The milk study protocol: A longitudinal, prospective cohort study of the relationship between human milk metabolic hormone concentration, maternal body composition, and early growth and satiety development in Samoan infants aged 1-4 months.

BACKGROUND: Current research suggests that energy transfer through human milk influences infant nutritional development and initiates metabolic programming, influencing eating patterns into adulthood. To date, this research has predominantly been conducted among women in high income settings and/or among undernourished women. We will investigate the relationship between maternal body composition, metabolic hormones in human milk, and infant satiety to explore mechanisms of developmental satiety programming and implications for early infant growth and body composition in Samoans; a population at high risk and prevalence for overweight and obesity. Our aims are (1) to examine how maternal body composition influences metabolic hormone transfer from mother to infant through human milk, and (2) to examine the influences of maternal metabolic hormone transfer and infant feeding patterns on early infant growth and satiety. METHODS: We will examine temporal changes in hormone transfers to infants through human milk in a prospective longitudinal cohort of n = 80 Samoan mother-infant dyads. Data will be collected at three time points (1, 3, & 4 months postpartum). At each study visit we will collect human milk and fingerpick blood samples from breastfeeding mother-infant dyads to measure the hormones leptin, ghrelin, and adiponectin. Additionally, we will obtain body composition measurements from the dyad, observe breastfeeding behavior, conduct semi-structured interviews, and use questionnaires to document infant hunger and feeding cues and satiety responsiveness. Descriptive statistics, univariate and multivariate analyses will be conducted to address each aim. DISCUSSION: This research is designed to advance our understanding of variation in the developmental programming of satiety and implications for early infant growth and body composition. The use of a prospective longitudinal cohort alongside data collection that utilizes a mixed methods approach will allow us to capture a more accurate representation on both biological and cultural variables at play in a population at high risk of overweight and obesity.

Effects of sleep deprivation on food-related Pavlovian-instrumental transfer: a randomized crossover experiment.

Recent research suggests that insufficient sleep elevates the risk of obesity. Although the mechanisms underlying the relationship between insufficient sleep and obesity are not fully understood, preliminary evidence suggests that insufficient sleep may intensify habitual control of behavior, leading to greater cue-elicited food-seeking behavior that is insensitive to satiation. The present study tested this hypothesis using a within-individual, randomized, crossover experiment. Ninety-six adults underwent a one-night normal sleep duration (NSD) condition and a one-night total sleep deprivation (TSD) condition. They also completed the Pavlovian-instrumental transfer paradigm in which their instrumental responses for food in the presence and absence of conditioned cues were recorded. The sleep × cue × satiation interaction was significant, indicating that the enhancing effect of conditioned cues on food-seeking responses significantly differed across sleep × satiation conditions. However, this effect was observed in NSD but not TSD, and it disappeared after satiation. This finding contradicted the hypothesis but aligned with previous literature on the effect of sleep disruption on appetitive conditioning in animals-sleep disruption following learning impaired the expression of appetitive behavior. The present finding is the first evidence for the role of sleep in Pavlovian-instrumental transfer effects. Future research is needed to further disentangle how sleep influences motivational mechanisms underlying eating.

Oxytocin-receptor-expressing neurons in the lateral parabrachial nucleus activate widespread brain regions predominantly involved in fluid satiation.

Fluid satiation is an important signal and aspect of body fluid homeostasis. Oxytocin-receptor-expressing neurons (OxtrPBN) in the dorsolateral subdivision of the lateral parabrachial nucleus (dl LPBN) are key neurons which regulate fluid satiation. In the present study, we investigated brain regions activated by stimulation of OxtrPBN neurons in order to better characterise the fluid satiation neurocircuitry in mice. Chemogenetic activation of OxtrPBN neurons increased Fos expression (a proxy marker for neuronal activation) in known fluid-regulating brain nuclei, as well as other regions that have unclear links to fluid regulation and which are likely involved in regulating other functions such as arousal and stress relief. In addition, we analysed and compared Fos expression patterns between chemogenetically-activated fluid satiation and physiological-induced fluid satiation. Both models of fluid satiation activated similar brain regions, suggesting that the chemogenetic model of stimulating OxtrPBN neurons is a relevant model of physiological fluid satiation. A deeper understanding of this neural circuit may lead to novel molecular targets and creation of therapeutic agents to treat fluid-related disorders.

