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International Journal of Food Sciences... Dec 2017Coffee and caffeine consumption has global popularity. However, evidence for the potential of these dietary constituents to influence energy intake, gut physiology, and... (Review)
Review
Coffee and caffeine consumption has global popularity. However, evidence for the potential of these dietary constituents to influence energy intake, gut physiology, and appetite perceptions remains unclear. The purpose of this review was to examine the evidence regarding coffee and caffeine's influence on energy intake and appetite control. The literature was examined for studies that assessed the effects of caffeine and coffee on energy intake, gastric emptying, appetite-related hormones, and perceptual measures of appetite. The literature review indicated that coffee administered 3-4.5 h before a meal had minimal influence on food and macronutrient intake, while caffeine ingested 0.5-4 h before a meal may suppress acute energy intake. Evidence regarding the influence of caffeine and coffee on gastric emptying, appetite hormones, and appetite perceptions was equivocal. The influence of covariates such as genetics of caffeine metabolism and bitter taste phenotype remain unknown; longer controlled studies are needed.
Topics: Appetite; Caffeine; Coffee; Energy Intake; Humans
PubMed: 28446037
DOI: 10.1080/09637486.2017.1320537 -
Microbiome Jul 2021Feelings of hunger and satiety are the key determinants for maintaining the life of humans and animals. Disturbed appetite control may disrupt the metabolic health of... (Review)
Review
Feelings of hunger and satiety are the key determinants for maintaining the life of humans and animals. Disturbed appetite control may disrupt the metabolic health of the host and cause various metabolic disorders. A variety of factors have been implicated in appetite control, including gut microbiota, which develop the intricate interactions to manipulate the metabolic requirements and hedonic feelings. Gut microbial metabolites and components act as appetite-related signaling molecules to regulate appetite-related hormone secretion and the immune system, or act directly on hypothalamic neurons. Herein, we summarize the effects of gut microbiota on host appetite and consider the potential molecular mechanisms. Furthermore, we propose that the manipulation of gut microbiota represents a clinical therapeutic potential for lessening the development and consequence of appetite-related disorders. Video abstract.
Topics: Animals; Appetite; Appetite Regulation; Gastrointestinal Microbiome; Humans; Immune System
PubMed: 34284827
DOI: 10.1186/s40168-021-01093-y -
Neuron Aug 2017Prior mouse genetic research has set the stage for a deep understanding of appetite regulation. This goal is now being realized through the use of recent technological... (Review)
Review
Prior mouse genetic research has set the stage for a deep understanding of appetite regulation. This goal is now being realized through the use of recent technological advances, such as the ability to map connectivity between neurons, manipulate neural activity in real time, and measure neural activity during behavior. Indeed, major progress has been made with regard to meal-related gut control of appetite, arcuate nucleus-based hypothalamic circuits linking energy state to the motivational drive, hunger, and, finally, limbic and cognitive processes that bring about hunger-mediated increases in reward value and perception of food. Unexpected findings are also being made; for example, the rapid regulation of homeostatic neurons by cues that predict future food consumption. The aim of this review is to cover the major underpinnings of appetite regulation, describe recent advances resulting from new technologies, and synthesize these findings into an updated view of appetite regulation.
Topics: Agouti-Related Protein; Animals; Appetite; Appetite Regulation; Arcuate Nucleus of Hypothalamus; Gastrointestinal Tract; Humans; Neural Pathways; Neurons
PubMed: 28817798
DOI: 10.1016/j.neuron.2017.06.014 -
Nature Metabolism Jul 2022The overconsumption of highly caloric and palatable foods has caused a surge in obesity rates in the past half century, thereby posing a healthcare challenge due to the... (Review)
Review
The overconsumption of highly caloric and palatable foods has caused a surge in obesity rates in the past half century, thereby posing a healthcare challenge due to the array of comorbidities linked to heightened body fat accrual. Developing treatments to manage body weight requires a grasp of the neurobiological basis of appetite. In this Review, we discuss advances in neuroscience that have identified brain regions and neural circuits that coordinate distinct phases of eating: food procurement, food consumption, and meal termination. While pioneering work identified several hypothalamic nuclei to be involved in feeding, more recent studies have explored how neuronal populations beyond the hypothalamus, such as the mesolimbic pathway and nodes in the hindbrain, interconnect to modulate appetite. We also examine how long-term exposure to a calorically dense diet rewires feeding circuits and alters the response of motivational systems to food. Understanding how the nervous system regulates eating behaviour will bolster the development of medical strategies that will help individuals to maintain a healthy body weight.
