Control Of Food Intake Research Articles

The Kidney Beans ( Phaseolus vulgaris ) Pods Extract Affects the Central and Peripheral Serotonergic Systems in Rats With High-Calorie Diet-Induced Obesity

Background: Overweight and obesity have become a global epidemic that presents a risk to health. Serotonin is involved in the regulation of many important functions of the body as in the periphery (as a hormone), as well as in the central nervous system as a neurotransmitter, which can be involved in central mechanisms that control food intake. The present work aimed to study the features of serotonin metabolism functioning under the effect of the kidney beans ( Phaseolus vulgaris ) pods extract in experimental obesity, which was induced by the consumption of high-calorie diet. Phaseolus vulgaris is the plant that possesses plenty of curative and therapeutic properties in particular for the treatment of diabetes mellitus, obesity, and cardiovascular diseases. It has been known that plant extracts, unlike synthetic drugs, can be used practically without toxic effects. Methods: Experiments were carried out on four groups of white nonlinear male rats (10 rats per group) during a 10-week period. Studies of the serotonergic system functioning were performed using ion-exchange chromatography, spectrofluorimetric and spectrophotometric methods. Results: The consumption of kidney beans ( Phaseolus vulgaris ) pods extract has a therapeutic effect on the obesity development in rats, as evidenced by changes in the functioning of the central and peripheral serotonergic systems. Tryptophan and serotonin levels have increased in duodenum mucosa compared to the obese rats, also had shown an increase of the serotonin synthesis enzymes activity (tryptophan hydroxylase and tryptophan decarboxylase) and a simultaneous decrease in the activity of monoamine oxidase. Central tryptophan and serotonin levels, as well as the activity of enzymes of the serotonin synthesis have increased compared to the obese rats while a simultaneous decrease in the activity of monoamine oxidase was observed. Conclusions: The obtained results indicated a therapeutic effect of the kidney beans ( Phaseolus vulgaris ) pods extract on the dysfunction of the serotonergic system under obesity development. J Endocrinol Metab. 2021;11(5):123-133 doi: https://doi.org/10.14740/jem650

Effects of oxytocin and antagonist antidote atosiban on body weight and food intake of female mice, Mus musculus

Growing evidence suggests that oxytocin (OT) plays an important factor for the control of food intake, body weight, and energy metabolism in human and non-human animals. It has reported previously, the downregulation in oxytocin receptors (OTRs) expression is linked with the development of obesity, but exogenous OT reverse body weight and food intake in obese animal model. It is important to know that, whether intraperitoneal administration crosses blood brain barrier. Therefore, in the present experiment, we study the impact of intraperitoneal administration of synthetic OT 0.0116 mg/kg and antagonist atosiban (OTA) 1 mg/kg on food intake, and body weight of female mice, Mus musculus for different duration i.e. 30, 60, and 90 days. In this study, it was observed that there was significant decrease (p<0.001, one-way analysis of variance [ANOVA]) in the body weight (BW), food intake, and gonadosmatic indices (GSI) after the intraperitoneal exposure of OT at dose 0.0116 mg/kg up to 90 days and inhibits via antagonist atosiban. These results indicates that intraperitoneal administration of OT can be used for treatment for longer duration without any side effects and maintains homeostasis in physiologic system regulates body weight and gonadal weight in female mice, which represent an important therapeutic tool for the obesity and metabolic disorder in female.

A Role for Peripheral Anandamide and 2-Arachidonoylglycerol in Short-Term Food Intake and Orexigenic Hypothalamic Responses in a Species with Continuous Nutrient Delivery.