Cumulative effect of obesity phenotypes on body weight and body mass index.

BACKGROUND: Obesity originates from an imbalance between energy intake and expenditure. Changes in energy intake components (satiation, postprandial satiety, emotional eating) and energy expenditure have been linked to obesity and are referred to as obesity phenotypes. We aim to study if these obesity phenotypes have a cumulative effect on body weight and body mass index (BMI). SUBJECT/METHODS: This is a cross-sectional study of adult patients with obesity (BMI > 30 kg/m2) who completed the validated tests to measure the obesity phenotypes. A total of 464 were included in this study. INTERVENTIONS/METHODS: We defined higher calories to fullness during an ad libitum meal as abnormal satiation, accelerated time to half gastric emptying with scintigraphy as abnormal postprandial satiety, higher anxiety score on the Hospital Anxiety and Depression Scale as hedonic eating behavior, and decreased percentage of measured resting energy expenditure as abnormal energy expenditure. The primary analysis was done on the number of phenotypes ( ≤ 1 and ≥ 2) with body weight and BMI using an independent t-test. RESULTS: Our cohort included 464 patients (mean [SD] age 42.0 [10.9] years, 79% females, weight 111.2 [22.9] kg, BMI 38.9 [7.0] kg/m2). There were 294 patients who had ≤ 1 phenotype, and 170 patients with ≥ 2 phenotypes with no baseline demographical differences (i.e., age and sex). Having ≥ 2 phenotypes was associated with higher body weight (115 [25] kg vs. 109 [21] kg; p = 0.004), BMI (40 [8] kg/m2 vs. 38 [7] kg/m2; p = 0.02) and waist (118 [15] cm vs. 115 [13] cm; p = 0.04) and hip (129 [14] cm vs. 125 [13] cm; p = 0.01) circumferences compared to ≤ 1 phenotype. CONCLUSION: Obesity phenotypes are associated with an additive effect on the body weight and BMI. Patients who have multiple obesity phenotypes may require a more aggressive approach to enhance weight loss.

The role of gastric function in control of food intake (and body weight) in relation to obesity, as well as pharmacological and surgical interventions.

PURPOSE: The objectives of this review are to summarize the role of gastric motor functions in the development of satiation (defined broadly as postprandial fullness) and satiety (reduced appetite or postponing desire to eat after a meal) and their impact on weight change. The specific topics are the methods of measurement of gastric emptying and accommodation and their impact on food intake, satiation, and satiety. A second focus contrasts bariatric surgery to endoscopic gastroplasty that alter gastric emptying and incretin responses in markedly divergent manners. BACKGROUND: The hormone, GLP-1, retards gastric emptying and increases gastric accommodation through vagally-mediated effects. Indeed, these effects provide the basis for the association of altered gastric emptying in the appetite and weight loss responses to pharmacological interventions particularly by those acting on receptors of incretin agonists such as liraglutide and the dual agonists, tirzepatide and cotadutide, all of which retard gastric emptying. In fact, retardation of gastric emptying and gastrointestinal adverse effects have been shown to contribute in part to the weight loss in response to this class of pharmacological agents. SUMMARY: The motor functions of the stomach are relevant to postprandial fullness and to interventions aimed at weight loss in people with obesity.

Visual cues and food intake: A preregistered replication of Wansink et al. (2005).

