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Objective Fullness is a cardinal symptom in functional dyspepsia (FD). The use of real-time symptom assessment might provide more insight into factors, such as daily stress, that can influence fullness. Therefore, this study aimed to use the experience sampling method (a real-time, repeated-measurement method making use of repeated questionnaires available at random moments for a limited amount of time) to assess the association between stress and fullness in patients with FD and healthy controls (HCs). Methods Thirty-five patients with FD (25 female, mean age = 44.7 years) and 34 HCs (24 female, mean age = 44.1 years) completed the experience sampling method (a maximum of 10 random moments per day) for 7 consecutive days. Stress and fullness were rated on an 11-point Numeric Rating Scale. Data between patients with FD and HCs were statistically compared using a Student samples t test and linear mixed-effects models with repeated measures (level 1) nested within participants (level 2). Results Average fullness scores were 2.23 (standard error = 0.37) points higher in patients with FD compared with HCs (p < .001). Average stress scores were 1.37 (standard error = 0.30) points higher in patients with FD compared with HCs (p = .002). In FD, fullness scores increased with 0.14 for every 1-point increase in concurrent stress scores (p = .010). Fullness scores at t = 0 increased with 0.12 for every 1-point increase in stress scores at t = -1 (p = .019). T = 0 stress scores were not associated with change in t = -1 fullness scores. No associations between concurrent symptom scores were found for HCs. Conclusions Concurrent and preceding stress scores are positively associated with fullness scores in patients with FD, but not in HCs. These findings indicate that increased levels of stress may precede feelings of fullness in patients with FD.

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.

Peripheral glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) are secreted from enteroendocrine cells, and their plasma concentrations increase in response to eating. While the satiating effect of gut-derived CCK on food intake control is well documented, the effect of peripheral GLP-1 is less clear. There is evidence that native GLP-1 can inhibit food intake only in the fed state but not in the fasting state. We therefore hypothesised that other gut peptides released during a meal might influence the subsequent effect of endogenous GLP-1 and investigated whether CCK could do so. We found that intraperitoneal injection of CCK in food-restricted mice inhibited food intake during the first 30 min segment of a one-hour session of ad libitum chow intake and that mice compensated by increasing their intake during the second half of the session. Importantly, this compensatory behaviour was abolished by an intraperitoneal injection of GLP-1 administered following an intraperitoneal injection of CCK and prior to the one-hour session. In vivo activation of the FFA1 receptor with orally administered TAK875 increased plasma CCK concentration and, consistent with the effect of exogenous CCK, we found that prior oral administration of TAK875 increased the eating inhibitory effect of peripherally administered GLP-1. To examine the role of the vagus nerve in this effect, we utilised a saporin-based lesioning procedure to selectively ablate the CCK receptor-expressing gastrointestinal vagal afferent neurones (VANs). We found that the combined anorectic effect of TAK875 and GLP-1 was significantly attenuated in the absence of CCK receptor expressing VANs. Taken together, our results indicate that endogenous CCK interacts with GLP-1 to promote satiation and that activation of the FFA1 receptor can initiate this interaction by stimulating the release of CCK. This article is protected by copyright. All rights reserved.

Non-communicable diseases (NCDs) affect many people in Myanmar where meals often contain high amounts of oil and salt that can lead to obesity and hypertension. Therefore, healthy Myanmar curry recipes and set menus were developed following the INMUCAL-Nutrients V.4.0 guidelines. Results from sensory evaluation and nutritional values before and after consumption were compared. Satiation and satiety were analysed using a visual analogue scale (VAS). Menus as pork curry and pork rib with fermented bamboo shoot curry were selected. After menu formulation, fat, saturated fat, and sodium decreased, while fibre increased (p

Dairy snacks are available in various physical forms and their consumption is linked to improved metabolic health. The objective of this study was to determine the effect of dairy snacks of different physical forms on short-term food intake (FI), subjective appetite, and the stress hormone, cortisol, in children. Following a repeated-measures crossover design, 40 children aged 9–14 years randomly consumed 1 of 5 isoenergetic (180 kcal) snacks per study session. These snacks included solid (potato chips, cookies, and cheese), semi-solid (Greek yogurt), and fluid (2% fat milk) snacks. FI was measured 120 min after snack consumption. Subjective appetite was measured at 0 (immediately before the snack), 15, 30, 45, 60, 90, and 120 min. Salivary cortisol (n = 18) was measured after the Greek yogurt and cookie snacks at 0, 30, 60, 90, and 120 min. FI did not differ between snacks (P = 0.15). The Greek yogurt (P < 0.0001) and cheese (P = 0.0009) snacks reduced average appetite compared with the 2% fat milk snack. Salivary cortisol levels were not affected by snack (P = 0.84). This study demonstrates that dairy snacks are as effective as other popular snacks at influencing subsequent FI. However, solid and semi-solid dairy snacks are more effective at repressing subjective appetite than a fluid dairy snack. Registered at ClinicalTrials.gov (NCT02484625). Novelty: Milk, Greek yogurt and cheese have a similar effect on short-term food intake in children as popular potato chips and cookie snacks. Solid, semi-solid and liquid snacks have a similar effect on short-term food intake in children.

Protein quality has an important role in increasing satiety. Evidence suggests that whey protein (WP) provides satiety via gastrointestinal hormone secretion. Hydrolysed collagen supplementation can also stimulate the production of incretins and influence satiety and food intake. Thus, we sought to compare the effect of acute supplementation of WP or hydrolysed collagen on post-intervention appetite and energy consumption. This was a randomised, double-blind, crossover pilot study with ten healthy adult women (22·4 years/old) who were submitted to acute intake (single dose) of a beverage containing WP (40 g of concentrated WP) or hydrolysed collagen (40 g). Subjective appetite ratings (feelings of hunger, desire to eat and full stomach) were measured using the Visual Analog Scale (VAS), energy intake was quantified by ad libitum cheese bread consumption 2 hours after supplementation and blood was collected for leptin and glucose determination. There was no difference between treatment groups in the perception of hunger (P = 0·983), desire to eat (P = 0·326), full stomach feeling (P = 0·567) or food consumption (P = 0·168). Leptin concentrations at 60 min post supplementation were higher when subjects received hydrolysed collagen (P = 0·006). Acute supplementation with hydrolysed collagen increased leptin levels in comparison with WP, but had no effect on appetite measured by feelings of hunger, desire to eat, full stomach feeling (VAS) or energy consumption.