The endocannabinoid system (ECS) plays a pivotal role in the complex control and regulation of food intake. Pharmacological ECS activation could improve health in energy-deficient stages by increasing food intake, at least in intermittent feeders. However, knowledge of the mechanism regulating appetite in species with continued nutrient delivery is incomplete. The objectives of this pilot study were to investigate the effect of the intraperitoneal (i.p.) administration of the endocannabinoids (ECs) anandamide (AEA) and 2-arachidonoylglycerol (2-AG) on food intake, plasma EC concentrations and hypothalamic orexigenic signaling, and to study how the circulatory EC tone changes in response to short-term food deprivation in dairy cows, a species with continuous nutrient delivery. The administration of EC resulted in higher food intake during the first hour after treatment. Plasma AEA concentrations were significantly increased 2.5 h after AEA injection, whereas plasma 2-AG concentrations remained unchanged 2.5 h after 2-AG injection. The hypothalamic immunoreactivity of cannabinoid receptor 1, agouti-related protein, and orexin-A was not affected by either treatment; however, neuropeptide Y and agouti-related protein mRNA abundances were downregulated in the arcuate nucleus of AEA-treated animals. Short-term food deprivation increased plasma 2-AG, while plasma AEA remained unchanged. In conclusion, i.p.-administered 2-AG and AEA increase food intake in the short term, but only AEA accumulates in the circulation. However, plasma 2-AG concentrations are more responsive to food deprivation than AEA.

Oxytocin and Food Intake Control: Neural, Behavioral, and Signaling Mechanisms.

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.

Rôle de la génétique et de l’épigénétique dans l’obésité de l’enfant et de l’adolescent

Obesity is a complex, multifactorial disease due to a dysfunction of the hypothalamic control of weight and food intake. The contribution of genetics is constant, but its impact is variable depending on the situations ranging from rare genetic obesities (around 5% of cases) to more frequently polygenic obesity (or common obesity) (95% of cases). Other factors as pre- and post-natal, societal or psychological determinants always interact closely with these genetic factors explaining the high variability of the phenotype and the complex pathophysiology. A true continuum exists between all these situations through the involvement of more or less rare genetic variants located in genes encoding key proteins in the central regulation of food intake. Rare forms of obesity are characterized by their common phenotype including a very early-onset severe obesity (BMI Z score greater than+3 SD early before the age of 3 years) with resistance to medical treatment, and major eating disorders characterized by difficulties in voluntary control of food intake. Central endocrine abnormalities such as hypogonadotropic hypogonadism or GH deficiency for example, and metabolic abnormalities due to abnormal adipose tissue distribution are also associated with variable degrees (Alström syndrome for example). Neuropsychological abnormalities are also present such as neurodevelopmental disorders (intellectual disability with variable intensity and/or adaptive development disorders which are part of many syndromes such as in Prader-Wili Syndrome; autism spectrum disorders (in SH2B1 or MYT1L deficiency for example), cognitive disorders with difficulties in emotional regulation (eg: Bardet-Biedl Syndrome or specific rare variants located on genes of the melanocortin pathway), behavioral or psychiatric disorders, sleep disorders and major hypothalamic dysfunctions (eg: Prader-Willi Syndrome, Smith Magenis syndrome). This better understanding of the mechanisms has made it possible to better precise the associated phenotypes and, recently, to lead to therapeutic innovations targeting these key genes. This evolution helps to quickly envisage the development of a real personalized medicine in early onset obesity using the combination of drug treatments targeted according to the identified genetic anomaly and/or a multidisciplinary global approach targeting the patient's phenotype or even the bariatric surgery in specific situations.

What Is the Impact of Energy Expenditure on Energy Intake?

Coupling energy intake (EI) to increases in energy expenditure (EE) may be adaptively, compensatorily, or maladaptively leading to weight gain. This narrative review examines if functioning of the homeostatic responses depends on the type of physiological perturbations in EE (e.g., due to exercise, sleep, temperature, or growth), or if it is influenced by protein intake, or the extent, duration, timing, and frequency of EE. As different measures to increase EE could convey discrepant neuronal or humoral signals that help to control food intake, the coupling of EI to EE could be tight or loose, which implies that some ways to increase EE may have advantages for body weight regulation. Exercise, physical activity, heat exposure, and a high protein intake favor weight loss, whereas an increase in EE due to cold exposure or sleep loss likely contributes to an overcompensation of EI, especially in vulnerable thrifty phenotypes, as well as under obesogenic environmental conditions, such as energy dense high fat—high carbohydrate diets. Irrespective of the type of EE, transient elevations in the metabolic rate seem to be general risk factors for weight gain, because a subsequent decrease in energy requirement is not compensated by an adequate adaptation of appetite and EI.

