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PloS One 2021The feeding pattern and control of energy intake in mice housed in groups are poorly understood. Here, we determined and quantified the normal feeding microstructure of...
The feeding pattern and control of energy intake in mice housed in groups are poorly understood. Here, we determined and quantified the normal feeding microstructure of social male and female mice of the C57BL/6J genetic background fed a chow diet. Mice at 10w, 20w and 30w of age showed the expected increase in lean and fat mass, being the latter more pronounced and variable in males than in females. Under ad libitum conditions, 20w and 30w old females housed in groups showed significantly increased daily energy intake when adjusted to body weight relative to age-matched males. This was the combined result of small increases in energy intake during the nocturnal and diurnal photoperiods of the day without major changes in the circadian pattern of energy intake or spontaneous ambulatory activity. The analysis of the feeding microstructure suggests sex- and age-related contributions of meal size, meal frequency and intermeal interval to the control of energy intake under stable energy balance, but not under negative energy balance imposed by prolonged fasting. During the night, 10-20w old females ate less frequently bigger meals and spent more time eating them resulting in reduced net energy intake relative to age-matched males. In addition, male and female mice at all ages tested significantly shortened the intermeal interval during the first hours of re-feeding in response to fasting without affecting meal size. Further, 20-30w old males lengthened their intermeal interval as re-feeding time increased to reach fed-levels faster than age-matched females. Collectively, our results suggest that the physiological mechanisms controlling meal size (satiation) and the non-eating time spent between meals (satiety) during stable or negative energy balance are regulated in a sex- and age-dependent manner in social mice.
Topics: Animals; Body Weight; Dietary Fats; Energy Intake; Energy Metabolism; Feeding Behavior; Female; Male; Mice; Mice, Inbred C57BL; Satiation
PubMed: 33539467
DOI: 10.1371/journal.pone.0246569 -
Nutrients Jan 2021Signals arising from the upper part of the gut are essential for the regulation of food intake, particularly satiation. This information is supplied to the brain partly... (Review)
Review
Signals arising from the upper part of the gut are essential for the regulation of food intake, particularly satiation. This information is supplied to the brain partly by vagal nervous afferents. The porcine model, because of its sizeable gyrencephalic brain, omnivorous regimen, and comparative anatomy of the proximal part of the gut to that of humans, has provided several important insights relating to the relevance of vagally mediated gut-brain relationships to the regulation of food intake. Furthermore, its large size combined with the capacity to become obese while overeating a western diet makes it a pivotal addition to existing murine models, especially for translational studies relating to obesity. How gastric, proximal intestinal, and portal information relating to meal arrival and transit are encoded by vagal afferents and their further processing by primary and secondary brain projections are reviewed. Their peripheral and central plasticities in the context of obesity are emphasized. We also present recent insights derived from chronic stimulation of the abdominal vagi with specific reference to the modulation of mesolimbic structures and their role in the restoration of insulin sensitivity in the obese miniature pig model.
Topics: Animals; Appetite; Brain; Digestive System Physiological Phenomena; Satiety Response; Stomach; Swine; Vagus Nerve
PubMed: 33573329
DOI: 10.3390/nu13020467 -
Critical Reviews in Food Science and... 2020Digestion and health properties of food do not solely rely on the sum of nutrients but are also influenced by food structure. Dairy products present an array of... (Review)
Review
Digestion and health properties of food do not solely rely on the sum of nutrients but are also influenced by food structure. Dairy products present an array of structures due to differences in the origin of milk components and the changes induced by processing. Some dairy structures have been observed to induce specific effects on digestion rates and physiological responses. However, the underlying mechanisms are not fully understood. Gastric digestion plays a key role in controlling digestion kinetics. The main objective of this review is to expose the relevance of gastric phase as the link between dairy structures and physiological responses. The focus is on human and animal studies, and physiological relevant digestion models. Data collected showed that the structure of dairy products have a profound impact on rate of nutrient bioavailability, absorption and physiological responses, suggesting gastric digestion as the main driver. Control of gastric digestion can be a tool for delivering specific rates of nutrient digestion. Therefore, the design of food structure targeting specific gastric behavior could be of great interest for particular population needs e.g. rapid nutrient digestion will benefit elderly, and slow nutrient digestion could help to enhance satiety.
Topics: Aged; Animals; Digestion; Humans; Milk; Nutrients; Nutritive Value; Satiation
PubMed: 32056441
DOI: 10.1080/10408398.2019.1707159 -
Cell Reports Dec 2022Organisms use several strategies to mitigate mitochondrial stress, including the activation of the mitochondrial unfolded protein response (UPR). The UPR in...