Imagine a bowl of soup that never emptied, no matter how many spoonfuls you ate-when and how would you know to stop eating? Satiation can play a role in regulating eating behavior, but research suggests visual cues may be just as important. In a seminal study by Wansink et al. (2005), researchers used self-refilling bowls to assess how visual cues of portion size would influence intake. The study found that participants who unknowingly ate from self-refilling bowls ate more soup than did participants eating from normal (not self-refilling) bowls. Despite consuming 73% more soup, however, participants in the self-refilling condition did not believe they had consumed more soup, nor did they perceive themselves as more satiated than did participants eating from normal bowls. Given recent concerns regarding the validity of research from the Wansink lab, we conducted a preregistered direct replication study of Wansink et al. (2005) with a more highly powered sample (N = 464 vs. 54 in the original study). We found that most results replicated, albeit with half the effect size (d = 0.45 instead of 0.84), with participants in the self-refilling bowl condition eating significantly more soup than those in the control condition. Like the original study, participants in the self-refilling condition did not believe they had consumed any more soup than participants in the control condition. These results suggest that eating can be strongly controlled by visual cues, which can even override satiation. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Effect of pregnancy on the expression of nutrient-sensors and satiety hormones in mice.

Small intestinal satiation pathways involve nutrient-induced stimulation of chemoreceptors leading to release of satiety hormones from intestinal enteroendocrine cells (ECCs). Whether adaptations in these pathways contribute to increased maternal food intake during pregnancy is unknown. To determine the expression of intestinal nutrient-sensors and satiety hormone transcripts and proteins across pregnancy in mice. Female C57BL/6J mice (10-12 weeks old) were randomized to mating and then tissue collection at early- (6.5 d), mid- (12.5 d) or late-pregnancy (17.5 d), or to an unmated age matched control group. Relative transcript expression of intestinal fatty acid, peptide and amino acid and carbohydrate chemoreceptors, as well as gut hormones was determined across pregnancy. The density of G-protein coupled receptor 93 (GPR93), free fatty acid receptor (FFAR) 4, cholecystokinin (CCK) and glucagon-like peptide1 (GLP-1) immunopositive cells was then compared between non-pregnant and late-pregnant mice. Duodenal GPR93 expression was lower in late pregnant than non-pregnant mice (P < 0.05). Ileal FFAR1 expression was higher at mid- than at early- or late-pregnancy. Ileal FFAR2 expression was higher at mid-pregnancy than in early pregnancy. Although FFAR4 expression was consistently lower in late-pregnant than non-pregnant mice (P < 0.001), the density of FFAR4 immunopositive cells was higher in the jejunum of late-pregnant than non-pregnant mice. A subset of protein and fatty acid chemoreceptor transcripts undergo region-specific change during murine pregnancy, which could augment hormone release and contribute to increased food intake. Further investigations are needed to determine the functional relevance of these changes.

Neurohormonal response patterns to hunger, satiation, and postprandial fullness in normal weight, anorexia nervosa, and obesity.

BACKGROUND: Food intake is regulated by homeostatic and hedonic systems that interact in a complex neuro-hormonal network. Dysregulation in energy intake can lead to obesity (OB) or anorexia nervosa (AN). However, little is known about the neurohormonal response patterns to food intake in normal weight (NW), OB, and AN. MATERIAL & METHODS: During an ad libitum nutrient drink (Ensure®) test (NDT), participants underwent three pseudo-continuous arterial spin labeling (pCASL) MRI scans. The first scan was performed before starting the NDT after a > 12 h overnight fast (Hunger), the second after reaching maximal fullness (Satiation), and the third 30-min after satiation (postprandial fullness). We measured blood levels of ghrelin, cholecystokinin (CCK), glucagon-like peptide (GLP-1), and peptide YY (PYY) with every pCASL-MRI scan. Semiquantitative cerebral blood flow (CBF) maps in mL/100 gr brain/min were calculated and normalized (nCBF) with the CBF in the frontoparietal white matter. The hypothalamus (HT), nucleus accumbens [NAc] and dorsal striatum [DS] were selected as regions of interest (ROIs). RESULTS: A total of 53 participants, 7 with AN, 17 with NW (body-mass index [BMI] 18.5-24.9 kg/m2 ), and 29 with OB (BMI ≥30 kg/m2 ) completed the study. The NW group had a progressive decrease in all five ROIs during the three stages of food intake (hunger, satiation, and post-prandial fullness). In contrast, participants with OB showed a minimal change from hunger to postprandial fullness in all five ROIs. The AN group had a sustained nCBF in the HT and DS, from hunger to satiation, with a subsequent decrease in nCBF from satiation to postprandial fullness. All three groups had similar hormonal response patterns with a decrease in ghrelin, an increase in GLP-1 and PYY, and no change in CCK. CONCLUSION: Conditions of regulated (NW) and dysregulated (OB and AN) energy intake are associated with distinctive neurohormonal activity patterns in response to hunger, satiation, and postprandial fullness.

