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The Journal of Nutrition Jun 2012Satiation and satiety are central concepts in the understanding of appetite control and both have to do with the inhibition of eating. Satiation occurs during an eating... (Review)
Review
Satiation and satiety are central concepts in the understanding of appetite control and both have to do with the inhibition of eating. Satiation occurs during an eating episode and brings it to an end. Satiety starts after the end of eating and prevents further eating before the return of hunger. Enhancing satiation and satiety derived from foodstuffs was perceived as a means to facilitate weight control. Many studies have examined the various sensory, cognitive, postingestive, and postabsorptive factors that can potentially contribute to the inhibition of eating. In such studies, careful attention to study design is crucial for correct interpretation of the results. Although sweetness is a potent sensory stimulus of intake, sweet-tasting products produce satiation and satiety as a result of their volume as well as their nutrient and energy content. The particular case of energy intake from fluids has generated much research and it is still debated whether energy from fluids is as satiating as energy ingested from solid foods. This review discusses the satiating power of foods and drinks containing nutritive and nonnutritive sweeteners. The brain mechanisms of food reward (in terms of "liking" and "wanting") are also addressed. Finally, we highlight the importance of reward homeostasis, which can help prevent eating in the absence of hunger, for the control of intake.
Topics: Beverages; Food; Humans; Nutritive Value; Satiety Response; Sweetening Agents
PubMed: 22573779
DOI: 10.3945/jn.111.149583 -
Nutrients Feb 2020Leptin is a hormone released by adipose tissue that plays a key role in the control of energy homeostasis through its binding to leptin receptors (LepR), mainly... (Review)
Review
Leptin is a hormone released by adipose tissue that plays a key role in the control of energy homeostasis through its binding to leptin receptors (LepR), mainly expressed in the hypothalamus. Most scientific evidence points to leptin's satiating effect being due to its dual capacity to promote the expression of anorexigenic neuropeptides and to reduce orexigenic expression in the hypothalamus. However, it has also been demonstrated that leptin can stimulate (i) thermogenesis in brown adipose tissue (BAT) and (ii) the browning of white adipose tissue (WAT). Since the demonstration of the importance of BAT in humans 10 years ago, its study has aroused great interest, mainly in the improvement of obesity-associated metabolic disorders through the induction of thermogenesis. Consequently, several strategies targeting BAT activation (mainly in rodent models) have demonstrated great potential to improve hyperlipidemias, hepatic steatosis, insulin resistance and weight gain, leading to an overall healthier metabolic profile. Here, we review the potential therapeutic ability of leptin to correct obesity and other metabolic disorders, not only through its satiating effect, but by also utilizing its thermogenic properties.
Topics: Adipose Tissue, Brown; Adipose Tissue, White; Animals; Energy Metabolism; Humans; Hypothalamus; Leptin; Obesity; Receptors, Leptin; Satiation; Thermogenesis
PubMed: 32069871
DOI: 10.3390/nu12020472 -
Nutrients Oct 2021The prevalence of obesity, and its comorbidities, particularly type 2 diabetes, cardiovascular and hepatic disease and certain cancers, continues to rise at an alarming...
The prevalence of obesity, and its comorbidities, particularly type 2 diabetes, cardiovascular and hepatic disease and certain cancers, continues to rise at an alarming rate worldwide [...].
Topics: Appetite Regulation; Energy Intake; Gastrointestinal Tract; Humans; Obesity; Satiation
PubMed: 34684635
DOI: 10.3390/nu13103635 -
Hormone Molecular Biology and Clinical... Sep 2014Abstract Eating is a simple behavior with complex functions. The unconscious neuroendocrine process that stops eating and brings a meal to its end is called satiation.... (Review)
Review
Abstract Eating is a simple behavior with complex functions. The unconscious neuroendocrine process that stops eating and brings a meal to its end is called satiation. Energy homeostasis is mediated accomplished through the control of meal size via satiation. It involves neural integrations of phasic negative-feedback signals related to ingested food and tonic signals, such as those related to adipose tissue mass. Energy homeostasis is accomplished through adjustments in meal size brought about by changes in these satiation signals. The best understood meal-derived satiation signals arise from gastrointestinal nutrient sensing. Gastrointestinal hormones secreted during the meal, including cholecystokinin, glucagon-like peptide 1, and PYY, mediate most of these. Other physiological signals arise from activation of metabolic-sensing neurons, mainly in the hypothalamus and caudal brainstem. We review both classes of satiation signal and their integration in the brain, including their processing by melanocortin, neuropeptide Y/agouti-related peptide, serotonin, noradrenaline, and oxytocin neurons. Our review is not comprehensive; rather, we discuss only what we consider the best-understood mechanisms of satiation, with a special focus on normally operating physiological mechanisms.
