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Journal of Neuroendocrinology Nov 2021There has been a long history of research on the effects of oxytocin on feeding behaviour. The classic-held view is that the neurohormone is anorexigenic at least in... (Review)
Review
There has been a long history of research on the effects of oxytocin on feeding behaviour. The classic-held view is that the neurohormone is anorexigenic at least in rodents, although the data for humans are not so clear cut. Likewise, a physiological role for oxytocin is disputed. Thus, although pharmacological, anatomical and physiological data suggest oxytocin may have a function in satiety signalling, this view is not supported by the latest research using the genetic recording and manipulation of oxytocin neurones. Here, we avoid a discussion of the pharmacological effects of oxytocin and examine evidence, from both sides of the argument, concerning whether the endogenous oxytocin system has a role in the regulation of normal feeding.
Topics: Animals; Feeding Behavior; Humans; Neurons; Oxytocin; Rodentia; Satiation
PubMed: 34495565
DOI: 10.1111/jne.13035 -
Medicina (Kaunas, Lithuania) Aug 2019Obesity is considered to be a 20th century pandemic, and its prevalence correlates with the increasing global pollution and the presence of chemical compounds in the... (Review)
Review
Obesity is considered to be a 20th century pandemic, and its prevalence correlates with the increasing global pollution and the presence of chemical compounds in the environment. Excessive adiposity results from an imbalance between energy intake and expenditure, but it is not merely an effect of overeating and lack of physical activity. Recently, several compounds that alter the mechanisms responsible for energy homeostasis have been identified and called "obesogens". This work presents the role of obesogens in the pathogenesis of obesity. We reviewed data from in vitro animal and human studies concerning the role of obesogens in the disturbance of energy homeostasis. We identified (i) the main groups and classes of obesogens, (ii) the molecular mechanisms of their action, (iii) their deleterious effect on adipose tissue function and control of appetite, and (iv) possible directions in limiting their influence on human metabolism. Obesogens have a multifactorial detrimental influence on energy homeostasis. Focusing on limiting exposure to obesogens and improving early life nutrition seems to be the most reasonable direction of action to prevent obesity in future generations.
Topics: Adipogenesis; Adipose Tissue; Animals; Appetite Regulation; Disease Susceptibility; Endocrine Disruptors; Energy Intake; Energy Metabolism; Environmental Pollutants; Epigenesis, Genetic; Female; Food Preferences; Gene-Environment Interaction; Homeostasis; Humans; Obesity; Pregnancy; Prenatal Exposure Delayed Effects; Satiety Response
PubMed: 31438630
DOI: 10.3390/medicina55090515 -
Nutrition Reviews Jul 2022Satiety is a complex state, influenced by numerous factors that go beyond food ingestion. Satiety influences food habits and behavior, thus affecting human health. This... (Review)
Review
Satiety is a complex state, influenced by numerous factors that go beyond food ingestion. Satiety influences food habits and behavior, thus affecting human health. This review provides an overview of physiological mechanisms involved in satiety and of methodologies to assess food intake and satiety in both animal models and humans. The following topics are highlighted: differences between satiety and satiation; how the central nervous system regulates food intake and satiety; the impact of different macronutrients on satiety; and how the manipulation of food composition might influence overall satiety. Bringing together knowledge on this myriad of satiety mechanisms and how we can study them is useful to better understand and control obesity and other eating disorders.
Topics: Animals; Eating; Feeding Behavior; Food; Humans; Rodentia; Satiation
PubMed: 35190825
DOI: 10.1093/nutrit/nuac010 -
Nutrients Mar 2021Food ingestion induces homeostatic sensations (satiety, fullness) with a hedonic dimension (satisfaction, changes in mood) that characterize the postprandial experience.... (Review)
Review
Food ingestion induces homeostatic sensations (satiety, fullness) with a hedonic dimension (satisfaction, changes in mood) that characterize the postprandial experience. Both types of sensation are secondary to intraluminal stimuli produced by the food itself, as well as to the activity of the digestive tract. Postprandial sensations also depend on the nutrient composition of the meal and on colonic fermentation of non-absorbed residues. Gastrointestinal function and the sensitivity of the digestive tract, i.e., perception of gut stimuli, are determined by inherent individual factors, e.g., sex, and can be modulated by different conditioning mechanisms. This narrative review examines the factors that determine perception of digestive stimuli and the postprandial experience.
