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Microbiota's Role in Diet-Driven Alterations in Food Intake: Satiety, Energy Balance, and Reward.
Rautmann, AW, de La Serre, CB
Nutrients. 2021;(9)
Abstract
The gut microbiota plays a key role in modulating host physiology and behavior, particularly feeding behavior and energy homeostasis. There is accumulating evidence demonstrating a role for gut microbiota in the etiology of obesity. In human and rodent studies, obesity and high-energy feeding are most consistently found to be associated with decreased bacterial diversity, changes in main phyla relative abundances and increased presence of pro-inflammatory products. Diet-associated alterations in microbiome composition are linked with weight gain, adiposity, and changes in ingestive behavior. There are multiple pathways through which the microbiome influences food intake. This review discusses these pathways, including peripheral mechanisms such as the regulation of gut satiety peptide release and alterations in leptin and cholecystokinin signaling along the vagus nerve, as well as central mechanisms, such as the modulation of hypothalamic neuroinflammation and alterations in reward signaling. Most research currently focuses on determining the role of the microbiome in the development of obesity and using microbiome manipulation to prevent diet-induced increase in food intake. More studies are necessary to determine whether microbiome manipulation after prolonged energy-dense diet exposure and obesity can reduce intake and promote meaningful weight loss.
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Gastric Sensory and Motor Functions and Energy Intake in Health and Obesity-Therapeutic Implications.
Cifuentes, L, Camilleri, M, Acosta, A
Nutrients. 2021;(4)
Abstract
Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.
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The Neurocircuitry of fluid satiation.
Ryan, PJ
Physiological reports. 2018;(12):e13744
Abstract
Fluid satiation, or quenching of thirst, is a critical homeostatic signal to stop drinking; however, its underlying neurocircuitry is not well characterized. Cutting-edge genetically encoded tools and techniques are now enabling researchers to pinpoint discrete neuronal populations that control fluid satiation, revealing that hindbrain regions, such as the nucleus of the solitary tract, area postrema, and parabrachial nucleus, primarily inhibit fluid intake. By contrast, forebrain regions such as the lamina terminalis, primarily stimulate thirst and fluid intake. One intriguing aspect of fluid satiation is that thirst is quenched tens of minutes before water reaches the circulation, and the amount of water ingested is accurately calibrated to match physiological needs. This suggests that 'preabsorptive' inputs from the oropharyngeal regions, esophagus or upper gastrointestinal tract anticipate the amount of fluid required to restore fluid homeostasis, and provide rapid signals to terminate drinking once this amount has been consumed. It is likely that preabsorptive signals are carried via the vagal nerve to the hindbrain. In this review, we explore our current understanding of the fluid satiation neurocircuitry, its inputs and outputs, and its interconnections within the brain, with a focus on recent studies of the hindbrain, particularly the parabrachial nucleus.
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[Satiation and satiety in the regulation of energy intake].
García-Flores, CL, Martínez Moreno, AG, Beltrán Miranda, CP, Zepeda-Salvador, AP, Solano Santos, LV
Revista medica de Chile. 2017;(9):1172-1178
Abstract
The study of the factors that regulate high energy food intake is especially relevant nowadays due to the high prevalence of overweight and obesity. Food intake regulation can be divided in two basic processes, namely satiation and satiety. Satiation is the process that determines the moment in which feeding stops and regulates the amount of ingested food during a single meal. Satiety is the interval between meals and regulates the time elapsed between two meals. The longer the interval, the lower energy intake. Each of these processes are regulated by different factors, which are here reviewed.
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The impact of gut hormones on the neural circuit of appetite and satiety: A systematic review.
Zanchi, D, Depoorter, A, Egloff, L, Haller, S, Mählmann, L, Lang, UE, Drewe, J, Beglinger, C, Schmidt, A, Borgwardt, S
Neuroscience and biobehavioral reviews. 2017;:457-475
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The brain-gut-axis is an interdependent system affecting neural functions and controlling our eating behaviour. In recent decades, neuroimaging techniques have facilitated its investigation. We systematically looked into functional and neurochemical brain imaging studies investigating how key molecules such as ghrelin, glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY), cholecystokinin (CCK), leptin, glucose and insulin influence the function of brain regions regulating appetite and satiety. Of the 349 studies published before July 2016 identified in the database search, 40 were included (27 on healthy and 13 on obese subjects). Our systematic review suggests that the plasma level of ghrelin, the gut hormone promoting appetite, is positively correlated with activation in the pre-frontal cortex (PFC), amygdala and insula and negatively correlated with activation in subcortical areas such as the hypothalamus. In contrast, the plasma levels of glucose, insulin, leptin, PYY, GLP-1 affect the same brain regions conversely. Our study integrates previous investigations of the gut-brain matrix during food-intake and homeostatic regulation and may be of use for future meta-analyses of brain-gut interactions.