The Kidney Beans (Phaseolus vulgaris) Pods Extract Affects the Central and Peripheral Serotonergic Systems in Rats With High-Calorie Diet-Induced Obesity

Background: Overweight and obesity have become a global epidemic that presents a risk to health. Serotonin is involved in the regulation of many important functions of the body as in the periphery (as a hormone), as well as in the central nervous system as a neurotransmitter, which can be involved in central mechanisms that control food intake. The present work aimed to study the features of serotonin metabolism functioning under the effect of the kidney beans ( Phaseolus vulgaris ) pods extract in experimental obesity, which was induced by the consumption of high-calorie diet. Phaseolus vulgaris is the plant that possesses plenty of curative and therapeutic properties in particular for the treatment of diabetes mellitus, obesity, and cardiovascular diseases. It has been known that plant extracts, unlike synthetic drugs, can be used practically without toxic effects. Methods: Experiments were carried out on four groups of white nonlinear male rats (10 rats per group) during a 10-week period. Studies of the serotonergic system functioning were performed using ion-exchange chromatography, spectrofluorimetric and spectrophotometric methods. Results: The consumption of kidney beans ( Phaseolus vulgaris ) pods extract has a therapeutic effect on the obesity development in rats, as evidenced by changes in the functioning of the central and peripheral serotonergic systems. Tryptophan and serotonin levels have increased in duodenum mucosa compared to the obese rats, also had shown an increase of the serotonin synthesis enzymes activity (tryptophan hydroxylase and tryptophan decarboxylase) and a simultaneous decrease in the activity of monoamine oxidase. Central tryptophan and serotonin levels, as well as the activity of enzymes of the serotonin synthesis have increased compared to the obese rats while a simultaneous decrease in the activity of monoamine oxidase was observed. Conclusions: The obtained results indicated a therapeutic effect of the kidney beans ( Phaseolus vulgaris ) pods extract on the dysfunction of the serotonergic system under obesity development. J Endocrinol Metab. 2021;11(5):123-133 doi: https://doi.org/10.14740/jem650

How does prolonged moderate intensity walking affect gait in children with cerebral palsy?

The mitogen-activated kinase phosphatase-3 (MKP-3) has gained great importance in the scientific community by acting as a regulator of the cell cycle through dephosphorylation of FoxO1, an important transcription factor involved in the insulin intracellular signaling cascade. When dephosphorylated and translocated to the nuclei, FoxO1 can promote the transcription of orexigenic neuropeptides (NPY/AgRP) in the hypothalamus, whereas insulin signaling is responsible for the disruption of this process. However, it is not understood if the hypothalamic activation of MKP-3 affects FoxO1 phosphorylation, and we hypothesized that MKP-3 overexpression reduces the capacity of the insulin signal to phosphorylate FoxO1. In the present study, we overexpressed the DUSP6 gene through an injection of adenovirus directly into the hypothalamic third ventricle of Swiss mice. The colocalization of the adenovirus was confirmed by the immunofluorescence assay. Then, MKP-3 overexpression resulted in a significant reduction of hypothalamic FoxO1 phosphorylation after insulin stimulation. This effect was independent of changes in Akt phosphorylation. Thus, the role of MKP-3 in the hypothalamus is closely associated with FoxO1 dephosphorylation and may provide a potential therapeutic target against hypothalamic disorders related to obesity and unbalanced food intake control.

Obesity as a Condition Determined by Food Addiction: Should Brain Endocannabinoid System Alterations Be the Cause and Its Modulation the Solution?