Objective Satiety, defined as the duration of the sensation of fullness, is usually measured by validated visual analog scales (VAS) for appetite. Gastric function plays a key role in food intake regulation. However, the association between gastric emptying (GE) and VAS appetite is unknown. Methods In this cross-sectional study, 134 participants (mean [SEM] age = 39 [0.8] years, mean [SEM] BMI = 38 [0.5] kg/m2 , 67% females) completed simultaneous measurements of GE and VAS appetite. After a 320-kcal meal, GE was measured by scintigraphy and appetite by validated 100-mm VAS for 240 minutes. Satiation was defined as calories consumed to terminate meal and was measured by an ad libitum meal. GE, VAS, and ad libitum meal tests were measured on the same day. Percent of meal retention in the stomach, VAS area under curve (AUC0-240 min ), and overall appetite score (OAS) were calculated. Pearson correlation (ρ) determined the association of GE with VAS appetite and satiation. Appetite components were also analyzed by quartiles based on GE120 min . Results GE120 min was correlated with sensation of VAS hungerAUC(0-240 min) (ρ = 0.24, p = 0.004), fullnessAUC(0-240 min) (ρ = 0.16, p = 0.05), and OASAUC(0-240 min) (ρ = 0.20, p = 0.02). Patients with rapid GE120 min had a mean increase in VAS hungerAUC(0-240 min) by 32 mm/min (15.62%, p = 0.03) compared with normal/slow GE120 min . Conclusions GE is associated with the sensations of appetite, and rapid GE is associated with increased appetite, which may contribute to weight gain.

Background: To date, several researchers have investigated the association between dietary fibre consumption and satiety. However, there is no study that includes both inulin and β-glucan to compare energy intake (EI) and satiety ratings. Aim: The current study investigated the effects of two dietary fibres, β-glucan and inulin, on satiety and food intake. Methods: The study was carried out among 24 woman over 18 years of age. The dietary fibres β-glucan (6 g/day) or inulin (6 g/day) were consumed by participants for five weeks. On the first and fifth week visits, the participants consumed a standard breakfast followed by an ad libitum test meal. Appetite was assessed using visual analogue scales (VAS) before and after breakfast. EI was measured at the test meal using plate waste. Results: Both dietary fibres significantly reduced the VAS scores of hunger, prospective food consumption and desire to eat, and increased satiety compared with the control group. However, the area under curve data for the VAS scores did not exhibit a significant difference. Significant reductions in EI and anthropometric values between the first and fifth week measures were observed in both dietary fibre groups. Statistically significant changes occurred in the body weight [-1.25 (1.27) kg], body mass index [-0.41 (0.42) kg/m2], waist circumference [-1.25 (1.04) cm] and waist/hip ratio [-0.01(0.01)] in the β-glucan group, whereas a statistically significant change occurred in body fat percentage in the inulin group [-2.16% (7.49)]. Conclusions: Overall, these findings demonstrate that the participants consuming β-glucan over the course of the five weeks had less EI, felt less hunger and had more satiety.

To eat or not to eat Melanocortin receptor 4 (MC4R) plays a role in regulating food intake: Its activation by a stimulating hormone inhibits appetite, whereas binding to a natural antagonist promotes appetite. Complementing a recent structure of MC4R in an inactive conformation, Israeli et al. present the structure bound to setmelanotide, a weight-control drug, and its G protein–signaling partner (see the Perspective by Farooqi). This work reveals the mechanism of MC4R activation and explains why setmelanotide acts as a potent agonist, whereas a structurally similar compound, SHU9119, is an inhibitor. The structure also provides insight into the contribution of mutations in MCR4 to weight-regulation disorders. Science , abf7958, this issue p. 808 ; see also abi8942, p. 792

Introduction Functional dyspepsia (FD) is a prevalent condition with multifactorial pathophysiology, including impaired gastric accommodation (GA), hypersensitivity to gastric distention, and delayed gastric emptying. Drink tests (DT) have been proposed as a potential biomarker for the presence and severity of gastric sensorimotor dysfunction. Thus, we aimed to summarize the state of knowledge on different DT and their potential as a biomarker for FD. Methods A PubMed and MEDLINE search was conducted for English language articles, reviews, meta-analyses, case series, and randomized controlled trials, including also published meeting abstracts. Results Several DT have been described in literature (e.g., different type of liquid, number of calories used, pace of drinking, and subject's awareness of the amount of liquid drunk). FD patients ingest significantly less volume in the different variants of the tests. The slow nutrient ("satiety drinking") test (SDT) studies show the most consistent separation between health and FD and correlation with GA. However, sensitivity to distention may be correlated with rapid DT. SDTs were used to evaluate the effect of several pharmacological agents, often showing concordance between their effects on GA and tolerated nutrient volume. This correlation was not found mainly for agents with central actions. Discussion An SDT is a potential diagnostic biomarker in FD, reflecting GA. Additional studies are required to confirm its role as a predictive biomarker for treatment outcome in FD.

Background: Dietary calcium has been proposed to reduce appetite in human studies. Postprandial satiety is mainly controlled by gut hormones. However, the effect of calcium on appetite and the role of gut hormones remain unclear. Objectives: We examined whether oral administration of calcium reduces food intake in rats and investigated the underlying mechanism. Methods: Male Sprague Dawley rats (8-12 wk old) were used after an overnight fastifffng. In a series of 2 trials with 1-wk interval between challenges, food intake was measured 0.5-24 h after oral gavage of a vehicle (saline containing 1.5% carboxymethyl cellulose) as the control treatment, or the vehicle containing various calcium compounds (calcium chloride (CaCl2), calcium carbonate, calcium lactate, in a random order) at 150 mg calcium/kg dose. A conditional taste aversion test was conducted. In separate experiments, plasma calcium and gut hormone concentrations were measured 15 or 30 min after oral administration of the calcium compounds. In anesthetized rats, portal peptide-YY (PYY) concentrations were measured after intraluminal administration of a liquid meal with or without additional calcium. Results: Oral CaCl2 reduced food intake acutely (30 min, similar to 20%, P < 0.05) compared with control rats, without taste aversion. Plasma PYY concentration was higher (100%, P < 0.05) in CaCl2-preloaded rats than in control rats, 15 min after administration. In anesthetized rats, luminal meal + CaCl2 induced a 4-fold higher increase in plasma PYY than the control treatment did. Oral administration of a calcium-sensing receptor (CaSR) agonist suppressed food intake (similar to 30%, P < 0.05), but CaCl2 and CaSR agonist did not suppress food intake under treatment with a PYY receptor antagonist. Furthermore, the CaSR antagonist attenuated the effect of CaCl2 on food intake. Conclusions: CaCl2 suppresses food intake partly by increasing CaSR-mediated PYY secretion in rats. Our findings could at least partially explain the satiating effect of calcium.