Topics: Brain; Conditioning, Psychological; Digestion; Eating; Female; Gastrointestinal Microbiome; Gastrointestinal Tract; Homeostasis; Humans; Intestinal Absorption; Intestinal Diseases; Male; Meals; Postprandial Period; Satiation; Sensation; Sex Characteristics
PubMed: 33801924
DOI: 10.3390/nu13030893 -
European Journal of Nuclear Medicine... May 2023Secretin activates brown adipose tissue (BAT) and induces satiation in both mice and humans. However, the exact brain mechanism of this satiety inducing,...
PURPOSE
Secretin activates brown adipose tissue (BAT) and induces satiation in both mice and humans. However, the exact brain mechanism of this satiety inducing, secretin-mediated gut-BAT-brain axis is largely unknown.
METHODS AND RESULTS
In this placebo-controlled, single-blinded neuroimaging study, firstly using [F]-fluorodeoxyglucose (FDG) PET measures (n = 15), we established that secretin modulated brain glucose consumption through the BAT-brain axis. Predominantly, we found that BAT and caudate glucose uptake levels were negatively correlated (r = -0.54, p = 0.037) during secretin but not placebo condition. Then, using functional magnetic resonance imaging (fMRI; n = 14), we found that secretin improved inhibitory control and downregulated the brain response to appetizing food images. Finally, in a PET-fMRI fusion analysis (n = 10), we disclosed the patterned correspondence between caudate glucose uptake and neuroactivity to reward and inhibition, showing that the secretin-induced neurometabolic coupling patterns promoted satiation.
CONCLUSION
These findings suggest that secretin may modulate the BAT-brain metabolic crosstalk and subsequently the neurometabolic coupling to induce satiation. The study advances our understanding of the secretin signaling in motivated eating behavior and highlights the potential role of secretin in treating eating disorders and obesity.
TRIAL REGISTRATION
EudraCT no. 2016-002373-35, registered 2 June 2016; Clinical Trials no. NCT03290846, registered 25 September 2017.
Topics: Adipose Tissue, Brown; Appetite; Brain; Secretin; Satiety Response; Brain-Gut Axis; Single-Blind Method; Magnetic Resonance Imaging; Positron-Emission Tomography; Glucose; Reward; Signal Transduction; Humans; Functional Neuroimaging; Feeding Behavior; Food
PubMed: 36764966
DOI: 10.1007/s00259-023-06124-4 -
Nature Feb 2022Ingested food and water stimulate sensory systems in the oropharyngeal and gastrointestinal areas before absorption. These sensory signals modulate brain appetite...
Ingested food and water stimulate sensory systems in the oropharyngeal and gastrointestinal areas before absorption. These sensory signals modulate brain appetite circuits in a feed-forward manner. Emerging evidence suggests that osmolality sensing in the gut rapidly inhibits thirst neurons upon water intake. Nevertheless, it remains unclear how peripheral sensory neurons detect visceral osmolality changes, and how they modulate thirst. Here we use optical and electrical recording combined with genetic approaches to visualize osmolality responses from sensory ganglion neurons. Gut hypotonic stimuli activate a dedicated vagal population distinct from mechanical-, hypertonic- or nutrient-sensitive neurons. We demonstrate that hypotonic responses are mediated by vagal afferents innervating the hepatic portal area (HPA), through which most water and nutrients are absorbed. Eliminating sensory inputs from this area selectively abolished hypotonic but not mechanical responses in vagal neurons. Recording from forebrain thirst neurons and behavioural analyses show that HPA-derived osmolality signals are required for feed-forward thirst satiation and drinking termination. Notably, HPA-innervating vagal afferents do not sense osmolality itself. Instead, these responses are mediated partly by vasoactive intestinal peptide secreted after water ingestion. Together, our results reveal visceral hypoosmolality as an important vagal sensory modality, and that intestinal osmolality change is translated into hormonal signals to regulate thirst circuit activity through the HPA pathway.
