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Taste and Food Choice
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
Autonomic reflexes are controlled by a second set of axons from the ventral gustatory NST, which travels caudally to the viscerosensory NST, to salivatory nuclei, and to the dorsal motor nucleus of the vagus, to invoke parasympathetic processes associated with digestion (Travers 1993). These include salivation, gastric reflexes, and cephalic phase releases of digestive enzymes and insulin. The dorsal motor nucleus of the vagus, whose output controls these processes, lies directly beneath the NST, and sends apical dendrites toward the taste area, though their contact with taste cells of the NST has not yet been demonstrated. These cephalic phase reflexes prepare the digestive system for the nutrients they are destined to receive when a sweet or other food-like taste is registered in the NST.
StomachGastric Secretions, Motility, Digestion and Vomiting
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Gastric secretion occurs in three phases: cephalic, gastric and intestinal. The cephalic phase is initiated by the thought, sight, taste and smell of food mediated via the vagus. Vagal stimulation activates enteric nerves to release gastrin-releasing peptide (GRP) and acetylcholine. GRP released near the G cells stimulates the secretion of gastrin into blood to activate parietal and chief cells. About 20%–30% of gastric secretions (HCl, gastrin and pepsinogen) released during a meal may occur as a result of the cephalic phase.
A Historical Overview of the Gastroenteropancreatic Regulatory Peptides
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Because Edkins’ gastrin hypothesis was not as readily accepted as the discovery of secretin by Bayliss and Starling, the work of Pavlov and colleagues suggesting the importance of nerves in controlling gastric acid secretion was not entirely forgotten and, hence, continued to be a focus of investigation. That the regulation of gastric acid secretion was mediated by a close interaction between the nervous and endocrine systems was probably first perceived by the Swedish pharmacologist Uvnas. Uvnas11a demonstrated that stimulation of the vagus nerve resulted in the release of gastrin but that, in the absence of gastrin, vagal stimulation was less effective in producing acid secretion. It is well recognized that the physiological release of certain hormones may, in part, be regulated by neural mechanisms (i.e., the so-called “cephalic-phase” responses). Conversely, it is entirely possible that circulating peptides may act on neural receptors to alter neuronal function in the peripheral nervous system or possibly, in certain areas, the central nervous system. Uvnas’ perception and demonstrations of the intimate relationship between the humoral entity gastrin and vagal nerve activity was clearly prescient.
Anodal stimulation of inhibitory control and craving in satiated restrained eaters
Published in Nutritional Neuroscience, 2023
Philipp A. Schroeder, Maryam Farshad, Jennifer Svaldi
Since craving and physiological hunger can vary tremendously throughout the day and since circadian changes can affect excitability changed from tDCS [71,72], we fixed the time of testing in this study. As a limitation, chronotypes were not systematically assessed, menstrual cycle was not tested, and breakfast times were held constant across participants. Due to the double-blind sham-controlled cross-over design, anticipatory effects are likely in both sham and anodal tDCS conditions. Accordingly, behavioral performance from the SST may not reflect actual basic inhibitory levels in our participants [39]. Moreover, the assumed effects on actual food-intake are hypothetical and require further investigations using standardized food intake and longitudinal observations of weight management. As further limitations, we wish to highlight the relatively small sample size which was just sufficient to detect tDCS effects on the sample level. Due the Coronavirus pandemic, recruitment for this study was discontinued before the anticipated sample was recruited. Finally, it is noticeable that cravings were overall very low due to the standardized breakfast and time of assessment; thus, the null observation regarding food craving may reflect a general floor effect [16–18]. Nevertheless, future studies should employ standardized meals for high control of food intake, but consider testing times with higher cravings (e.g. afternoon or evenings). Moreover, as more valid physiological markers for craving, future studies can employ bogus taste tests or cephalic phase responses [73,74].
The effect of intestinal glucose load on neural regulation of food craving
Published in Nutritional Neuroscience, 2021
Marion A. Stopyra, Hans-Christoph Friederich, Sebastian Sailer, Sabina Pauen, Martin Bendszus, Wolfgang Herzog, Joe J. Simon
Connolly and colleagues [32] also failed to find differences in brain response between orally ingested sucrose and non-nutrient sweetener while viewing food images. Together with Connolly's findings, our results suggest that caloric ingestion per se, whether administered orally or intragastrically, is not sufficient to evoke differences in subjective food craving and in the neural processing of reward and inhibitory control. Our findings therefore highlight the importance of the cephalic phase and orosensory stimulation during food consumption and the interactive effect with nutritional value in order to observe significant differences in brain activation. This conclusion is in line with Crézé and colleagues [8] that congruent taste signalling and caloric content are necessary in order to evoke the appropriate neurophysiological response.
At the heart of microbial conversations: endocannabinoids and the microbiome in cardiometabolic risk
Published in Gut Microbes, 2021
Ramsha Nabihah Khan, Kristal Maner-Smith, Joshua A. Owens, Maria Estefania Barbian, Rheinallt M. Jones, Crystal R. Naudin
The cephalic phase of gastric secretion occurs before food enters the stomach, and ECS activity has been found to elicit a cephalic phase response that enhances anticipation for meals.9,92 In rats, upon high-fat liquid meal feeding, signals via the vagus nerve led to increased intestinal AEA and 2-AG.93 Moreover, this increased AEA and 2-AG was associated with increased food consumption, while a CB1 antagonist inhibited food intake.93 Furthermore, an enhancement in endocannabinoid tone is linked to an increase in the preferential uptake of palatable (high-calorie) food.94 In other studies, sham-feeding emulsions consisting of linoleic acid, oleic acid and unsaturated free fatty acids contributed to an increase in jejunum endocannabinoid levels.95 Furthermore, in a two-bottle sham-feeding preference test, rats showed a strong preference for the 18:2 free fatty acid option (high-reward diet), rather than the mineral oil, but this effect was not observed when the CB1 receptor antagonists, URB447 and AM6545, were administered.95 Thus, the ECS modulates energy balance through the regulation of feeding behavior and associated hormones in various neural circuits associated with reward-related behaviors, such as the hypothalamus.