Purpose Satiety is a crucial factor in the attempt to reduce food intake for long-term body weight loss. Since there is evidence for a negative correlation between cerebral energy levels and food intake, the provision of the primary energy substrate glucose to the brain through oral ingestion of carbohydrates could trigger feelings of satiety. Therefore, we hypothesized that a low-calorie saccharide preload would increase satiety, reduce subsequent food intake, and thereby decrease overall calorie consumption. Methods In a randomized single-blind crossover study, 17 healthy young normal-weight men received saccharide (26 kcal in total) or placebo capsules 30 min before a standardized breakfast buffet. We analysed food intake from the test buffet as well as plasma glucose and serum insulin levels. Results The saccharide preload reduced food intake from the buffet by 168 (± 34) kcal (p p Conclusion A very low-calorie saccharide preload considerably reduces subsequent food intake leading to decreased overall calorie consumption. A saccharide preload before meals could, therefore, be a promising support for reducing caloric intake. German Clinical Trials Register DRKS00010281 (date of registration: 11.04.2016)

Understanding how to modulate appetite in humans is key to developing successful weight loss interventions. Here, we showed that postprandial glucose dips 2–3 h after a meal are a better predictor of postprandial self-reported hunger and subsequent energy intake than peak glucose at 0–2 h and glucose incremental area under the blood glucose curve at 0–2 h. We explore the links among postprandial glucose, appetite and subsequent energy intake in 1,070 participants from a UK exploratory and US validation cohort, who consumed 8,624 standardized meals followed by 71,715 ad libitum meals, using continuous glucose monitors to record postprandial glycaemia. For participants eating each of the standardized meals, the average postprandial glucose dip at 2–3 h relative to baseline level predicted an increase in hunger at 2–3 h (r = 0.16, P

BACKGROUND: Scant research has examined whether laboratory assessments of eating in the absence of hunger (EAH) relates to long-term diet quality. OBJECTIVE: This study investigates the association of EAH with diet quality during pregnancy. DESIGN: Pregnancy diet quality was assessed using 24-hour diet recalls collected in each pregnancy trimester. EAH was assessed in a counterbalanced, crossover laboratory feeding substudy in which participants completed two free access eating occasions following a standardized meal during their 2(nd) pregnancy trimester. PARTICIPANTS/SETTING: Data were collected from March 2015 to December 2016 from a subsample of participants (n=46) enrolled at ≤ 12 weeks gestation in an observational, prospective cohort study (the Pregnancy Eating Attributes Study) in North Carolina. INTERVENTION: Participants were presented with highly processed (HP) and minimally processed (MP) foods in two separate assessments. MAIN OUTCOME MEASURES: Scores for total Healthy Eating Index-2015 (HEI2015) and adherence to adequacy (HEI2015-adq) and moderation components (HEI2015-mod) were calculated from the diet recalls. Higher scores reflect better diet quality. STATISTICAL ANALYSES PERFORMED: Linear regressions estimated associations of pregnancy diet quality with EAH (energy, EAH-kcal; and percent offered, EAH-%) in each condition for all foods, and separately for sweet and savory foods. RESULTS: Lower pregnancy diet quality (all indicators) was associated with greater EAH-kcal and EAH-% of all foods and sweet foods in the HP condition. Each 100-kcal increase in EAH of HP foods was associated with a 2–3-point decrease (SE=0.7 – 0.8) in HEI2015 (P

The Western diet is poor in dietary fibre and previous efforts to increase fibre intake were not successful. The aim of this study was to develop sensorically appealing, fibre-enriched convenience foods. As a showcase, we prepared a fibre-enriched, fat-reduced Leberkas served in a roll and compared the reformulated product with the standard product. The design was a randomized, single-blinded cross-over study. A Leberkas meal enriched with 19.2 g of wheat fibre and resistant dextrin as well as fat- and energy-reduced (30% less calories) was served to 20 middle-aged healthy volunteers (10 male, 10 female) and compared to the standard product in a random order. Blood was repeatedly taken over a 4 h period to measure metabolic parameters as well as satiety hormones, such as glucagon-like-peptide 1, cholecystokinin, peptide YY. Satiety and consumer acceptance of the fibre-enriched meal were assessed by visual analogue scales and a questionnaire. The fibre-enriched meal showed very small significant effects at only single time points in postprandial blood glucose (at 120 min, p = 0.050) and glucoseAUC fibre 22,079 ± 2819, standard 22,912 ± 3583 (p = 0.030). The profiles of satiety hormones were comparable between both meals. No differences in subjective satiation, taste and consumer acceptance were observed between the two products, despite a marked reduction in fat and energy content of the reformulated product. It is possible to enrich a popular convenience product with dietary fibre and to markedly reduce energy content without loss of sensory qualities or satiety suggesting that development and promotion of healthier convenience foods may be a useful strategy to tackle obesity and other diet-related diseases.

Stimulation of gastrointestinal taste receptors affects eating behaviour. Intraduodenal infusion of tastants leads to increased satiation and reduced food intake, whereas intraileal infusion of tastants does not affect eating behaviour. Currently, it is unknown whether oral- or intragastric administration of tastants induces a larger effect on eating behaviour. This study investigated the effects of oral- and/or intragastric administration of quinine on food intake, appetite sensations and heart rate variability (HRV). In a blinded randomised crossover trial, thirty-two healthy volunteers participated in four interventions with a 1-week washout: oral placebo and intragastric placebo (OPGP), oral quinine and intragastric placebo (OQGP), oral placebo and intragastric quinine (OPGQ) and oral quinine and intragastric quinine (OQGQ). On test days, 150 min after a standardised breakfast, subjects ingested a capsule containing quinine or placebo and were sham-fed a mixture of quinine or placebo orally. At 50 min after intervention, subjects received an ad libitum meal to measure food intake. Visual analogue scales for appetite sensations were collected, and HRV measurements were performed at regular intervals. Oral and/or intragastric delivery of the bitter tastant quinine did not affect food intake (OPGP: 3273·6 (sem 131·8) kJ, OQGP: 3072·7 (sem 132·2) kJ, OPGQ: 3289·0 (sem 132·6) kJ and OQGQ: 3204·1 (sem 133·1) kJ, P = 0·069). Desire to eat and hunger decreased after OQGP and OPGQ compared with OPGP (P < 0·001 and P < 0·05, respectively), whereas satiation, fullness and HRV did not differ between interventions. In conclusion, sole oral sham feeding with and sole intragastric delivery of quinine decreased desire to eat and hunger, without affecting food intake, satiation, fullness or HRV.

The vagus nerve and the celiaco-mesenteric ganglia (CMG) are required for reduction of meal size (MS) and prolongation of the intermeal interval (IMI) by intraperitoneal (ip) sulfated cholecystokinin-8 (CCK-8). However, recently we have shown that the gut regulates these responses. Therefore, reevaluating the role of the vagus and the CMG in the feeding responses evoked by CCK is necessary because the gut contains the highest concentration of enteric, vagal and splanchnic afferents and CCK-A receptors, which are required for reduction of food intake by this peptide, compared to other abdominal organs. To address this necessity, we injected sulfated CCK-8 (0, 0.1, 0.5, 1 and 3 nmol/kg) in the aorta, near the gastrointestinal sites of action of the peptide, in three groups of free-feeding rats (n = 10 rats per group), subdiaphragmatic vagotomy (VGX), celiaco-mesenteric ganglionectomy (CMGX) and sham-operated, and recorded seven feeding responses. In the sham group, CCK-8 reduced MS (normal chow), prolonged the intermeal interval (IMI, time between first and second meals), increased satiety ratio (SR, IMI/MS), shortened duration of first meal, reduced total (24 hrs) food intake and reduced number of meals relative to saline vehicle. Vagotomy attenuated all of the previous responses except IMI length and SR, and CMGX attenuated all of those responses. In conclusion, the feeding responses evoked by sulfated CCK-8 require, independently, the vagus nerve and the CMG.

