Relationships Among the Brain, the Digestive System, and Eating Behavior Workshop Summary (2015) / Chapter Skim
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2 Interaction Between the Brain and the Digestive System
2 Interaction Between the Brain and the Digestive System
Pages 5-30
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OVERVIEW OF INTERACTIONS BETWEEN THE BRAIN AND THE DIGESTIVE SYSTEM2 In his overview of interactions between the brain and digestive system, Timothy Moran focused mainly on signals sent from the gastrointestinal (GI) tract to the brain via the vagus nerve and described how GI peptides released in response to the presence of nutrients trigger vagal nerve activity.
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• As described by Robert Ritter, the gut peptide cholecystokinin reduces food intake by modulating vagal afferent feedback to the brain. According to Ritter, non-GI peptides, such as leptin, and brain neuropeptides can trigger changes in vagal synaptic transmission and help reduce food intake.
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Vagal Afferent Feedback Signals Moran described the work of Hans-Rudolf Berthoud and colleagues, which has been instrumental in providing researchers with an understanding of the GI tract's overall vagal afferent innervation. Berthoud and Neuhuber (2000)
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Using cholecystokinin (CCK) as an example, Moran explored the role played by many gut peptides in regulating food intake by mediating the response between nutrient activity in the small intestine and vagal afferent signaling (see Figure 2-1)
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Crosstalk in the Hindbrain The vagus nerve enters the brain in an area of the brain known as the caudal medulla, with the vagal afferents and vagal efferents entering struc
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, while the vagal efferents enter the dorsal motor nucleus. The adjacency of the vagal afferents and efferents is what allows for some of the vagovagal reflexes that Moran suspects may contribute to some vagal afferent responses.
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. HOW TASTE RECEPTORS IN THE GUT INFLUENCE EATING BEHAVIOR5 Taste cells in the tongue are among the first cells in the GI tract that come into contact with food.
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As summarized by Margolskee, researchers recently have identified tastelike cells in the gut that play an important role in integrating physiological responses during digestion. Taste-like cells in the gut are not actual taste cells, although they have a number of characteristics in common with true oral taste cells: they are morphologically similar under both light and electron microscopy and produce many of the same taste signaling proteins.
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. Subsequently, E nrique Rozengurt's group identified a number of T2R bitter taste receptors in the stomach and small intestine (Wu et al., 2002)
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They also found essentially the entire taste transduction pathway as it was known to exist in oral taste cells, in gut endocrine cells, and particularly in L cells expressing GLP-1 (Jang et al., 2007)
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Oral Taste Cells and the Expression of Gut Proteins Margolskee noted that researchers have observed a number of gut hormones, including GLP1, GIP (gastric inhibitory peptide) , and CCK, expressed in multiple types of oral taste cells.
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He focused on CCK because scientists know more about how it modulates vagal afferent activity compared with what is known about other GI peptides. GI Peptides GI peptides are localized in specialized enteroendocrine cells scattered among the cells of the absorptive and secretory mucosa of the GI tract, from the stomach through the colon.
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. The Cellular Mechanisms by Which GI Peptides Modulate Vagal Afferent Activity Ritter elaborated on what Moran had discussed about CCK reducing food intake through its effect on vagal afferent neurons.
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Indeed, interaction between leptin and gut hormones begins in the GI tract, at the peripheral vagal afferents. About 45 percent of vagal afferents that innervate the tomach and s small intestine express both CCK and leptin receptors (Peters et al., 2006)
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Conclusion Based on this growing body of evidence, Ritter proposed a model in need of further study: CCK and other gut peptides activate vagal afferents and provide the primary signal for satiation, but the signal is modulated by leptin and perhaps other endocrine signals. Ritter described the vagal afferent ending as a "paintbrush that paints the .
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. Dubé then described in detail two empirical studies she and her colleagues conducted based on the Dutch Eating Behavior Questionnaire (DEBQ)
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In contrast, participants who were told that the bar was healthy reported significantly greater hunger after consumption when consumption was imposed compared with when they were given free choice. Again, for Dubé, these results highlight the need for scientific study of eating behavior and the complex interplay among different brain systems within a broader behavioral context.
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report that parental food rules can influence eating behavior, with some parents using food to reward or punish and encourage or discourage good or bad noneating behavior. Parents applying a control food rule typically use high-calorie
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as additional relevant studies. Impact of the Broader Social, Commercial, and Cultural Environment on Eating Behavior Dubé explained that plentiful correlational evidence collected at the population level over the past few decades links changes in eating behavior and BMI with various changes in the food environment.
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During his presentation, Moran had emphasized that vagal afferents innervating the stomach were stimulated by load volume, not content. A member of the audience observed that Moran had presented gastric load data from experiments using glucose and asked whether other macro nutrients produced the same effect.
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For example, would subsequent eating behavior differ if umami were placed in the gut instead of glucose? And do different amino acids placed in the gut have different satiety potency?
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on gustducin and TRPM5 knockout mice, suggesting that there may be oral and postingestive gut endocrine fat sensors tied to some taste proteins. "But a lot of work is yet to be done," he said.
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In sum, he said, "It's a very complex system where we need to understand each of the parts and understand how it functions in totality." The Role of Animal Models in Understanding Human Eating Behavior When asked about the use of animal models to study human eating behavior, Dubé opined that many processes can be studied with rats even at the presymbolic level of decision making. She pointed to Peter Shizgal's work on decision making in rats, which has documented how multiple sensory information and biological needs are integrated into a common currency driving the nature and quantity of food choices (Shizgal and Conover, 1996)
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Moran added that many of the hormones being studied for their peripheral pathway effects have the ability to cross the blood-brain barrier and directly impact brain reward pathways. Gut Peptides: Hormone Versus Paracrine Signaling and the Impact of Overall Metabolic State An audience member noted that many studies have found no relationship between levels of gut hormones circulating in the blood and subjective measures of appetite or food intake.
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can induce changes in vagal afferent signaling that lead to decreased nutrient sensing and decreased caloric feedback. When asked whether overstimulation or macronutrient content drives decreased sensitivity, Ritter replied that there is evidence for both mechanisms.
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Studying the Social Context of Eating Behavior Dubé also was asked how population-level data, such as the soft drink consumption data that she presented, could be used to generate hypotheses about eating behavior and how better-quality population data could be collected. She replied by emphasizing that the very rigorous standard for collecting population data for epidemiological study needs to be applied in the study of food environments, accounting for sampling and other research methods.
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