Reversal of Conditioned Food Aversion Using a Cognitive Intervention: A Sham-Controlled, Randomized, Parallel Study.

BACKGROUND: Aversive conditioning weakens the gratifying value of a comfort meal. The aim was to determine the effect of a cognitive intervention to reverse aversive conditioning and restore hedonic postprandial response. METHODS: This was a randomized, sham-controlled, single-blind, parallel study that was conducted on 12 healthy women (n = 6 in each group). The reward value of a comfort meal was measured on different days: at initial exposure, after aversive conditioning (administration of the same meal with a masked fat overload on the previous day) and after a cognitive intervention (disclosing the aversive conditioning paradigm in the test group vs. no explanation in the control group). The primary outcome, digestive wellbeing, was determined using graded scales at regular intervals before and after ingestion. RESULTS: At initial exposure, the comfort meal produced a rewarding experience that was impaired using aversive conditioning; upon re-exposure to the original meal, the cognitive intervention increased meal wanting and liking; improved digestive wellbeing and mood; tended to reduce postprandial satiety, bloating/fullness; and abolished discomfort/pain, thereby restoring the hedonic value of the comfort meal. By contrast, sham intervention had no effects, and the postprandial sensations remained like the responses to the offending meal. CONCLUSION: In this proof-of-concept study, we demonstrate that in healthy women, a mild, short-term acquired aversion to a comfort meal can be reversed using a cognitive intervention. CLINICALTRIALS: gov ID: NCT05897411.

Sequential appetite suppression by oral and visceral feedback to the brainstem.

The termination of a meal is controlled by dedicated neural circuits in the caudal brainstem. A key challenge is to understand how these circuits transform the sensory signals generated during feeding into dynamic control of behaviour. The caudal nucleus of the solitary tract (cNTS) is the first site in the brain where many meal-related signals are sensed and integrated1-4, but how the cNTS processes ingestive feedback during behaviour is unknown. Here we describe how prolactin-releasing hormone (PRLH) and GCG neurons, two principal cNTS cell types that promote non-aversive satiety, are regulated during ingestion. PRLH neurons showed sustained activation by visceral feedback when nutrients were infused into the stomach, but these sustained responses were substantially reduced during oral consumption. Instead, PRLH neurons shifted to a phasic activity pattern that was time-locked to ingestion and linked to the taste of food. Optogenetic manipulations revealed that PRLH neurons control the duration of seconds-timescale feeding bursts, revealing a mechanism by which orosensory signals feed back to restrain the pace of ingestion. By contrast, GCG neurons were activated by mechanical feedback from the gut, tracked the amount of food consumed and promoted satiety that lasted for tens of minutes. These findings reveal that sequential negative feedback signals from the mouth and gut engage distinct circuits in the caudal brainstem, which in turn control elements of feeding behaviour operating on short and long timescales.

Feeding signals inhibit fluid-satiation signals in the mouse lateral parabrachial nucleus to increase intake of highly palatable, caloric solutions.