The review provides information on the effect of dietary fibers on the production of key gastrointestinal hormonal peptides that affect eating behavior and the formation of feelings of hunger and satiety. The mechanisms of action of dietary fiber on the production of appetite-regulating peptides are discussed. Modulation of gastrointestinal hormonal peptide secretion by dietary fibers is involved in the regulation of the balance of energy, appetite, and body weight. The aim of the research was to expand the understanding about the effects of dietary fiber on the secretion of major gastrointestinal hormonal peptides involved in appetite control, the formation of feelings of hunger, satiety and satiation. Results. Gastrointestinal hormones, as physiological regulators of food intake, play an essential role in the formation of feelings of hunger, satiety and satiation, helping to reduce appetite and maintain normal body weight. Various dietary fibers, depending on the physic-chemical properties, the amount and duration of the consumption period, can have a modulating effect on the secretion of the hunger hormone ghrelin and the hormones of satiety: leptin and intestinal peptides (glucagon-like peptide-1, cholecystokinin and YY peptide). Conclusion. Dietary fiber influence on processes of energy intake, food ingestion and nutrient absorption in gastrointestinal tract, enhance neuroendocrine responses, modulate release of appetite-regulating hormones involved in energy balance and regulation of feelings of hunger and satiety. The possibility to promote a favorable profile of the endogenic gastrointestinal hormones by inclusion of dietary fiber in food ration both in the form of the natural food and additionally as dietary supplements is of interest as one from strategies of over appetite control and normal body weight maintenance.

In the United States and Mexico, the obesity epidemic represents a significant public health problem. Although obesity is often attributed to a Western-style, high-fat diet and decreased activity, there is now compelling evidence that this, in part, occurs because of the developmental programming effects resulting from exposure to maternal overnutrition. Human and animal studies demonstrate that maternal obesity and high-fat diet result in an increased risk for childhood and adult obesity. The potential programming effects of obesity have been partly attributed to hyperphagia, which occurs as a result of increased appetite with reduced satiety neuropeptides or neurons. However, depending on maternal nutritional status during the nursing period, the programmed hyperphagia and obesity can be exacerbated or prevented in offspring born to obese mothers. The underlying mechanism of this phenomenon likely involves the plasticity of the appetite regulatory center and thus presents an opportunity to modulate feeding and satiety regulation and break the obesity cycle.

Objective: To identify how different eating behaviours are correlated, and to analyse which behaviour is a true predictor of food satisfaction while comparing the pattern in gender behaviours. Methods: The correlational study was conducted at the Department of Humanities, COMSATS University, Islamabad, Pakistan, from January to May, 2019, and comprised adult individuals of both genders from different universities and food outlets located in Islamabad. Data was collected using the adult eating behaviour questionnaire and satisfaction with food-related life scale. Data was analysed using SPSS version 25. Results: Of the 430 subjects, 183(42.5%) males and 247(57.4%) were females. All subscales of the adult eating behaviour questionnaire were correlated positively with the satisfaction with food-related life scale scale except for satiety responsiveness which showed negative correlation (r=-0.07). Enjoyment of food, food responsiveness and hunger subscales acted as true predictors of satisfaction with food-related life with correlation values of 0.37, 0.38 and 0.33 respectively. Significant difference was found across gender only on satiety responsiveness (p

Overweight and obesity are major risk factors for a number of chronic diseases, including diabetes, cardiovascular diseases, and cancer. Obesity rates are on the rise worldwide with women more frequently affected than men. Hedonic responses to food seem to play a key role in obesity, but the exact mechanisms and relationships are still poorly understood. In this study, we investigate the perceived pleasantness of food rewards in relation to satiety and calories consumed during an ad libitum meal in women. Using functional magnetic resonance imaging (fMRI) and a milkshake consumption task, we studied how experienced food values are encoded in women with healthy weight, overweight or obesity. Participants rated the pleasantness and intensity of high and low caloric milkshakes in the fMRI scanner during both the fasted and fed states. We found differences in the neural responses and experienced pleasantness of high and low caloric milkshakes depending on satiety and Body Mass Index (BMI). Women with both high ad libitum consumption levels and high BMI reported greater experienced pleasantness for milkshakes. In contrast, among women with low ad libitum consumption levels, greater BMI was associated with less experienced pleasantness. At the neural level, satiety affected women with obesity to a lesser degree than women with healthy weight. Thus, having obesity was associated with altered relationships between food consumption and the hedonic responses to food rewards as well as reduced satiety effects in women.

Several clinical trials have found that consuming more protein than the recommended dietary allowance not only reduces body weight (BW), but also enhances body composition by decreasing fat mass while preserving fat-free mass (FFM) in both low-calorie and standard-calorie diets. Fairly long-term clinical trials of 6–12 months reported that a high-protein diet (HPD) provides weight-loss effects and can prevent weight regain after weight loss. HPD has not been reported to have adverse effects on health in terms of bone density or renal function in healthy adults. Among gut-derived hormones, glucagon-like peptide-1, cholecystokinin, and peptide tyrosine-tyrosine reduce appetite, while ghrelin enhances appetite. HPD increases these anorexigenic hormone levels while decreasing orexigenic hormone levels, resulting in increased satiety signaling and, eventually, reduced food intake. Additionally, elevated diet-induced thermogenesis (DIT), increased blood amino acid concentration, increased hepatic gluconeogenesis, and increased ketogenesis caused by higher dietary protein contribute to increased satiety. The mechanism by which HPD increases energy expenditure involves two aspects: first, proteins have a markedly higher DIT than carbohydrates and fats. Second, protein intake prevents a decrease in FFM, which helps maintain resting energy expenditure despite weight loss. In conclusion, HPD is an effective and safe tool for weight reduction that can prevent obesity and obesity-related diseases. However, long-term clinical trials spanning more than 12 months should be conducted to further substantiate HPD effects.

Research demonstrates that exercise acutely reduces appetite by stimulating the secretion of gut-derived satiety hormones. Currently there is a paucity of research examining the impact of postexercise nutrient intake on appetite regulation. The objective of this study was to examine how postexercise fasting versus feeding impacts the postexercise appetite response. In a randomized crossover intervention, 14 participants (body mass index: 26.9 ± 3.5 kg·m−2; age: 26.8 ± 6.7 years) received 1 of 2 recovery beverages: (i) water control (FAST) or (ii) sweetened-milk (FED) after completing a 45-min (65%–70% peak oxygen uptake) evening exercise session (∼1900 h). Energy intake was assessed through a fasted ad libitum breakfast meal and 3-day food diaries. Perceived appetite was assessed using visual analogue scales. Appetite-regulating hormones glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY), and acyl-ghrelin were assessed pre-exercise, 1 h after exercise, and the morning following exercise. FAST increased subjective hunger compared with FED (P < 0.05). PYY and GLP-1 after exercise were decreased and acyl-ghrelin was increased in FAST, with these differences disappearing the day after exercise (P < 0.05). Ad libitum energy intake at breakfast the following morning did not differ between trials. Overall, in the absence of postexercise macronutrient consumption, there was a pronounced increase in objective and subjective appetite after exercise. The orexigenic effects of postexercise fasting, however, were not observed the morning following exercise. Novelty Postexercise fasting leads to reduced GLP-1 and PYY and increased hunger. Reduced GLP-1 and PYY after exercise is blunted by postexercise nutrient intake. Energy intake the day after exercise is not influenced by postexercise fasting.