Obesity is a complex disorder, and the number of people affected is growing every day. In recent years, research has confirmed the hypothesis that food addiction is a determining factor in obesity. Food addiction is a behavioral disorder characterized by disruptions in the reward system in response to hedonic eating. The endocannabinoid system (ECS) plays an important role in the central and peripheral control of food intake and reward-related behaviors. Moreover, both obesity and food addiction have been linked to impairments in the ECS function in various brain regions integrating peripheral metabolic signals and modulating appetite. For these reasons, targeting the ECS could be a valid pharmacological therapy for these pathologies. However, targeting the cannabinoid receptors with inverse agonists failed when used in clinical contexts as a consequence of the induction of affective disorders. In this context, new classes of drugs acting either on CB1 and/or CB2 receptors or on synthetic and degradation enzymes of endogenous cannabinoids are being studied. However, further investigation is necessary to find safe and effective treatments that can exert anti-obesity effects, normalizing reward-related behaviors without causing important adverse mood effects.

Eating behavior and obesity of women: estrogens and anorexigenic effect of estradiol

Eating behavior is a complex interaction of physiological, psychological, social, and genetic factors that affect the time of eating, the amount of food consumed, and food preferences. Obesity has reached epidemic proportions in the world and it is the leading cause of morbidity and mortality. According to an analysis of 20 prospective studies, the years of life lost due to obesity have now exceeded the years of life lost due to smoking. The epidemic of obesity in the world determines the relevance of research aimed at identifying the factors that contribute to the emergence of this pathological condition. We studied mainly foreign literature on the effect of estrogens on women’s eating behavior and the physiology of adipose tissue. After puberty, women are at greater risk of developing eating disorders than men, possibly due to a more labile psyche. Estrogens contribute to the accumulation of subcutaneous fat, and low estrogen level in menopausal women contributes to an increase in the amount of visceral fat. It is believed that the anorectic effects of estrogens are mediated by the central nervous system, this statement is based on the fact that direct injections of estradiol into the paraventricular nucleus or the arcuate/ventromedial nucleus are most effective for reducing food intake, body weight and increasing motor activity. There is every reason to believe that further clinical, women-focused studies that provide a better understanding of the intracellular signaling pathways responsible for the estrogenic control of food intake will provide new insights into the mechanisms responsible for the greater prevalence of obesity and eating disorders in women.

Brain adiponectin signaling controls peripheral insulin response in Drosophila

The brain plays a key role in energy homeostasis, detecting nutrients, metabolites and circulating hormones from peripheral organs and integrating this information to control food intake and energy expenditure. Here, we show that a group of neurons in the Drosophila larval brain expresses the adiponectin receptor (AdipoR) and controls systemic growth and metabolism through insulin signaling. We identify glucose-regulated protein 78 (Grp78) as a circulating antagonist of AdipoR function produced by fat cells in response to dietary sugar. We further show that central AdipoR signaling inhibits peripheral Juvenile Hormone (JH) response, promoting insulin signaling. In conclusion, we identify a neuroendocrine axis whereby AdipoR-positive neurons control systemic insulin response.

Serotonin activates paraventricular thalamic neurons through direct depolarization and indirect disinhibition from zona incerta.