Chemogenetic activation of oxytocin receptor-expressing neurons in the parabrachial nucleus (OxtrPBN neurons) acts as a satiation signal for water. In this research, we investigated the effect of activating OxtrPBN neurons on satiation for different types of fluids. Chemogenetic activation of OxtrPBN neurons in male and female transgenic OxtrCre mice robustly suppressed the rapid, initial (15-min) intake of several solutions after dehydration: water, sucrose, ethanol and saccharin, but only slightly decreased intake of Ensure®, a highly caloric solution (1 kcal/mL; containing 3.72 g protein, 3.27 g fat, 13.42 g carbohydrates, and 1.01 g dietary fibre per 100 mL). OxtrPBN neuron activation also suppressed cumulative, longer-term (2-h) intake of lower caloric, less palatable solutions, but not highly caloric, palatable solutions. These results suggest that OxtrPBN neurons predominantly control initial fluid-satiation responses after rehydration, but not longer-term intake of highly caloric, palatable solutions. The suppression of fluid intake was not because of anxiogenesis, but because OxtrPBN neuron activation decreased anxiety-like behaviour. To investigate the role of different PBN subdivisions on the intake of different solutions, we examined FOS as a proxy marker of PBN neuron activation. Different PBN subdivisions were activated by different solutions: the dorsolateral PBN similarly by all fluids; the external lateral PBN by caloric but not non-caloric solutions; and the central lateral PBN primarily by highly palatable solutions, suggesting PBN subdivisions regulate different aspects of fluid intake. To explore the possible mechanisms underlying the minimal suppression of Ensure® after OxtrPBN neuron activation, we demonstrated in in vitro slice recordings that the feeding-associated agouti-related peptide (AgRP) inhibited OxtrPBN neuron firing in a concentration-related manner, suggesting possible inhibition by feeding-related neurocircuitry of fluid satiation neurocircuitry. Overall, this research suggests that although palatable beverages like sucrose- and ethanol-containing beverages activate fluid satiation signals encoded by OxtrPBN neurons, these neurons can be inhibited by hunger-related signals (agouti-related peptide, AgRP), which may explain why these fluids are often consumed in excess of what is required for fluid satiation.

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)age = 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.

A corticoamygdalar pathway controls reward devaluation and depression using dynamic inhibition code.

Reward devaluation adaptively controls reward intake. It remains unclear how cortical circuits causally encode reward devaluation in healthy and depressed states. Here, we show that the neural pathway from the anterior cingulate cortex (ACC) to the basolateral amygdala (BLA) employs a dynamic inhibition code to control reward devaluation and depression. Fiber photometry and imaging of ACC pyramidal neurons reveal reward-induced inhibition, which weakens during satiation and becomes further attenuated in depression mouse models. Ablating or inhibiting these neurons desensitizes reward devaluation, causes reward intake increase and ultimate obesity, and ameliorates depression, whereas activating the cells sensitizes reward devaluation, suppresses reward consumption, and produces depression-like behaviors. Among various ACC neuron subpopulations, the BLA-projecting subset bidirectionally regulates reward devaluation and depression-like behaviors. Our study thus uncovers a corticoamygdalar circuit that encodes reward devaluation via blunted inhibition and suggests that enhancing inhibition within this circuit may offer a therapeutic approach for treating depression.

Macronutrients effects on satiety and food intake in older and younger adults: A randomised controlled trial.