The serum hormone concentrations were studied in a group of male F1 (C57BL/6×DBA/2) mice in different states of food activity (satiety, 24-h food deprivation, and cognitive load against the background of food deprivation). The hormonal response depended on food activity: the content of leptin, triiodothyronine, and testosterone decreased in hungry animals, while during cognitive load (learning), we observed a decrease in the concentrations of ghrelin, leptin, thyroxine, and testosterone. The exceptions were neuropeptide Y (its concentration increased in hungry animals) and corticosterone (its level remained unchanged). The use of hierarchical cluster analysis allowed identifying functional organization of the relationships within the hormonal ensemble that underwent plastic changes depending on the state of the organism. It was shown that the hormonal ensemble was system-organized in the form of a "core" that determines stability of the system and the "field", within which functional interactions of the hormones are preserved.

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.

The satiating efficiency of food has been increasingly quantified using the Satiety Quotient (SQ). The SQ integrates both the energy content of food ingested during a meal and the associated change in appetite sensations. This systematic review examines the available evidence regarding its methodological use and clinical utility. A literature search was conducted in six databases considering studies from 1900 to April 2020 that used SQ in adults, adolescents and children. All study designs were included. From the initial 495 references found, fifty-two were included. Of the studies included, thirty-three were acute studies (twenty-nine in adults and four in adolescents) and nineteen were longitudinal studies in adults. A high methodological heterogeneity in the application of the SQ was observed between studies. Five main utilisations of the SQ were identified: its association with (i) energy intake; (ii) anthropometric variables; (iii) energy expenditure/physical activity; (iv) sleep quality and quantity and (v) to classify individuals by their satiety responsiveness (i.e. low and high satiety phenotypes). Altogether, the studies suggest the SQ as an interesting clinical tool regarding the satiety responsiveness to a meal and its changes in responses to weight loss in adults. The SQ might be a reliable clinical indicator in adults when it comes to both obesity prevention and treatment. There is a need for more standardised use of the SQ in addition to further studies to investigate its validity in different contexts and populations, especially among children and adolescents.

Cholecystokinin (CCK) and leptin are satiety-controlling peptides, yet their interactive roles remain unclear. Here, we addressed this issue using in vitro and in vivo models. In rat C6 glioma cells, leptin pre-treatment enhanced Ca2+ mobilization by a CCK agonist (CCK-8s). This leptin action was reduced by Janus kinase inhibitor (AG490) or PI3-kinase inhibitor (LY294002). Meanwhile, leptin stimulation alone failed to mobilize Ca2+ even in cells overexpressing leptin receptors (C6-ObRb). Leptin increased nuclear immunoreactivity against phosphorylated STAT3 (pSTAT3) whereas CCK-8s reduced leptin-induced nuclear pSTAT3 accumulation in these cells. In the rat ventromedial hypothalamus (VMH), leptin-induced action potential firing was enhanced, whereas nuclear pSTAT3 was reduced by co-stimulation with CCK-8s. To further analyse in vivo signalling interplay, a CCK-1 antagonist (lorglumide) was intraperitoneally injected in rats following 1-h restricted feeding. Food access was increased 3-h after lorglumide injection. At this timepoint, nuclear pSTAT3 was increased whereas c-Fos was decreased in the VMH. Taken together, these results suggest that leptin and CCK receptors may both contribute to short-term satiety, and leptin could positively modulate CCK signalling. Notably, nuclear pSTAT3 levels in this experimental paradigm were negatively correlated with satiety levels, contrary to the generally described transcriptional regulation for long-term satiety via leptin receptors.

Traditional theories of neuroeconomics focus on reinforcement learning and reward value. We propose here a novel reframing of reinforcement learning and motivation that includes a hippocampal-dependent regulatory mechanism which balances cue-induced behavioral excitation with behavioral inhibition. This mechanism enables interoceptive cues produced by respective food or drug satiety to antagonize the ability of excitatory food- and drug-related environmental cues to retrieve the memories of food and drug reinforcers, thereby suppressing the power of those cues to evoke appetitive behavior. When the operation of this mechanism is impaired, ability of satiety signals to inhibit appetitive behavior is weakened because the relative balance between inhibition and simple excitation is shifted toward increased retrieval of food and drug memories by environmental cues. In the present paper, we (1) describe the associative processes that constitute this mechanism of hippocampal-dependent behavior inhibition; (2) describe how a prevailing obesity-promoting diet and drugs of abuse produce hippocampal pathophysiologies that can selectively impair this inhibitory function; and (3) propose how glucagon-like peptide 1 (GLP-1), an incretin hormone that is recognized as an important satiety signal, may work to protect the hippocampal-dependent inhibition. Our perspective may add to neuroscientific and neuroeconomic analyses of both overeating and drug abuse by outlining the role of hippocampal-dependent memory processes in the control of both food and drug seeking behaviors. In addition, this view suggests that consideration should be given to diet- and drug induced hippocampal pathophysiologies, as potential novel targets for the treatment of dysregulated energy and drug intake.

Background Type 2 resistant starch (RS2) has been shown to improve metabolic health outcomes and may increase satiety and suppress appetite and food intake in humans. Objective This study assessed whether 12 weeks of daily RS2 supplementation could influence appetite perception, food intake, and appetite-related gut hormones in adults with prediabetes, relative to the control (CTL) group. Design The study was a randomized controlled trial and analysis of secondary study end points. Participants/setting Sixty-eight adults (body mass index ≥27) aged 35 to 75 years with prediabetes were enrolled in the study at Pennington Biomedical Research Center (2012 to 2016). Fifty-nine subjects were included in the analysis. Intervention Participants were randomized to consume 45 g/day of high-amylose maize (RS2) or an isocaloric amount of the rapidly digestible starch amylopectin (CTL) for 12 weeks. Main outcome measures Subjective appetite measures were assessed via visual analogue scale and the Eating Inventory; appetite-related gut hormones (glucagon-like peptide 1, peptide YY, and ghrelin) were measured during a standard mixed-meal test; and energy and macronutrient intake were assessed by a laboratory food intake (buffet) test, the Remote Food Photography Method, and SmartIntake app. Statistical analyses performed Data were analyzed using linear mixed models, adjusting for treatment group and time as fixed effects, with a significance level of α=.05. Results RS2 had no effect on subjective measures of appetite, as assessed by visual analogue scale (P>0.05) and the Eating Inventory (P≥0.24), relative to the CTL group. There were no effects of RS2 supplementation on appetite-related gut hormones, including glucagon-like peptide 1 (P=0.61), peptide YY (P=0.34), and both total (P=0.26) and active (P=0.47) ghrelin compared with the CTL. RS2 had no effect on total energy (P=0.30), carbohydrate (P=0.11), protein (P=0.64), or fat (P=0.37) consumption in response to a buffet meal test, relative to the CTL. In addition, total energy (P=0.40), carbohydrate (P=0.15), protein (P=0.46), and fat (P=0.53) intake, as quantified by the Remote Food Photography Method, were also unaffected by RS2, relative to the CTL. Conclusions RS2 supplementation did not increase satiety or reduce appetite and food intake in adults with prediabetes.