Topics: Appetite; Body Weight; Diet; Feeding Behavior; Humans; Obesity
PubMed: 35879462
DOI: 10.1038/s42255-022-00611-y -
The Proceedings of the Nutrition Society Feb 2021The enteroendocrine system is located in the gastrointestinal (GI) tract, and makes up the largest endocrine system in the human body. Despite that, its roles and... (Review)
Review
The enteroendocrine system is located in the gastrointestinal (GI) tract, and makes up the largest endocrine system in the human body. Despite that, its roles and functions remain incompletely understood. Gut regulatory peptides are the main products of enteroendocrine cells, and play an integral role in the digestion and absorption of nutrients through their effect on intestinal secretions and gut motility. Several peptides, such as cholecystokinin, polypeptide YY and glucagon-like peptide-1, have traditionally been reported to suppress appetite following food intake, so-called satiety hormones. In this review, we propose that, in the healthy individual, this system to regulate appetite does not play a dominant role in normal food intake regulation, and that there is insufficient evidence to wholly link postprandial endogenous gut peptides with appetite-related behaviours. Instead, or additionally, top-down, hedonic drive and neurocognitive factors may have more of an impact on food intake. In GI disease however, supraphysiological levels of these hormones may have more of an impact on appetite regulation as well as contributing to other unpleasant abdominal symptoms, potentially as part of an innate response to injury. Further work is required to better understand the mechanisms involved in appetite control and unlock the therapeutic potential offered by the enteroendocrine system in GI disease and obesity.
Topics: Appetite; Appetite Regulation; Enteroendocrine Cells; Gastrointestinal Diseases; Gastrointestinal Hormones; Gastrointestinal Tract; Humans; Nutritional Physiological Phenomena; Obesity; Postprandial Period; Satiation
PubMed: 32364087
DOI: 10.1017/S0029665120006965 -
Current Opinion in Clinical Nutrition... Jul 2021The popularity of ketogenic diets in the treatment of obesity has increased dramatically over the last years, namely due to their potential appetite suppressant effect.... (Review)
Review
PURPOSE OF REVIEW
The popularity of ketogenic diets in the treatment of obesity has increased dramatically over the last years, namely due to their potential appetite suppressant effect. The purpose of this review was to examine the latest evidence regarding the impact of ketogenic diets on appetite.
RECENT FINDINGS
The majority of the studies published over the last 2 years adds to previous evidence and shows that ketogenic diets suppress the increase in the secretion of the hunger hormone ghrelin and in feelings of hunger, otherwise see when weight loss is induced by non-ketogenic diets. Research done using exogenous ketones point out in the same direction. Even though the exact mechanisms by which ketogenic diets suppress appetite remain to be fully determined, studies show that the more ketotic participants are (measured as β-hydroxybutyrate plasma concentration), the smaller is the increase in ghrelin and hunger and the larger is the increase in the release of satiety peptides. Further evidence for a direct effect of ketones on appetite comes from studies using exogenous ketones.
SUMMARY
The appetite suppressant effect of ketogenic diets may be an important asset for improving adherence to energy restricted diets and weight loss outcomes.