Topics: Animals; Brain; Gastrointestinal Hormones; Gastrointestinal Tract; Humans; Neurosecretory Systems; Nutritional Physiological Phenomena; Satiation
PubMed: 25390024
DOI: 10.1515/hmbci-2014-0010 -
Nutrients Jan 2023The objectives of this paper are to first present physiological and ecological aspects of the unique motivational state of sodium appetite, then to focus on systemic... (Review)
Review
The objectives of this paper are to first present physiological and ecological aspects of the unique motivational state of sodium appetite, then to focus on systemic physiology and brain mechanisms. I describe how laboratory protocols have been developed to allow the study of sodium appetite under controlled conditions, and focus on two such conditions specifically. The first of these is the presentation a sodium-deficient diet (SDD) for at least one week, and the second is accelerated sodium loss using SDD for 1-2 days coupled with the diuretic furosemide. The modality of consumption is also considered, ranging from a free intake of high concentration of sodium solution, to sodium-rich food or gels, and to operant protocols. I describe the pivotal role of angiotensin and aldosterone in these appetites and discuss whether the intakes or appetite are matched to the physiological need state. Several brain systems have been identified, most recently and microscopically using molecular biological methods. These include clusters in both the hindbrain and the forebrain. Satiation of sodium appetite is often studied using concentrated sodium solutions, but these can be consumed in apparent excess, and I suggest that future studies of satiation might emulate natural conditions in which excess consumption does not occur, using either SDD only as a stimulus, offering a sodium-rich food for the assessment of appetite, or a simple operant task.
Topics: Appetite; Sodium; Diuretics; Furosemide; Satiation; Sodium, Dietary
PubMed: 36771327
DOI: 10.3390/nu15030620 -
Physiology & Behavior Oct 2016The idea that food intake is motivated by (or in anticipation of) 'hunger' arising from energy depletion is apparent in both public and scientific discourse on eating... (Review)
Review
The idea that food intake is motivated by (or in anticipation of) 'hunger' arising from energy depletion is apparent in both public and scientific discourse on eating behaviour. In contrast, our thesis is that eating is largely unrelated to short-term energy depletion. Energy requirements meal-to-meal are trivial compared with total body energy stores, and energy supply to the body's tissues is maintained if a meal or even several meals are missed. Complex and exquisite metabolic machinery ensures that this happens, but metabolic regulation is only loosely coupled with the control of energy intake. Instead, food intake needs to be controlled because the limited capacity of the gut means that processing a meal presents a significant physiological challenge and potentially hinders other activities. We illustrate the relationship between energy (food) intake and energy expenditure with a simple analogy in which: (1) water in a bathtub represents body energy content, (2) water in a saucepan represents food in the gut, and (3) the bathtub is filled via the saucepan. Furthermore, (4) it takes hours to process and pass the full energy (macronutrient) content of the saucepan to the bathtub, and (5) both the saucepan and bathtub resist filling, representing negative feedbacks on appetite (desire to eat). This model is consistent with the observations that appetite is reduced acutely by energy intake (a meal added to the limited capacity of the saucepan/gut), but not increased by an acute increase in energy expenditure (energy removed from the large store of energy in the bathtub/body). The existence of relatively very weak but chronic negative feedback on appetite proportional to body fatness is supported by observations on the dynamics of energy intake and weight gain in rat dietary obesity. (We use the term 'appetite' here because 'hunger' implies energy depletion.) In our model, appetite is motivated by the accessibility of food and the anticipated and experienced pleasure of eating it. The latter, which is similar to food reward, is determined primarily by the state of emptiness of the gut and food liking related to the food's sensory qualities and macronutrient value and the individual's dietary history. Importantly, energy density adds value because energy dense foods are less satiating kJ for kJ and satiation limits further intake. That is, energy dense foods promote energy intake by virtue (1) of being more attractive and (2) having low satiating capacity kJ for kJ, and (1) is partly a consequence of (2). Energy storage is adapted to feast and famine and that includes unevenness over time of the costs of obtaining and ingesting food compared with engaging in other activities. However, in very low-cost food environments with energy dense foods readily available, risk of obesity is high. This risk can be and is mitigated by dietary restraint, which in its simplest form could mean missing the occasional meal. Another strategy we discuss is the energy dilution achieved by replacing some sugar in the diet with low-calorie sweeteners. Perhaps as or more significant, though, is that belief in short-term energy balancing (the energy depletion model) may undermine attempts to eat less. Therefore, correcting narratives of eating to be consistent with biological reality could also assist with weight control.
Topics: Animals; Appetite; Energy Intake; Energy Metabolism; Feeding Behavior; Humans; Models, Biological; Obesity; Satiation
PubMed: 27059321
DOI: 10.1016/j.physbeh.2016.03.038 -
Physiological Reports Jun 2018Fluid satiation, or quenching of thirst, is a critical homeostatic signal to stop drinking; however, its underlying neurocircuitry is not well characterized.... (Review)
Review
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.