Smoothies are a popular breakfast option. However, liquids may evoke weaker satiation than nutritionally comparable semi-solid and solid foods. This study examined consumption of cereal and milk (CM) or a nutritionally comparable fruit smoothie (FS) for breakfast on subsequent dietary behaviours, in a controlled laboratory setting. Twenty-five participants (age 25 ± 6 y) completed three trials, receiving either CM or FS for breakfast. Afterwards, participants remained isolated for 4 h with

Background: Stevia is a zero-calorie alternative to caloric sugars. Substituting caloric sweeteners with noncaloric sweeteners reduces available energy, but their effects on appetite, subsequent food intake, and neurocognitive responses are still unclear. Objective: The aim was to examine whether sweetness with or without calories influences food intake, appetite, blood glucose concentrations, and attentional bias (AB) to food cues. Methods: This was a randomized, controlled, double-blind crossover study. Healthy participants [n = 20; aged 27 ± 5 y, 55% female; BMI (kg/m2): 21.8 ± 1.5] completed 5 visits, consuming 5 study beverages: 330 mL water (control, no sweet taste, no calories) and either 330 mL water containing 40 g glucose or sucrose (sweet taste; calories, both 160 kcal), maltodextrin (no sweet taste; calories, 160 kcal), or 240 ppm stevia (sweet taste, no calories). Glucose and stevia beverages were matched for sweetness. Subjective appetite ratings and blood glucose were measured at baseline and at 15, 30, and 60 min postprandially. At 15 min participants performed a visual-dot probe task to assess AB to food cues; at 30 min, participants were offered an ad libitum lunch; food intake was measured. Results: Subjective appetite ratings showed that preload sweetness and calorie content both affected appetite. The total AUC for glycemia was significantly higher after the caloric beverages (mean ± SD: maltodextrin, 441 ± 57.6; glucose, 462 ± 68.1; sucrose, 425 ± 53.6 mmol × min × L-1 ) compared with both stevia (320 ± 34.2 mmol × min × L-1) and water (304 ± 32.0 mmol × min × L-1) (all P < 0.001). Total energy intake (beverage and meal) was significantly lower after the stevia beverage (727 ± 239 kcal) compared with water (832 ± 198 kcal, P = 0.013), with no significant difference between the water and caloric beverages (P = 1.00 for water vs. maltodextrin, glucose, and sucrose). However, food-related AB did not differ across conditions (P = 0.140). Conclusions: This study found a beneficial and specific effect of a stevia beverage consumed prior to a meal on appetite and energy intake in healthy adults. This trial is registered at clinicaltrials.gov as NCT03711084.

Scarce research has examined the links between stress, anxiety, and gastrointestinal (GI) symptoms during competition, despite that they are positively correlated in the general population. A total of 186 endurance athletes completed the Perceived Stress Scale (PSS)-14, Anxiety Sensitivity Index (ASI)-3, and State-Trait Inventory for Cognitive and Somatic Anxiety (STICSA) before races. Afterwards, they reported the severity of in-race GI symptoms. Associations between high levels of stress and anxiety (defined as the top tertile) and GI distress (≥3 on a 0-10 scale) were examined using logistic regression. Athletes with high PSS-14 scores did not have greater odds of GI symptoms, except nausea (odds ratio [OR] = 2.21, 95% confidence interval [CI] 1.02-4.78). High scores on the STICSA-trait were associated with nausea (OR = 3.43, 95% CI 1.57-7.50) and regurgitation/reflux (OR = 3.31, 95% CI 1.26-8.73). Among a sub-sample of 125 participants that completed STICSA-state questionnaires, higher anxiety was associated with nausea (OR = 5.57, 95% CI 1.96-15.83), regurgitation/reflux (OR = 3.75, 95% CI 1.17-12.00), fullness (OR = 2.98, 95% CI 1.05-8.49), and cramping (OR = 3.99, 95% CI 1.36-11.68). The ORs remained relatively stable after adjusting for age, gender, experience, body mass index, type of race, and race duration. ASI-3 scores were not associated with symptoms. Individuals with higher levels of anxiety, especially on the morning of a race, may be prone GI distress, particularly nausea, regurgitation/reflux, and cramping.

Background and Aims: For a healthy food to be introduced to the consumer’s diet, it has to be attractive, yet testing for food acceptance and the sensory postprandial responses is still not standardized. The main objective of this study was to demonstrate that healthier foods can be obtained without impact on the responses to ingestion. Methods: A randomized, cross-over, double-blind, pilot study in non-obese, healthy men (n=8) comparing the responses to a standard sausage rich in animal fat (mortadella) versus a modified product based on a plant-derived fat analogue and an aroma. Palatability and postprandial sensations were measured on 10 cm scales and brain activity was evaluated by functional magnetic resonance imaging before and after each meal on separate days. Results: Both meals were rated equally palatable and induced the same degree of homeostatic sensations (satiety, fullness) with a similar hedonic dimension (improved mood and digestive well-being). Both meals induced similar changes in brain connectivity: decreased activity in the frontal-parietal, basal ganglia and thalamus, visual occipital, sensory-motor, temporal superior and in the “default-mode” networks, while increased activity was detected in the network associated with white matter. Conclusion: A substantial improvement in the nutritional profile of food can be achieved without affecting the responses to ingestion.

Mangos are an understudied fruit rich in fiber and polyphenols that have been linked to better metabolic outcomes and promotion of satiety. The purpose of this study was to examine the effect of mango consumption on postprandial glucose, insulin, and satiety responses. Using a randomized crossover study design, 23 overweight and obese men and women consumed 100 kcal snacks of fresh mangos or isocaloric low-fat cookies on two separate occasions. Insulin and satiety hormones were measured at baseline and 45 min post-snack consumption. Glucose was measured at baseline, 30, 60, 90, and 120 min after snack consumption. Satiety questionnaires were completed at baseline and every 20 min for 120 min post-consumption. Both mangos and low-fat cookies increased insulin, with a significantly lower increase for mangos compared with low-fat cookies at 45 min post-snack consumption (