Topics: Appetite; Appetite Regulation; Diet, Ketogenic; Ghrelin; Humans; Hunger; Weight Loss
PubMed: 33883420
DOI: 10.1097/MCO.0000000000000760 -
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 -
Journal of Neuroendocrinology Sep 2023Serotonin is a neurotransmitter that is synthesized and released from the brainstem raphe nuclei to affect many brain functions. It is well known that the activity of... (Review)
Review
Serotonin is a neurotransmitter that is synthesized and released from the brainstem raphe nuclei to affect many brain functions. It is well known that the activity of raphe serotonergic neurons is changed in response to the changes in feeding status to regulate appetite via the serotonin receptors. Likewise, changes in volume status are known to alter the activity of raphe serotonergic neurons and drugs targeting serotonin receptors were shown to affect sodium appetite. Therefore, the central serotonin system appears to regulate ingestion of both food and salt, although neural mechanisms that induce appetite in response to hunger and sodium appetite in response to volume depletion are largely distinct from each other. In this review, we discuss our current knowledge regarding the regulation of ingestion - appetite and sodium appetite - by the central serotonin system.
Topics: Appetite; Sodium; Serotonin; Raphe Nuclei; Brain Stem; Appetite Regulation
PubMed: 37525500
DOI: 10.1111/jne.13328 -
Nutrients Apr 2022Chronic circadian disruption (CCD), such as occurs during rotating shiftwork, and insufficient sleep are each independently associated with poor health outcomes,... (Randomized Controlled Trial)
Randomized Controlled Trial
Chronic circadian disruption (CCD), such as occurs during rotating shiftwork, and insufficient sleep are each independently associated with poor health outcomes, including obesity and glucose intolerance. A potential mechanism for poor health is increased energy intake (i.e., eating), particularly during the circadian night, when the physiological response to energy intake is altered. However, the contributions of CCD and insufficient sleep to subjective hunger, appetite, food preference, and appetitive hormones are not clear. To disentangle the influences of these factors, we studied seventeen healthy young adults in a 32-day in-laboratory study designed to distribute sleep, wakefulness, and energy intake equally across all phases of the circadian cycle, thereby imposing CCD. Participants were randomized to the Control (1:2 sleep:wake ratio, = 8) or chronic sleep restriction (CSR, 1:3.3 sleep:wake ratio, = 9) conditions. Throughout each waking episode the participants completed visual analog scales pertaining to hunger, appetite, and food preference. A fasting blood sample was collected to assess appetitive hormones. CCD was associated with a significant decrease in hunger and appetite in a multitude of domains in both the Control and CSR groups. This change in hunger was significantly correlated with changes in the ghrelin/leptin ratio. These findings further our understanding of the contributions of CCD and insufficient sleep on subjective hunger and appetite as well as of their possible contributions to adverse health behaviors.
Topics: Appetite; Food Preferences; Ghrelin; Humans; Hunger; Sleep; Sleep Deprivation; Young Adult
PubMed: 35565768
DOI: 10.3390/nu14091800 -
Neuropharmacology Aug 2019To maintain sodium homeostasis, animals will readily seek and ingest salt when salt-depleted, even at concentrations that they typically find aversive when sodium... (Review)
Review
To maintain sodium homeostasis, animals will readily seek and ingest salt when salt-depleted, even at concentrations that they typically find aversive when sodium replete. This innate behaviour is known as sodium (or salt) appetite. Salt appetite is subserved by a conserved brain network that senses sodium need and promotes the ingestion of salty substances when sodium-deficient. The subfornical organ (SFO) is a circumventricular organ that has diverse roles encompassing cardiovascular regulation, energy balance, immune responses, reproduction, and hydromineral balance. The SFO acts as a central sensor of sodium need and is essential for the generation of salt appetite. In this review, we discuss recent findings on the neurochemical and circuit-level organisation of the SFO in the context of sodium appetite. This article is part of the Special Issue entitled 'Hypothalamic Control of Homeostasis'.
Topics: Animals; Appetite; Homeostasis; Humans; Sodium Chloride, Dietary; Subfornical Organ
PubMed: 30118727
DOI: 10.1016/j.neuropharm.2018.08.012