Topics: Brain; Brain Mapping; Drinking; Homeostasis; Humans; Neural Pathways; Prosencephalon; Rhombencephalon; Satiation; Thirst
PubMed: 29932494
DOI: 10.14814/phy2.13744 -
Cerebellum (London, England) Oct 2023Given the importance of the cerebellum in controlling movements, it might be expected that its main role in eating would be the control of motor elements such as chewing... (Review)
Review
Given the importance of the cerebellum in controlling movements, it might be expected that its main role in eating would be the control of motor elements such as chewing and swallowing. Whilst such functions are clearly important, there is more to eating than these actions, and more to the cerebellum than motor control. This review will present evidence that the cerebellum contributes to homeostatic, motor, rewarding and affective aspects of food consumption.Prediction and feedback underlie many elements of eating, as food consumption is influenced by expectation. For example, circadian clocks cause hunger in anticipation of a meal, and food consumption causes feedback signals which induce satiety. Similarly, the sight and smell of food generate an expectation of what that food will taste like, and its actual taste will generate an internal reward value which will be compared to that expectation. Cerebellar learning is widely thought to involve feed-forward predictions to compare expected outcomes to sensory feedback. We therefore propose that the overarching role of the cerebellum in eating is to respond to prediction errors arising across the homeostatic, motor, cognitive, and affective domains.
Topics: Feeding Behavior; Hunger; Satiation; Cerebellum; Learning; Eating
PubMed: 36121552
DOI: 10.1007/s12311-022-01476-3 -
Journal of Neuroendocrinology Mar 2020Microglia have been known for decades as key immune cells that shape the central nervous system (CNS) during development and respond to brain pathogens and injury in... (Review)
Review
Microglia have been known for decades as key immune cells that shape the central nervous system (CNS) during development and respond to brain pathogens and injury in adult life. Recent findings now suggest that these cells also play a highly complex role in several other functions of the CNS. In this review, we provide a brief overview of the established microglial functions in development and disease. We also discuss emerging research suggesting that microglia are important for both cognitive function and the regulation of food intake. With respect to cognitive function, current data suggest microglia are not indispensable for neurogenesis, synaptogenesis or cognition in the healthy young adult, although they crucially modulate and support these functions. In doing so, they are likely important in supporting the balance between apoptosis and survival of newborn neurones and in orchestrating appropriate synaptic remodelling in response to a learning stimulus. We also explore the possibility of a role for microglia in feeding and satiety. Microglia have been implicated in both appetite suppression with sickness and obesity and in promoting feeding under some conditions and we discuss these findings here, highlighting the contribution of these cells to healthy brain function.
Topics: Animals; Brain; Cognition; Humans; Microglia; Neurons; Satiation
PubMed: 32097992
DOI: 10.1111/jne.12838 -
Appetite Mar 2018For the past several decades, vagal and hormonal gut-brain negative feedback signaling mechanisms that promote satiety and subsequent suppression of food intake have... (Review)
Review
For the past several decades, vagal and hormonal gut-brain negative feedback signaling mechanisms that promote satiety and subsequent suppression of food intake have been explored. In addition, a separate positive feedback process termed "appetition," involving postoral signaling from the gut to the brain, has been shown to promote food intake and produce flavor-nutrient preference conditioning. Afferent fibers emerging from the vagus nerve form the main pathway by which information is relayed from the abdominal viscera to the hindbrain and eventually other higher brain regions involved in food intake. Using a specialized subdiaphragmatic vagal deafferentation technique, it was observed that gut vagal and splanchnic afferents play a role in the negative feedback control of satiety after nutrient intake; however, these afferents are not required for nutrient reinforcement or flavor-nutrient preference conditioning, thereby highlighting the distinction between the processes of satiation and appetition. By linking these physiological and behavioral processes to a neurochemical mechanism, it was found that striatal dopamine release induced by intragastric glucose infusion is involved in sweet appetite conditioning. The mechanisms underlying appetition are still being investigated but may involve other nondopaminergic neurochemical systems and/or presently undiscovered hormonal mediators. Future work to delineate the biological mechanisms whereby appetition drives increased intake and conditioned food preference in response to ingestion should take a multifaceted approach by integrating hormonal, neurophysiological, and behavioral techniques.
Topics: Animals; Appetite; Brain; Choice Behavior; Diet; Dopamine; Eating; Food Preferences; Gastrointestinal Tract; Humans; Reinforcement, Psychology; Reward; Satiation; Taste; Vagus Nerve
PubMed: 28007490
DOI: 10.1016/j.appet.2016.12.009