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Current Obesity Reports Mar 2016Effective strategies to combat recent rises in obesity levels are limited. The accumulation of excess body fat results when energy intake exceeds that expended. Energy... (Review)
Review
Effective strategies to combat recent rises in obesity levels are limited. The accumulation of excess body fat results when energy intake exceeds that expended. Energy balance is controlled by hypothalamic responses, but these can be overridden by hedonic/reward brain systems. This override, combined with unprecedented availability of cheap, energy-dense, palatable foods, may partly explain the increase in overweight and obesity. The complexity of the processes that regulate feeding behaviour has driven the need for further fundamental research. Full4Health is an EU-funded project conceived to advance our understanding of hunger and satiety mechanisms. Food intake has an impact on and is also affected by the gut-brain signalling which controls hunger and appetite. This review describes selected recent research from Full4Health and how new mechanistic findings could be exploited to adapt and control our physiological responses to food, potentially providing an alternative solution to addressing the global problems related to positive energy balance.
Topics: Appetite; Eating; Food, Formulated; Humans; Hunger; Obesity; Satiation
PubMed: 26762623
DOI: 10.1007/s13679-015-0184-5 -
Obesity Reviews : An Official Journal... Feb 2015Exercise is widely regarded as one of the most valuable components of behaviour that can influence body weight and therefore help in the prevention and management of... (Review)
Review
Exercise is widely regarded as one of the most valuable components of behaviour that can influence body weight and therefore help in the prevention and management of obesity. Indeed, long-term controlled trials show a clear dose-related effect of exercise on body weight. However, there is a suspicion, particularly fuelled by media reports, that exercise serves to increase hunger and drive up food intake thereby nullifying the energy expended through activity. Not everyone performing regular exercise will lose weight and several investigations have demonstrated a huge individual variability in the response to exercise regimes. What accounts for this heterogeneous response? First, exercise (or physical activity) through the expenditure of energy will influence the energy balance equation with the potential to generate an energy deficit. However, energy expenditure also influences the control of appetite (i.e. the physiological and psychological regulatory processes underpinning feeding) and energy intake. This dynamic interaction means that the prediction of a resultant shift in energy balance, and therefore weight change, will be complicated. In changing energy intake, exercise will impact on the biological mechanisms controlling appetite. It is becoming recognized that the major influences on the expression of appetite arise from fat-free mass and fat mass, resting metabolic rate, gastric adjustment to ingested food, changes in episodic peptides including insulin, ghrelin, cholecystokinin, glucagon-like peptide-1 and tyrosine-tyrosine, as well as tonic peptides such as leptin. Moreover, there is evidence that exercise will influence all of these components that, in turn, will influence the drive to eat through the modulation of hunger (a conscious sensation reflecting a mental urge to eat) and adjustments in postprandial satiety via an interaction with food composition. The specific actions of exercise on each physiological component will vary in strength from person to person (according to individual physiological characteristics) and with the intensity and duration of exercise. Therefore, individual responses to exercise will be highly variable and difficult to predict.
Topics: Appetite; Appetite Regulation; Energy Intake; Energy Metabolism; Exercise; Homeostasis; Humans; Obesity; Physical Fitness; Satiation
PubMed: 25614205
DOI: 10.1111/obr.12257 -
Clinics and Research in Hepatology and... Feb 2022Food intake and energy expenditure are key regulators of body weight. To regulate food intake, the brain must integrate physiological signals and hedonic cues. The brain... (Review)
Review
Food intake and energy expenditure are key regulators of body weight. To regulate food intake, the brain must integrate physiological signals and hedonic cues. The brain plays an essential role in modulating the appropriate responses to the continuous update of the body energy-status by the peripheral signals and the neuronal pathways that generate the gut-brain axis. This regulation encompasses various steps involved in food consumption, include satiation, satiety, and hunger. It is important to have a comprehensive understanding of the mechanisms that regulate food consumption as well as to standardize the vocabulary for the steps involved. This review discusses the current knowledge of the regulation and the contribution peripheral and central signals at each step of the cycle to control appetite. We also highlight how food intake has been measured. The increasingly complex understanding of regulation and action mechanisms intervening in the gut-brain axis offers ambitious targets for new strategies to control appetite.
Topics: Appetite; Eating; Homeostasis; Humans; Hunger; Satiation
PubMed: 34481092
DOI: 10.1016/j.clinre.2021.101794 -
Cell Jan 2020The function of central appetite neurons is instructing animals to ingest specific nutrient factors that the body needs. Emerging evidence suggests that individual... (Review)
Review
The function of central appetite neurons is instructing animals to ingest specific nutrient factors that the body needs. Emerging evidence suggests that individual appetite circuits for major nutrients-water, sodium, and food-operate on unique driving and quenching mechanisms. This review focuses on two aspects of appetite regulation. First, we describe the temporal relationship between appetite neuron activity and consumption behaviors. Second, we summarize ingestion-related satiation signals that differentially quench individual appetite circuits. We further discuss how distinct appetite and satiation systems for each factor may contribute to nutrient homeostasis from the functional and evolutional perspectives.