Older adults are advised to increase their protein intake to maintain their muscle mass. However, protein is considered the most satiating macronutrient and this recommendation may cause a decrease in total energy intake. To date, satiety studies comparing all three macronutrients have been undertaken in young adults, and it is unclear if the same response is seen in older adults. The objective of this study was to compare the effect of preloads high in protein, fat, and carbohydrate but equal in energy (∼300 kcal) and volume (250 ml) on energy intake, perceived appetite, and gastric emptying in younger and older adults. Twenty older and 20 younger adults completed a single-blinded randomised crossover trial involving three study visits. Participants consumed a standard breakfast, followed by a preload milkshake high in either carbohydrate, fat, or protein. Three hours after the preload, participants were offered an ad libitum meal to assess food intake. Visual analogue scales were used to measure perceived appetite and gastric emptying was measured via the 13C-octanoic acid breath test. There was no significant effect of preload type or age on energy intake either at the ad libitum meal, self-recorded food intake for the rest of the test day or subjective appetite ratings. There was a significant effect of preload type on gastric emptying latency phase and ascension time, and an effect of age on gastric emptying latency and lag phase such that older adults had faster emptying. In conclusion, energy intake, and perceived appetite were not affected by macronutrient content of the preloads in both younger and older adults, but gastric emptying times differed.

A qualitative exploration of perceived barriers and facilitators to following an intuitive eating style.

BACKGROUND: Intuitive eating involves following internal cues of hunger and satiety to guide eating choices as opposed to responding to external signals, strong emotions, or dietary rules. This style of eating has consistently been shown to be related to better physical and psychological health indicators, and more interventions are being designed and studied to promote this eating style. The current study aimed to identify anticipated facilitators and barriers to following this style of eating among a group of college students enrolled in a larger study of intuitive eating. METHOD: Following a week of tracking their current eating as part of a larger study, college students read a description of intuitive eating. They then answered three open-ended questions about following intuitive eating including facilitators, barriers, and perceived ability to follow long term. Responses were coded using thematic analysis to identify themes across responses. RESULTS: Among 100 participants, 86 % were female, 46 % were Hispanic (41 % non-Hispanic White, 13 % other race/ethnicity), mean age was 24.3 years, and mean body mass index was 26.2. The most commonly anticipated participant-reported facilitators of intuitive eating were being in touch with the body's needs and hunger cues, positive perceptions of intuitive eating, and health considerations. The most commonly anticipated barriers were logistical constraints (e.g., busyness and mealtimes), difficulty with hunger cues and reactions to food, and negative perceptions of intuitive eating. The majority of participants (64 %) would consider following this style of eating long term. DISCUSSION: This study provides information that can be used to improve efforts aimed at promoting intuitive eating to college students, including marketing intuitive eating interventions, and clarifying misunderstandings of its key tenets that might serve as barriers.

[What is the relationship between alcohol and obesity?] / Quelle relation entre alcool et obésité ?

The prevalence of alcohol consumption and obesity continues to increase. The aim of this literature review was to give an overview of the association between these two health and socioeconomic problems. Ethanol must be considered as an orexigenic molecule, acting on the cerebral regulation of hunger and satiety and on the mesolimbic reward system. Moreover, studies showed that alcohol blocks the fatty acid beta oxidation, promoting the storage of lipids. Observational and experimental studies struggle to find a solid correlation between the two entities, but they have several biases and limitations. Experts agree to consider ethanol ingestion as a potential contributing factor of the higher obesity rates observed in the last decades.

Les prévalences de la consommation d'alcool et de l'obésité ne cessent d'augmenter. L'objectif de cette revue de la littérature est de donner un aperçu de l'association entre ces deux problématiques sanitaires et socio-économiques. L'éthanol, agissant sur la régulation cérébrale de la faim et de la satiété ainsi que sur le système mésolimbique de la récompense, est à considérer comme une substance orexigène. En outre, il bloque la bêta-oxydation des lipides, prédisposant à leur stockage. Malgré des évidences scientifiques discordantes, qui sont cependant conditionnées par des biais et limitations, les experts sont d'accord de considérer la consommation de boissons alcoolisées comme un probable facteur contribuant à l'incrémentation du taux d'obésité observé lors des dernières décennies.

Hyperexcited limbic neurons represent sexual satiety and reduce mating motivation.