Background: Satiation is a key component of food intake regulation as it brings an eating episode to an end. The effect of sex on satiation measurement has not been characterized. Methods: This retrospective cohort study aimed to investigate the effect of sex on satiation measurement in adult participants across all body mass indices (BMI). We measured satiation with a nutrient-drink test to assess volume to fullness (VTF) and maximum tolerated volume (MTV), and/or an ad libitum meal test to assess calories consumed to fullness (CTF). We performed univariate and multiple regression analyses to estimate the contribution of sex to VTF, MTV, and CTF, compared to other biological variables, such as age, weight, height, BMI, waist-to-hip circumference (W/H), and lean mass percentage (LM%), that are known to affect these parameters. Findings: We included 959 participants (mean age 39 [SD 12] years; 70·7% female, and BMI 33 kg/m2 [8]). Females had higher BMI, W/H, and LM%. VTF, MTV, and CTF were lower in females: 704 [323] vs. 783 [328] mL, p=0·001; 1226 [384] vs. 1419 [410] mL, p

Despite the utility of social cognitive theory for facilitating individual behavior changes needed for initial weight loss, this model has been less effective in facilitating adherence to recommended lifestyle changes required for sustainable weight-loss maintenance. One potential reason for the limited long-term effectiveness of lifestyle interventions guided by this model is that the model does not consider the important influence that biology can have on weight-relevant behaviors, during both weight loss and weight-loss maintenance, via sensations of hunger and satiety and changes in energy metabolism (expenditure and fat oxidation). We describe here a proposed revision to social cognitive theory that allows for biological factors to exist in reciprocal determinism with behavioral, environmental, and personal factors, with the goal of creating a theoretical basis for lifestyle interventions with greater personalization in order to facilitate better long-term adherence and improve weight-loss maintenance.

Exercise Satiation is a novel theoretical conceptualization for problematic exercise often observed in eating disorders. Problematic exercise is present across the spectrum of eating disorder presentations and is a cardinal symptom of eating disorders that has been difficult to treat historically. Conceptualizing exercise in the context of Reward Satiation similar to other biological drives such as eating could provide new insights into the etiology, maintenance, and treatment of problematic exercise in eating disorders. Through this understanding, we may be able to provide and increase adherence to interventions that target these mechanisms and as such, reduce impairment associated with problematic exercise for those with eating disorders. Using the Research Domain Criteria (RDoC) framework, we propose and discuss potential research avenues to explore Exercise Satiation in the context of eating disorders.

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 [...]

Background: The taste of carbohydrates may drive their intake. Sensitivity to carbohydrate taste varies among individuals, thus, it is important to understand how differences in sensitivity influence eating behaviour and body mass. Objective: The aims of this study were to assess associations among carbohydrate taste sensitivity, habitual and acute food intake, and body mass, as well as assess the reliability of the carbohydrate detection threshold (DT) test within and across days. Methods: Carbohydrate DT was assessed six times across three sessions in 36 healthy adult participants (22 female) using a three-alternate forced choice methodology. Moreover, 24 h diet records were completed on the days prior to testing sessions, and food intake at a buffet lunch was collected following each session. Anthropometry was also measured. Linear mixed regression models were fitted. Results: The DT test required at least three measures within a given day for good reliability (ICC = 0.76), but a single measure had good reliability when compared at the same time across days (ICC = 0.54–0.86). Carbohydrate DT was associated with BMI (kg/m2: β = −0.38, p = 0.014), habitual carbohydrate intake (g: β = −41.8, p = 0.003) and energy intake (kJ: β = −1068, p = 0.019) from the 24-h diet records, as well as acute intake of a buffet lunch (food weight (g): β = −76.1, p = 0.008). Conclusions: This suggests that individuals who are more sensitive to carbohydrate are more likely to consume greater quantities of carbohydrates and energy, resulting in a greater body mass.

The intent of this review is to survey physiological, psychological, and societal obstacles to the control of eating and body weight maintenance and offer some evidence-based solutions. Physiological obstacles are genetic and therefore not amenable to direct abatement. They include an absence of feedback control against gaining weight; a non-homeostatic relationship between motivations to be physically active and weight gain; dependence of hunger and satiation on the volume of food ingested by mouth and processed by the gastrointestinal tract and not on circulating metabolites and putative hunger or satiation hormones. Further, stomach size increases from overeating and binging, and there is difficulty in maintaining weight reductions due to a decline in resting metabolism, increased hunger, and enhanced efficiency of energy storage. Finally, we bear the evolutionary burden of extraordinary human capacity to store body fat. Of the psychological barriers, human craving for palatable food, tendency to overeat in company of others, and gullibility to overeat when offered large portions, can be overcome consciously. The tendency to eat an unnecessary number of meals during the wakeful period can be mitigated by time-restricted feeding to a 6–10 hour period. Social barriers of replacing individual physical work by labor-saving appliances, designing built environments more suitable for car than active transportation; government food macronutrient advice that increases insulin resistance; overabundance of inexpensive food; and profit-driven efforts by the food industry to market energy-dense and nutritionally compromised food are best overcome by informed individual macronutrient choices and appropriate timing of exercise with respect to meals, both of which can decrease insulin resistance. The best defense against overeating, weight gain, and inactivity is the understanding of factors eliciting them and of strategies that can avoid and mitigate them.

The neuropeptide oxytocin is produced in the paraventricular hypothalamic nucleus and the supraoptic nucleus of the hypothalamus. In addition to its extensively studied influence on social behavior and reproductive function, central oxytocin signaling potently reduces food intake in both humans and animal models and has potential therapeutic use for obesity treatment. In this review, we highlight rodent model research that illuminates various neural, behavioral, and signaling mechanisms through which oxytocin’s anorexigenic effects occur. The research supports a framework through which oxytocin reduces food intake via amplification of within-meal physiological satiation signals rather than by altering between-meal interoceptive hunger and satiety states. We also emphasize the distributed neural sites of action for oxytocin’s effects on food intake and review evidence supporting the notion that central oxytocin is communicated throughout the brain, at least in part, through humoral-like volume transmission. Finally, we highlight mechanisms through which oxytocin interacts with various energy balance-associated neuropeptide and endocrine systems (e.g., agouti-related peptide, melanin-concentrating hormone, leptin), as well as the behavioral mechanisms through which oxytocin inhibits food intake, including effects on nutrient-specific ingestion, meal size control, food reward-motivated responses, and competing motivations.

The aim of the study was to investigate the effect of prebiotic fibres on appetite-regulating hormones, subjective feeling of appetite and energy intake in subjects with type 2 diabetes. Data presented are secondary outcomes of a study investigating the effect of prebiotics on glucagon-like peptide-1 and glycaemic regulation. We conducted a randomised and placebo-controlled crossover trial to evaluate the effects of 16 g/d of inulin-type fructans or a control supplement (maltodextrin) for 6 weeks in randomised order, with a 4-week washout period in-between, on appetite in thirty-five men and women with type 2 diabetes. Data were collected at visits before and after each treatment: plasma concentration of the satiety-related peptides ghrelin and peptide YY (PYY) were assessed during a standardised mixed meal. The subjective sensation of appetite was evaluated in response to an ad libitum lunch by rating the visual analogue scale. Twenty-nine individuals (twelve women) were included in the analyses. Compared to control treatment, the prebiotics did not affect ghrelin (P =0⋅71) or the ratings of hunger (P = 0⋅62), satiety (P = 0⋅56), fullness (P = 0⋅73) or prospective food consumption (P = 0⋅98). Energy intake also did not differ between the treatments. However, the response of PYY increased significantly after the control treatment with mean (sem) 11⋅1 (4⋅3) pg/ml when compared to the prebiotics −0⋅3 (4⋅3) pg/ml (P = 0⋅013). We observed no effect of inulin-type fructans on appetite hormones, subjective feeling of appetite or energy intake in patients with type 2 diabetes.