Topics: Ganglia, Sensory; Intestines; Osmolar Concentration; Osmotic Pressure; Satiation; Sensory Receptor Cells; Thirst; Vagus Nerve; Water
PubMed: 35082448
DOI: 10.1038/s41586-021-04359-5 -
Reviews in Endocrine & Metabolic... Sep 2020Protein-rich diets are surging in popularity for weight loss. An increase in diet-induced thermogenesis, better preservation of fat-free mass, and enhanced satiety with... (Review)
Review
Protein-rich diets are surging in popularity for weight loss. An increase in diet-induced thermogenesis, better preservation of fat-free mass, and enhanced satiety with greater dietary protein intakes may lead to increased energy expenditure and decreased energy intake; and thus promote a more negative energy balance that facilitates weight loss. Results from large randomized trials and meta-analyses of many smaller trials indicate that high-protein diets typically induce significantly greater amounts of weight loss than conventional low-fat or high-carbohydrate diets during the early, rapid weight loss phase (3-6 months), but differences between diets are attenuated and no longer significant during the late, slow weight loss phase (12-24 months). Gradually decreasing adherence may be responsible for this observation; in fact, dietary adherence, rather than macronutrient composition, is likely the major predictor of long-term weight loss success. Recently, some randomized trials evaluated the efficacy of high-protein (vs. normal-protein) diets consumed ad libitum during weight loss maintenance, i.e. after clinically significant weight loss. Weight regain may be smaller with high-protein diets in the short-term (3-12 months), but longer studies are needed to confirm this. Given the lack of conclusive evidence in favor of high-protein diets, or any other dietary pattern, it is reasonable to conclude that no individual nutrient is a friend or a foe when it comes to weight loss and its maintenance. Therefore, any diet that best suits one's dietary habits and food preferences is likely to be better adhered to, and thus lead to more successful long-term weight loss.
Topics: Diet, High-Protein; Dietary Proteins; Energy Metabolism; Humans; Obesity; Satiation; Thermogenesis; Weight Loss
PubMed: 32740867
DOI: 10.1007/s11154-020-09576-3 -
Neuroscience and Biobehavioral Reviews Jan 2022This paper reviews evidence demonstrating a bidirectional relationship between memory and eating in humans and rodents. In humans, amnesia is associated with impaired... (Review)
Review
This paper reviews evidence demonstrating a bidirectional relationship between memory and eating in humans and rodents. In humans, amnesia is associated with impaired processing of hunger and satiety cues, disrupted memory of recent meals, and overconsumption. In healthy participants, meal-related memory limits subsequent ingestive behavior and obesity is associated with impaired memory and disturbances in the hippocampus. Evidence from rodents suggests that dorsal hippocampal neural activity contributes to the ability of meal-related memory to control future intake, that endocrine and neuropeptide systems act in the ventral hippocampus to provide cues regarding energy status and regulate learned aspects of eating, and that consumption of hypercaloric diets and obesity disrupt these processes. Collectively, this evidence indicates that diet-induced obesity may be caused and/or maintained, at least in part, by a vicious cycle wherein excess intake disrupts hippocampal functioning, which further increases intake. This perspective may advance our understanding of how the brain controls eating, the neural mechanisms that contribute to eating-related disorders, and identify how to treat diet-induced obesity.
Topics: Eating; Feeding Behavior; Hippocampus; Humans; Obesity; Satiation
PubMed: 34813827
DOI: 10.1016/j.neubiorev.2021.10.051 -
The Journal of Nutrition May 2022Glucose induces the release of gastrointestinal (GI) satiation hormones, such as glucagon-like peptide 1 (GLP-1) and peptide tyrosine tyrosine (PYY), in part via the... (Randomized Controlled Trial)
Randomized Controlled Trial
The Role of D-allulose and Erythritol on the Activity of the Gut Sweet Taste Receptor and Gastrointestinal Satiation Hormone Release in Humans: A Randomized, Controlled Trial.
BACKGROUND
Glucose induces the release of gastrointestinal (GI) satiation hormones, such as glucagon-like peptide 1 (GLP-1) and peptide tyrosine tyrosine (PYY), in part via the activation of the gut sweet taste receptor (T1R2/T1R3).