Transient sexual experiences can have long-lasting effects on behavioral decisions, but the neural coding that accounts for this change is unclear. We found that the ejaculation experience selectively activated estrogen receptor 2 (Esr2)-expressing neurons in the bed nucleus of the stria terminalis (BNST)-BNSTEsr2-and led to persistent decreases in firing threshold for days, during which time the mice displayed sexual satiety. Inhibition of hyperexcited BNSTEsr2 elicited fast mating recovery in satiated mice of both sexes. In males, such hyperexcitability reduced mating motivation and was partially mediated by larger HCN (hyperpolarization-activated cyclic nucleotide-gated) currents. Thus, BNSTEsr2 not only encode a specific mating action but also represent a persistent state of sexual satiety, and alterations in a neuronal ion channel contribute to sexual experience-dependent long-term changes to mating drive.

The complex pattern of the effects of prolonged frequent exercise on appetite control, and implications for obesity.

From a public health perspective, much of the interest in the relationship between exercise and appetite rests on the implications for energy balance and obesity. Energy balance reflects a dynamic 2-way interaction between energy expenditure (EE) and energy intake (EI). Physical activity and exercise, and appetite are the behavioural components of EE and EI, respectively. Beyond EE, exercise is a powerful and complex physiological stimulus acting on several bodily systems. There are multiple effects of frequent and prolonged exercise on appetite which include inter alia an increase in fasting hunger, an enhancement of post-prandial satiety, a modulation of the hedonic responses to food and improvements in eating behaviour traits. These lead to variable adjustments in EI and in a reduction in the susceptibility to overconsumption. Frequent and prolonged physical activity and exercise behaviour can strengthen and sensitise the appetite control system, whilst physical inactivity and sedentariness (low level of EE) fails to downregulate EI and can permit overconsumption. Not all of the effects of exercise operate uniformly to drive appetite in the same direction. The complexity of the interaction between EE and EI means that the effects of prolonged exercise are characterised by substantial individual heterogeneity. This leads to variable effects on energy balance and body mass.

Low glycemic index common bean snack increased satiety without modifying energy intake in adults with normal weight: randomized crossover trials.

This study aimed to evaluate the short-term effect of a common bean baked snack (CBBS) and cooked bean consumption on energy intake, satiety, glycemic response, and palatability in subjects with normal weight (Study 1) and overweight (Study 2) and to determine the glycemic index of CBBS (Study 3). For studies 1 and 2, satiety and glycemic response were measured over 45 min after consuming CBBS, cooked beans or white bread preload, and energy intake at an ad libitum test meal was calculated. Energy intake remained similar after consuming the three preloads in both studies. Compared to white bread, CBBS consumption increased fullness by 52% in subjects with normal weight but not in those with overweight. The CBBS calculated glycemic index was considered low (42). Consumption of low glycemic index CBBS increased satiety in adults with a normal weight. Long-term trials assessing the effects on body weight management are necessary.

Validation of a Mobile App-Based Visual Analog Scale for Appetite Measurement in the Real World: A Randomized Digital Clinical Trial.

There has been no validated digital tool for measuring appetite with a visual analog scale (VAS) through a mobile app using participants' smart phones for data collection in virtual settings. To fill the gap, we developed a digital VAS and conducted a digital cross-over clinical trial by comparing appetite responses measured by this digital tool versus paper-based VAS in 102 participants in a free-living environment. Participants consumed either a 230 or 460 kcal breakfast in randomized order in two virtual sessions, and their appetite was measured over the next 4 h using both tools. The results revealed no significant difference in hunger, fullness, satiety, or desire to eat measured by digital and paper VAS. Paper VAS resulted in a higher prospective consumption score than digital VAS; the difference (1.1 out of 100 points) was statistically significant but not practically relevant. Bland and Altman analysis also indicated consistency in the results from the two methods. In conclusion, digital VAS on a smart phone is a validated tool for appetite measurement in the real world; it provides a new way for researchers to leverage participants' mobile devices for appetite data collection in digital trials.