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.

Milk whey is effective in enhancing satiety mainly due to its protein composition. Peptides and amino acids derived from digestion of whey protein can act as suppressants of appetite by stimulation of receptors of satiety gut hormones. But, the protein fraction of whey can vary depending on species of animal, season, lactation period, etc. The aim of this study is to evaluate the satiety effect of milk whey from different species of ruminants (cow, sheep, goat and a mixture of them) through a simulated in vitro digestion, which performed the whole gastrointestinal process, from oral digestion to colonic fermentation. The satiety effect of each sample was measured by the production of satiating hormones (CCK and GLP-1) secreted by enteroendocrine cell line (STC-1) after 2 hours of incubation with non-digested, digested and fermented whey. Digested samples have shown to be potent CCK and GLP-1 secretagogues followed by fermented and non-digested samples, showing that the last one showed a weak hormone stimulation. Digested goat whey was the most efficient stimulator of GLP-1 (86.33 ± 4.55 pg mL-1) and fermented mixture whey produced the major release of CCK (80.78±1.81 pg mL-1). This study demonstrates that milk whey is a suitable ingredient to stimulate satiety through the effect of peptides, amino acids produced from digestion, and metabolites released by fermentation.

Background This study aimed to investigate the dynamic interactions among three neural systems that are implicated in substance and behavioral addictions in response to food cues in young adults. These include an impulsive system involving the striatum, a reflective system involving the prefrontal cortex, and a homeostasis sensing system involving the insular cortex. Methods College students (N = 45) with various levels of body mass index were recruited. Functional magnetic resonance imaging data were acquired while participants performed food-related Go/NoGo tasks, with low-calorie and high-calorie food cues. Participants were scanned under both food satiety and deprivation conditions. Dynamic causal modeling was applied to the data to examine the causal architecture of coupled or distributed dynamics among the aforementioned systems. Results Participants showed difficulty inhibiting responses to high-calorie foods as suggested by higher false alarm rate and decision bias for low-calorie food Go task. This difficulty was enhanced during the food deprivation condition. Deprivation increased neural activity of both the insula and the striatum bilaterally in response to high-calorie foods during Go trials and anterior cingulate cortex and dorsolateral prefrontal cortex activity during NoGo trials. Dynamic causal modeling analysis revealed that food deprivation modulated the communications between the insula, striatum, and dorsolateral prefrontal cortex, and the modulations were positively associated with body mass index. Conclusions The results support tripartite views of decision making. Deprivation states, such as hunger, trigger insular activity, which modulates the balance between impulsive and reflective systems when facing tempting food cues.

Chronic sleep restriction, or inadequate sleep, is associated with increased risk of cardiometabolic disease. Laboratory studies demonstrate that sleep restriction causes impaired whole-body insulin sensitivity and glucose disposal. Evidence suggests that inadequate sleep also impairs adipose tissue insulin sensitivity and the NEFA rebound during intravenous glucose tolerance tests, yet no studies have examined the effects of sleep restriction on high-fat meal lipemia. We assessed the effect of 5 h time in bed (TIB) per night for four consecutive nights on postprandial lipemia following a standardized high-fat dinner (HFD). Furthermore, we assessed whether one night of recovery sleep (10 h TIB) was sufficient to restore postprandial metabolism to baseline. We found that postprandial triglyceride (TG) area under the curve was suppressed by sleep restriction (P = 0.01), but returned to baseline values following one night of recovery. Sleep restriction decreased NEFAs throughout the HFD (P = 0.02) and NEFAs remained suppressed in the recovery condition (P = 0.04). Sleep restriction also decreased participant-reported fullness or satiety (P = 0.03), and decreased postprandial interleukin-6 (P < 0.01). Our findings indicate that four nights of 5 h TIB per night impair postprandial lipemia and that one night of recovery sleep may be adequate for recovery of TG metabolism, but not for markers of adipocyte function.

Purpose Obesity is associated with alterations in appetite, gastrointestinal hormone levels and excessive fat mass. We previously published a double-blind, placebo-controlled, randomized, 16-week trial on effects of once-daily glucagon-like peptide-1 (GLP-1) analog, liraglutide on weight, satiation, and gastric functions in obese volunteers. The aim of this substudy is to compare to placebo the effects of liraglutide on appetite, taste preference, regional body fat stores, and anthropometric measurements. Methods Forty obese adults received standard instruction for weight management, monthly behavioral intervention utilizing motivational interviews, and 16-week treatment of once-daily liraglutide (escalated to 3 mg SQ daily). At baseline and 16 weeks, the following were measured: appetite and taste preferences rated every 30 min for 5 h after ingesting 300 mL Ensure®; maximal tolerated volume (MTV) with a nutrient drink test; fasting and postprandial bioactive GLP-1 (7–36) and peptide YY (PYY) levels; total and regional body fat with dual-energy X-ray absorptiometry, and waist and hip circumference. Results Thirty-five participants (17 liraglutide; 18 placebo) completed the trial. Compared to placebo group, liraglutide group had significant reductions in MTV; prospective food consumption score; desire to eat something sweet, salty, savory or fatty; and an increase in perceived fullness. Postprandial plasma levels of GLP-1 decreased and PYY levels increased with liraglutide relative to baseline. Significant reductions in total body, trunk, and upper and lower body fat without reduction in lean body mass were observed. Conclusion Liraglutide 3 mg SQ modulates appetite, taste preference, gut hormones, and regional body fat stores in adults with obesity without reduction in lean body mass.

Metabolites are active controllers of cellular physiology, but their role in complex behaviors is less clear. Here we report metabolic changes that occur during the transition between hunger and satiety in Drosophila melanogaster. To analyze these data in the context of fruit fly metabolic networks, we developed Flyscape, an open-access tool. We show that in response to eating, metabolic profiles change in quick, but distinct ways in the heads and bodies. Consumption of a high sugar diet dulls the metabolic and behavioral differences between the fasted and fed state, and reshapes the way nutrients are utilized upon eating. Specifically, we found that high dietary sugar increases TCA cycle activity, alters neurochemicals, and depletes 1-carbon metabolism and brain health metabolites N-acetyl-aspartate and kynurenine. Together, our work identifies the metabolic transitions that occur during hunger and satiation, and provides a platform to study the role of metabolites and diet in complex behavior., The relationship between metabolomic and behavioral changes is not well understood. Here, the authors analyze metabolome changes in D. melanogaster heads and bodies during hunger and satiety, and develop the Flyscape tool to visualize the resulting metabolic networks and integrate them with other omics data.