Organisms use several strategies to mitigate mitochondrial stress, including the activation of the mitochondrial unfolded protein response (UPR). The UPR in Caenorhabditis elegans, regulated by the transcription factor ATFS-1, expands on this recovery program by inducing an antimicrobial response against pathogens that target mitochondrial function. Here, we show that the mammalian ortholog of ATFS-1, ATF5, protects the host during infection with enteric pathogens but, unexpectedly, by maintaining the integrity of the intestinal barrier. Intriguingly, ATF5 supports intestinal barrier function by promoting a satiety response that prevents obesity and associated hyperglycemia. This consequently averts dysregulated glucose metabolism that is detrimental to barrier function. Mechanistically, we show that intestinal ATF5 stimulates the satiety response by transcriptionally regulating the gastrointestinal peptide hormone cholecystokinin, which promotes the secretion of the hormone leptin. We propose that ATF5 protects the host from enteric pathogens by promoting intestinal barrier function through a satiety-response-mediated metabolic control mechanism.
Topics: Animals; Caenorhabditis elegans Proteins; Satiety Response; Caenorhabditis elegans; Mitochondria; Unfolded Protein Response; Mammals
PubMed: 36516750
DOI: 10.1016/j.celrep.2022.111789 -
International Journal of Obesity (2005) Dec 2020Early attempts at the objective measurement of food intake in humans followed many heuristic pioneer studies in laboratory animals, which revealed how homeostatic and... (Review)
Review
Early attempts at the objective measurement of food intake in humans followed many heuristic pioneer studies in laboratory animals, which revealed how homeostatic and hedonic factors interact to shape the daily eating patterns. Early studies in humans examined the characteristics of intake responses at discrete ingestive events. Described for the first time in 1969, the edogram consisted of a parallel recording of chewing and swallowing responses during standardized lunches, allowing parameters of the "microstructure of meals" to be quantified under varying conditions of deprivation or sensory stimulation, in parallel with overall meal size, meal duration, and eating rate. Edographic studies showed consistent changes in the microstructure of meals in response to palatability level (increased eating rate, decreased chewing time and number of chews per food unit, shorter intrameal pauses, and increased prandial drinking under improved palatability). Longer premeal deprivation affected the eating responses at the beginning of meals (decreased chewing time and number of chews per food unit) but not at the end. Eating rate decelerated during the course of meals in normal-weight participants but not in participants with obesity. These observations largely agreed with contemporary works using other objective measurement methods. They were confirmed and expanded in later studies, notably in the investigation of satiation mechanisms affecting weight control. Importantly, research has demonstrated that the parameters of the microstructure of meals not only reflect the influence of stimulatory/inhibitory factors but can, per se, exert a causal role in satiation and satiety. The early edographic recording instruments were improved over the years and taken out of laboratory settings in order to address the measurement of spontaneous intake responses in free-living individuals. Much remains to be done to make these instruments entirely reliable under the immense variety of situations where food consumption occurs.
Topics: Appetite; Deglutition; Eating; Energy Intake; Humans; Mastication; Meals; Satiation
PubMed: 32843712
DOI: 10.1038/s41366-020-00653-w -
The American Journal of Gastroenterology Aug 2022Cannabidiol (CBD), a CBR2 agonist with limited psychic effects, antagonizes CB1/CB2 receptors. Allelic variation CNR1 (gene for CBR1) rs806378 and FAAH rs324420 were... (Randomized Controlled Trial)
Randomized Controlled Trial
INTRODUCTION
Cannabidiol (CBD), a CBR2 agonist with limited psychic effects, antagonizes CB1/CB2 receptors. Allelic variation CNR1 (gene for CBR1) rs806378 and FAAH rs324420 were associated with altered gut motility and sensation. This study aimed to compare the pharmacodynamics and clinical effects of a 4-week treatment with pharmaceutical-grade CBD vs placebo and assess the interactions of FAAH and CNR1 gene variants on the effects of CBD in patients with functional dyspepsia (FD).
METHODS
We performed a randomized, double-blinded, placebo-controlled (1:1 ratio) study of CBD b.i.d. (20 mg/kg/d according to the US Food and Drug Administration escalation guidance) in FD patients with nondelayed gastric emptying (GE) at baseline. Symptoms were assessed by validated daily symptom diary (0-4 scale for upper abdominal pain, nausea, and bloating), weekly assessment of adequate relief, Leuven Postprandial Distress Scale (8 symptoms, adjectival scores rated 0-4 for severity), and quality of life (Short-Form Nepean Dyspepsia Index [average of 10 dimensions each on a 5-point scale]). After the 4-week treatment, all patients underwent measurements of GE of solids, gastric volumes, and Ensure nutrient satiation test. Statistical analysis compared 2 treatments for all endpoints and the effects of CBD in association with FAAH rs324420 and CNR1 rs806378.
