as duodenal chemoreceptive vagal afferents, to directly transmit meal-related feedback signals to the brain (29). CCK also activates CCK-1 receptors in the circular muscle layer of the pylorus, causing it to contract. This slows gastric emptying, resulting in gastric distension and the indirect activation of gastric mechanoreceptive vagal afferents (29).The monoamine 5-HT is produced by platelets, endothelial cells, mast cells, serotonergic neurons, and enterochromaffin cells (13). Its wide distribution in the gastrointestinal tract and vasculature have made 5-HT a strong candidate for involvement in peripheral mechanisms of satiety. Parenteral administration of 5-HT reduces food intake by reducing meal size and duration (11). Like CCK, 5-HT is released from intestinal enteroendocrine cells in response to nutrients (21). In addition, 5-HT is also released in response to gastric distension (22). Gastrointestinal release of 5-HT, like CCK, activates vagal afferent fibers (22,27).Given the complex pharmacology of 5-HT receptor subtypes, and the emphasis on central 5-HT in feeding (5, 6), the identification of roles for specific 5-HT receptors in peripheral mechanisms of feeding control has been challenging. The 5-HT type-3 (5-HT3) receptor was long discounted from having an important role in the control of food intake. Systemic administration of antagonists at 5-HT3 receptors usually produced negative results and occasionally decreased food intake (7, 23, 30, 32). For some time, the only consistent data for...

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A disturbance of gastric function in bulimia nervosa

Cited by 38 publications

References 25 publications

Satiety and test meal intake among women with binge eating disorder

Satiety and test meal intake among women with binge eating disorder

An interoceptive model of bulimia nervosa: A neurobiological systematic review

Serotonin-3 receptors in gastric mechanisms of cholecystokinin-induced satiety

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