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Physiologic and Neural Controls of Eating.
Moran, TH, Ladenheim, EE
Gastroenterology clinics of North America. 2016;(4):581-599
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Multiple physiologic and neural systems contribute to the controls over what and how much we eat. These systems include signaling involved in the detection and signaling of nutrient availability, signals arising from consumed nutrients that provide feedback information during a meal to induce satiation, and signals related to the rewarding properties of eating. Each of these has a separate neural representation, but important interactions among these systems are critical to the overall controls of food intake.
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Dietary fiber and satiety: the effects of oats on satiety.
Rebello, CJ, O'Neil, CE, Greenway, FL
Nutrition reviews. 2016;(2):131-47
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This review examines the effect of β-glucan, the viscous soluble fiber in oats, on satiety. A literature search for studies that examined delivery of the fiber in whole foods or as an extract was conducted. Viscosity interferes with the peristaltic mixing process in the small intestine to impede digestion and absorption of nutrients, which precipitates satiety signals. From measurements of the physicochemical and rheological properties of β-glucan, it appears that viscosity plays a key role in modulating satiety. However, the lack of standardized methods to measure viscosity and the inherent nature of appetite make it difficult to pinpoint the reasons for inconsistent results of the effects of oats on satiety. Nevertheless, the majority of the evidence suggests that oat β-glucan has a positive effect on perceptions of satiety.
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Nutrients, satiety, and control of energy intake.
Tremblay, A, Bellisle, F
Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme. 2015;(10):971-9
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In the context of the worldwide epidemic of obesity affecting men and women of all ages, it is important to understand the mechanisms that control human appetite, particularly those that allow the adjustment of energy intake to energy needs. Satiety is one important psycho-biological mechanism whose function is to inhibit intake following the ingestion of a food or a beverage. According to the classical theories of appetite control, satiety is influenced by macronutrient intake and/or metabolism. Satiety also seems to be modified by micronutrients, non-nutrients, and some bioactive food constituents. Under optimal conditions, satiety should be well connected with hunger and satiation in a way that spontaneously leads to a close match between energy intake and expenditures. However, the current obesity epidemic suggests that dysfunctions often affect satiety and energy intake. In this regard, this paper presents a conceptual integration that hopefully will help health professionals address satiety issues and provide the public with informed advice to facilitate appetite control.
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Gut-brain nutrient signaling. Appetition vs. satiation.
Sclafani, A
Appetite. 2013;:454-8
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Multiple hormonal and neural signals are generated by ingested nutrients that limit meal size and suppress postmeal eating. However, the availability of sugar-rich and fat-rich foods can override these satiation/satiety signals and lead to overeating and obesity. The palatable flavor of these foods is one factor that promotes overeating, but sugar and fat also have postoral actions that can stimulate eating and increase food preferences. This is revealed in conditioning studies in which rodents consume flavored solutions paired with intragastric sugar or fat infusions. The significant flavor preferences and increased intake produced by the nutrient infusions appear to involve stimulatory gut-brain signals, referred to here as appetition signals, that are distinct from the satiation signals that suppress feeding. Newly developed rapid conditioning protocols may facilitate the study of postoral appetition processes.
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Factors that determine energy compensation: a systematic review of preload studies.
Almiron-Roig, E, Palla, L, Guest, K, Ricchiuti, C, Vint, N, Jebb, SA, Drewnowski, A
Nutrition reviews. 2013;(7):458-73
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Insufficient energy compensation after a preload (meal, snack, or beverage) has been associated with excess energy intake, but experimental studies have used heterogeneous methodologies, making energy compensation difficult to predict. The aim of this systematic review was to analyze the relative contributions of two key variables, preload physical form and intermeal interval (IMI), to differences in energy compensation. Forty-eight publications were included, from which percent energy compensation (%EC) data were extracted for 253 interventions (121 liquid, 69 semisolid, 20 solid, and 43 composite preloads). Energy compensation ranged from -370% (overconsumption, mostly of liquids) to 450% (overcompensation). A meta-regression analysis of studies reporting positive energy compensation showed that IMI (as the predominant factor) together with preload physical form and energy contributed significantly to %EC differences, accounting for 50% of the variance, independently from gender and BMI. Energy compensation was maximized when the preload was in semisolid/solid form and the IMI was 30-120 min. These results may assist in the interpretation of studies assessing the relative efficacy of interventions to enhance satiety, including functional foods and weight management products.