RESULTS
CBD and placebo effects on physiological functions and patient response outcomes were not significantly different. There were borderline CBD treatment-by-genotype interactions: rs806378 CNR1 with Leuven Postprandial Distress Scale ( P = 0.06) and GE solids ( P = 0.12).
DISCUSSION
Approved doses of CBD used off-label do not relieve FD with normal baseline GE of solids or alter gastric motor functions and satiation. CBD treatment-by-gene interactions suggest potential benefits for postprandial distress with CNR1 rs806378 T allele.
Topics: Amidohydrolases; Cannabidiol; Double-Blind Method; Dyspepsia; Gastric Emptying; Humans; Quality of Life; Receptor, Cannabinoid, CB1; Satiation
PubMed: 35537858
DOI: 10.14309/ajg.0000000000001805 -
The International Journal of Eating... Dec 2023Gastrointestinal symptoms, particularly postprandial fullness, are frequently reported in eating disorders. Limited data exist evaluating how these symptoms change in...
Preliminary data that psychological treatment and baseline anxiety are associated with a decrease in postprandial fullness and early satiation for individuals with bulimia nervosa and related other specified feeding or eating disorder.
OBJECTIVE
Gastrointestinal symptoms, particularly postprandial fullness, are frequently reported in eating disorders. Limited data exist evaluating how these symptoms change in response to outpatient psychological treatment. The current study sought to describe the course of postprandial fullness and early satiation across psychological treatment for adults with bulimia nervosa and related other specified feeding or eating disorders and to test if anxiety moderates treatment response.
METHODS
Secondary data analysis was conducted on questionnaire data provided by 30 individuals (80% white, M(SD) = 31.43(13.44) years; 90% female) throughout treatment and six-month follow-up in a pilot trial comparing mindfulness and acceptance-based treatment with cognitive-behavioral therapy for bulimia nervosa. Participants completed items from the Rome IV Diagnostic Questionnaire for Adult Functional Gastrointestinal Disorders and the State Trait Anxiety Inventory.
RESULTS
Postprandial fullness and early satiation both significantly decreased over time (ds = 1.23-1.54; p's < .001). Baseline trait anxiety moderated this outcome, such that greater decreases were observed for those with higher baseline anxiety (p = .02).
DISCUSSION
Results extend prior work in inpatient samples by providing preliminary data that postprandial fullness and early satiation decrease with outpatient psychological treatment for bulimia nervosa. Baseline anxiety moderated this effect for postprandial fullness. Future work should replicate findings in a larger sample and test anxiety as a mechanism underlying postprandial fullness in eating disorders.
PUBLIC SIGNIFICANCE
The current study found that common gastrointestinal symptoms (postprandial fullness and early satiation) decrease over the course of outpatient psychotherapy for adults with full and subthreshold bulimia nervosa. Postprandial fullness decreased more across time for those high in anxiety.
Topics: Adult; Humans; Female; Male; Bulimia Nervosa; Preliminary Data; Feeding and Eating Disorders; Anxiety; Satiation; Anorexia Nervosa
PubMed: 37746867
DOI: 10.1002/eat.24068 -
Comprehensive Physiology Jul 2020This article in the Neural and Endocrine Section of Comprehensive Physiology discusses the physiology and pathophysiology of the pancreatic hormone amylin. Shortly after... (Review)
Review
This article in the Neural and Endocrine Section of Comprehensive Physiology discusses the physiology and pathophysiology of the pancreatic hormone amylin. Shortly after its discovery in 1986, amylin has been shown to reduce food intake as a satiation signal to limit meal size. Amylin also affects food reward, sensitizes the brain to the catabolic actions of leptin, and may also play a prominent role in the development of certain brain areas that are involved in metabolic control. Amylin may act at different sites in the brain in addition to the area postrema (AP) in the caudal hindbrain. In particular, the sensitizing effect of amylin on leptin action may depend on a direct interaction in the hypothalamus. The concept of central pathways mediating amylin action became more complex after the discovery that amylin is also synthesized in certain hypothalamic areas but the interaction between central and peripheral amylin signaling remains currently unexplored. Amylin may also play a dominant pathophysiological role that is associated with the aggregation of monomeric amylin into larger, cytotoxic molecular entities. This aggregation in certain species may contribute to the development of type 2 diabetes mellitus but also cardiovascular disease. Amylin receptor pharmacology is complex because several distinct amylin receptor subtypes have been described, because other neuropeptides [e.g., calcitonin gene-related peptide (CGRP)] can also bind to amylin receptors, and because some components of the functional amylin receptor are also used for other G-protein coupled receptor (GPCR) systems. © 2020 American Physiological Society. Compr Physiol 10:811-837, 2020.