OBJECTIVES
The primary objective was to investigate the importance of T1R2/T1R3 for the release of cholecystokinin (CCK), GLP-1, and PYY in response to D-allulose and erythritol by assessing the effect of the T1R2/T1R3 antagonist lactisole on these responses and as secondary objectives to study the effect of the T1R2/T1R3 blockade on gastric emptying, appetite-related sensations, and GI symptoms.
METHODS
In this randomized, controlled, double-blind, crossover study, 18 participants (5 men) with a mean ± SD BMI (in kg/m2) of 21.9 ± 1.7 and aged 24 ± 4 y received an intragastric administration of 25 g D-allulose, 50 g erythritol, or tap water, with or without 450 parts per million (ppm) lactisole, respectively, in 6 different sessions. 13C-sodium acetate was added to all solutions to determine gastric emptying. At fixed time intervals, blood and breath samples were collected, and appetite-related sensations and GI symptoms were assessed. Data were analyzed with linear mixed-model analysis.
RESULTS
D-allulose and erythritol induced a significant release of CCK, GLP-1, and PYY compared with tap water (all PHolm < 0.0001, dz >1). Lactisole did not affect the D-allulose- and erythritol-induced release of CCK, GLP-1, and PYY (all PHolm > 0.1). Erythritol significantly delayed gastric emptying, increased fullness, and decreased prospective food consumption compared with tap water (PHolm = 0.0002, dz = -1.05; PHolm = 0.0190, dz = 0.69; and PHolm = 0.0442, dz = -0.62, respectively).
CONCLUSIONS
D-allulose and erythritol stimulate the secretion of GI satiation hormones in humans. Lactisole had no effect on CCK, GLP-1, and PYY release, indicating that D-allulose- and erythritol-induced GI satiation hormone release is not mediated via T1R2/T1R3 in the gut.
Topics: Cholecystokinin; Cross-Over Studies; Erythritol; Female; Fructose; Gastrointestinal Hormones; Glucagon-Like Peptide 1; Humans; Male; Peptide YY; Satiation; Taste; Tyrosine; Water
PubMed: 35135006
DOI: 10.1093/jn/nxac026 -
Nutrition Research (New York, N.Y.) May 2020To reduce the health burden of obesity, it is important to identify safe and practical treatments that are effective for weight loss while concurrently preventing weight... (Review)
Review
To reduce the health burden of obesity, it is important to identify safe and practical treatments that are effective for weight loss while concurrently preventing weight regain. Diet-induced weight loss is usually followed by a concomitant increase in ghrelin secretion and feelings of hunger, which may compromise weight loss goals and increase the risk of weight regain. The aim of this review is to describe the status of knowledge regarding the impact of ketosis, induced by diet or exogenous ketones (ketone esters), on appetite and the potential mechanisms involved. Ketogenic diets (KDs) have been shown to prevent an increase in ghrelin secretion, otherwise seen with weight loss, as well as to reduce hunger and/or prevent hunger. However, the exact threshold of ketosis needed to induce appetite suppression, as well as the exact mechanisms that mediate such an effect, has yet to be elucidated. Use of exogenous ketones may provide an alternative to KDs, which have poor long-term adherence due to their restrictive nature. Ketone esters have been shown to have concentration-dependent effects on food intake and body weight in rodent models, with effects becoming apparent when 30% of total dietary energy comes from ketone esters (threshold effect). In humans, acute consumption of a ketone ester drink reduced feelings of hunger and increased satiety compared to a dextrose drink. With the emerging widespread acceptance of KDs and exogenous ketones in mainstream media and the diet culture, it is important to fully understand their role on appetite control and weight management and the potential mechanisms mediating this role.
Topics: 3-Hydroxybutyric Acid; Animals; Appetite Regulation; Body Weight; Diet, Ketogenic; Diet, Reducing; Dietary Supplements; Eating; Esters; Female; Ghrelin; Humans; Hydroxybutyrates; Ketones; Ketosis; Male; Obesity; Satiation
PubMed: 32193016
DOI: 10.1016/j.nutres.2020.02.010