Topics: Animals; Appetite; Appetite Regulation; Brain; Feeding Behavior; Homeostasis; Humans; Hunger; Nervous System Physiological Phenomena; Neurons; Satiation; Sodium; Thirst
PubMed: 31923398
DOI: 10.1016/j.cell.2019.11.040 -
Cell Metabolism Oct 2022Late eating has been linked to obesity risk. It is unclear whether this is caused by changes in hunger and appetite, energy expenditure, or both, and whether molecular... (Randomized Controlled Trial)
Randomized Controlled Trial
Late eating has been linked to obesity risk. It is unclear whether this is caused by changes in hunger and appetite, energy expenditure, or both, and whether molecular pathways in adipose tissues are involved. Therefore, we conducted a randomized, controlled, crossover trial (ClinicalTrials.gov NCT02298790) to determine the effects of late versus early eating while rigorously controlling for nutrient intake, physical activity, sleep, and light exposure. Late eating increased hunger (p < 0.0001) and altered appetite-regulating hormones, increasing waketime and 24-h ghrelin:leptin ratio (p < 0.0001 and p = 0.006, respectively). Furthermore, late eating decreased waketime energy expenditure (p = 0.002) and 24-h core body temperature (p = 0.019). Adipose tissue gene expression analyses showed that late eating altered pathways involved in lipid metabolism, e.g., p38 MAPK signaling, TGF-β signaling, modulation of receptor tyrosine kinases, and autophagy, in a direction consistent with decreased lipolysis/increased adipogenesis. These findings show converging mechanisms by which late eating may result in positive energy balance and increased obesity risk.
Topics: Adult; Appetite; Eating; Energy Intake; Energy Metabolism; Ghrelin; Humans; Hunger; Leptin; Metabolic Networks and Pathways; Obesity; Overweight; Transforming Growth Factor beta; Tyrosine; p38 Mitogen-Activated Protein Kinases
PubMed: 36198293
DOI: 10.1016/j.cmet.2022.09.007 -
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 -
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 -
Applied Physiology, Nutrition, and... Oct 2015In 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,... (Review)
Review
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.
Topics: Appetite; Appetite Regulation; Energy Intake; Female; Food; Humans; Male; Obesity; Satiation
PubMed: 26394262
DOI: 10.1139/apnm-2014-0549 -
Cell Metabolism Oct 2022Morning loaded calorie intake in humans has been advocated as a dietary strategy to improve weight loss. This is also supported by animal studies suggesting time of... (Randomized Controlled Trial)
Randomized Controlled Trial
Morning loaded calorie intake in humans has been advocated as a dietary strategy to improve weight loss. This is also supported by animal studies suggesting time of eating can prevent weight gain. However, the underlying mechanisms through which timing of eating could promote weight loss in humans are unclear. In a randomized crossover trial (NCT03305237), 30 subjects with obesity/overweight underwent two 4-week calorie-restricted but isoenergetic weight loss diets, with morning loaded or evening loaded calories (45%:35%:20% versus 20%:35%:45% calories at breakfast, lunch, and dinner, respectively). We demonstrate no differences in total daily energy expenditure or resting metabolic rate related to the timing of calorie distribution, and no difference in weight loss. Participants consuming the morning loaded diet reported significantly lower hunger. Thus, morning loaded intake (big breakfast) may assist with compliance to weight loss regime through a greater suppression of appetite.
Topics: Animals; Appetite; Diet, Reducing; Energy Intake; Energy Metabolism; Healthy Volunteers; Humans; Hunger; Obesity; Weight Loss
PubMed: 36087576
DOI: 10.1016/j.cmet.2022.08.001 -
Cell Metabolism May 2023Restricting caloric intake effectively reduces body weight, but most dieters fail long-term adherence to caloric deficit and eventually regain lost weight. Hypothalamic...
Restricting caloric intake effectively reduces body weight, but most dieters fail long-term adherence to caloric deficit and eventually regain lost weight. Hypothalamic circuits that control hunger drive critically determine body weight; yet, how weight loss sculpts these circuits to motivate food consumption until lost weight is regained remains unclear. Here, we probe the contribution of synaptic plasticity in discrete excitatory afferents on hunger-promoting AgRP neurons. We reveal a crucial role for activity-dependent, remarkably long-lasting amplification of synaptic activity originating from paraventricular hypothalamus thyrotropin-releasing (PVH) neurons in long-term body weight control. Silencing PVH neurons inhibits the potentiation of excitatory input to AgRP neurons and diminishes concomitant regain of lost weight. Brief stimulation of the pathway is sufficient to enduringly potentiate this glutamatergic hunger synapse and triggers an NMDAR-dependent gaining of body weight that enduringly persists. Identification of this activity-dependent synaptic amplifier provides a previously unrecognized target to combat regain of lost weight.
Topics: Humans; Hunger; Agouti-Related Protein; Hypothalamus; Neurons; Body Weight
PubMed: 36965483
DOI: 10.1016/j.cmet.2023.03.002