Topics: Animals; Brain; Diabetes Mellitus; Eating; Feeding Behavior; Humans; Islet Amyloid Polypeptide; Receptors, Islet Amyloid Polypeptide; Satiation; Signal Transduction
PubMed: 32941692
DOI: 10.1002/cphy.c190034 -
The Proceedings of the Nutrition Society May 2021High-protein meals and foods are promoted for their beneficial effects on satiety, weight loss and glucose homeostasis. However, the mechanisms involved and the...
High-protein meals and foods are promoted for their beneficial effects on satiety, weight loss and glucose homeostasis. However, the mechanisms involved and the long-term benefits of such diets are still debated. We here review how the characterisation of intestinal gluconeogenesis (IGN) sheds new light on the mechanisms by which protein diets exert their beneficial effects on health. The small intestine is the third organ (in addition to the liver and kidney) contributing to endogenous glucose production via gluconeogenesis. The particularity of glucose produced by the intestine is that it is detected in the portal vein and initiates a nervous signal to the hypothalamic nuclei regulating energy homeostasis. In this context, we demonstrated that protein diets initiate their satiety effects indirectly via IGN and portal glucose sensing. This induction results in the activation of brain areas involved in the regulation of food intake. The μ-opioid-antagonistic properties of protein digests, exerted in the portal vein, are a key link between IGN induction and protein-enriched diet in the control of satiety. From our results, IGN can be proposed as a mandatory link between nutrient sensing and the regulation of whole-body homeostasis. The use of specific mouse models targeting IGN should allow us to identify several metabolic functions that could be controlled by protein diets. This will lead to the characterisation of the mechanisms by which protein diets improve whole-body homeostasis. These data could be the basis of novel nutritional strategies targeting the serious metabolic consequences of both obesity and diabetes.
Topics: Animals; Gluconeogenesis; Glucose; Intestines; Mice; Obesity; Satiation
PubMed: 33190653
DOI: 10.1017/S0029665120007922 -
Food & Function Aug 2022Lipid emulsions (LEs) with tailored digestibility have the potential to modulate satiation or act as delivery systems for lipophilic nutrients and drugs. The digestion...
Lipid emulsions (LEs) with tailored digestibility have the potential to modulate satiation or act as delivery systems for lipophilic nutrients and drugs. The digestion of LEs is governed by their interfacial emulsifier layer which determines their gastric structuring and accessibility for lipases. A plethora of LEs that potentially modulate digestion have been proposed in recent years, however, validations of altered LE digestion remain scarce. Here, we report on the digestion and satiation of three novel LEs stabilized by whey protein isolate (WPI), thermo-gelling methylcellulose (MC), or cellulose nanocrystals (CNCs) in comparison to an extensively studied surfactant-stabilized LE. LE digestion and satiation were determined in terms of gastric emptying, postprandial plasma hormone and metabolite levels characteristic for lipid digestion, perceived hunger/fullness sensations, and postprandial food intake. No major variations in gastric fat emptying were observed despite distinct gastric structuring of the LEs. The plasma satiation hormone and metabolite response was fastest and highest for WPI-stabilized LEs, indicating a limited capability of proteins to prevent lipolysis due to fast hydrolysis under gastric conditions and displacement by lipases. MC-stabilized LEs show a similar gastric structuring as surfactant-stabilized LEs but slightly reduced hormone and metabolite responses, suggesting that thermo-gelling MC prevents lipase adsorption more effectively. Ultimately, CNC-stabilized LEs showed a drastic reduction (>70%) in plasma hormone and metabolite responses. This confirms the efficiency of particle (Pickering) stabilized LEs to prevent lipolysis proposed in literature based on experiments. Subjects reported more hunger and less fullness after consumption of LEs stabilized with MC and CNCs which were able to limit satiation responses. We do not find evidence for the widely postulated ileal brake, that delivery of undigested nutrients to the ileum triggers increased satiation. On the contrary, we find decreased satiation for LEs that are able to delay lipolysis. No differences in food intake were observed 5 h after LE consumption. In conclusion, LE interfacial design modulates digestion and satiation response in humans. In particular, Pickering LEs show extraordinary capability to prevent lipolysis and qualify as oral delivery systems for lipophilic nutrients and drugs.
Topics: Cellulose; Digestion; Emulsions; Hormones; Humans; Lipase; Lipids; Satiation; Surface-Active Agents
PubMed: 35942900
DOI: 10.1039/d2fo01247b