Paraventricular thalamus (PVT) is a midline thalamic area that receives dense GABA projections from zona incerta (ZI) for the regulation of feeding behaviours. Activation of central serotonin (5-HT) signalling is known to inhibit food intake. Although previous studies have reported both 5-HT fibres and receptors in the PVT, it remains unknown how 5-HT regulates PVT neurons and whether PVT 5-HT signalling is involved in the control of food intake. Using slice patch-clamp recordings in combination with optogenetics, we found that 5-HT not only directly excited PVT neurons by activating 5-HT7 receptors to modulate hyperpolarization-activated cyclic nucleotide-gated (HCN) channels but also disinhibited these neurons by acting on presynaptic 5-HT1A receptors to reduce GABA inhibition. Specifically, 5-HT depressed photostimulation-evoked inhibitory postsynaptic currents (eIPSCs) in PVT neurons innervated by channelrhodopsin-2-positive GABA axons from ZI. Using paired-pulse photostimulation, we found 5-HT increased paired-pulse ratios of eIPSCs, suggesting 5-HT decreases ZI-PVT GABA release. Furthermore, we found that exposure to a high-fat-high-sucrose diet for 2weeks impairedboth 5-HT inhibition of ZI-PVT GABA transmission and 5-HT excitation of PVT neurons. Using retrograde tracer in combination with immunocytochemistry and slice electrophysiology, we found that PVT-projecting dorsal raphe neurons expressed 5-HT and were inhibited by food deprivation. Together, our study reveals the mechanism by which 5-HT activates PVT neurons through both direct excitation and indirect disinhibition from the ZI. The downregulation in 5-HT excitation and disinhibition of PVT neurons may contribute to the development of overeating and obesity after chronic high-fat diet. KEY POINTS: Serotonin (5-HT) depolarizes and excites paraventricular thalamus (PVT) neurons. 5-HT7 receptors are responsible for 5-HT excitation of PVT neurons and the coupling of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels to 5-HT receptors in part mediates the excitatory effect of 5-HT. 5-HT depresses the frequency of spontaneous inhibitory but not excitatory postsynaptic currents in PVT neurons. 5-HT1A receptors contribute to the depressive effect of 5-HT on inhibitory transmissions. 5-HT inhibits GABA release from zona incerta (ZI) GABA terminals in PVT. Chronic high-fat diet not only impairs 5-HT inhibition of the ZI-PVT GABA transmission but also downregulates 5-HT excitation of PVT neurons. PVT-projecting dorsal raphe neurons express 5-HT and are inhibited by food deprivation.

Open pancreaticoduodenectomy: setting the benchmark of time to functional recovery

PurposeNo accepted benchmarks for open pancreaticoduodenectomy (PD) exist. The study assessed the time to functional recovery after open PD and how this could be affected by the magnitude of midline incision (MI).Materials and methodsProspective snapshot study during 1 year. Time to functional recovery (TtFR) was assessed for the entire cohort. Further analyses were conducted after excluding patients developing a Clavien-Dindo ≥ 2 morbidity and after stratifying for the relative length of MI.ResultsThe overall median TtFR was 7 days (n = 249), 6 days for uncomplicated patients (n = 124). A short MI (SMI, < 60% of xipho-pubic distance, n = 62) was compared to a long MI (LMI, n = 62) in uncomplicated patients. The choice of a SMI was not affected by technical issues and provided a significantly shorter TtFR (5 vs 6 days, p = 0.002) especially for pain control (4 vs. 5 days, p = 0.048) and oral food intake (5 vs. 6 days, p = 0.001).ConclusionFunctional recovery after open PD with MI is achieved within 1 week from surgery in half of the patients. This should be the appropriate benchmark for comparison with minimally invasive PD. Moreover, PD with a SMI is feasible, safe, and associated with a faster recovery.

Rhythmic neuronal activities of the rat nucleus of the solitary tract are impaired by high-fat diet - implications for daily control of satiety.

Temporal partitioning of daily food intake is crucial for survival and involves the integration of internal circadian states and external influences such as the light-dark cycle and dietary composition. These intrinsic and extrinsic factors are interdependent with misalignment of circadian rhythms promoting body weight gain, while consumption of a calorie-dense diet elevates the risk of obesity and blunts circadian rhythms. Recently, we defined the circadian properties of the dorsal vagal complex of the brainstem, a structure implicated in the control of food intake and autonomic tone, but whether and how 24h rhythms in this area are influenced by diet remains unresolved. Here we focused on a key structure of this complex, the nucleus of the solitary tract (NTS). We used a combination of immunohistochemical and electrophysiological approaches together with daily monitoring of body weight and food intake to interrogate how the neuronal rhythms of the NTS are affected by a high-fat diet. We report that short-term consumption of a high-fat diet increases food intake during the day and blunts NTS daily rhythms in neuronal discharge. Additionally, we found that a high-fat diet dampens NTS responsiveness to metabolic neuropeptides, and decreases orexin immunoreactive fibres in this structure. These alterations occur without prominent body weight gain, suggesting that a high-fat diet acts initially to reduce activity in the NTS to disinhibit mechanisms that suppress daytime feeding. KEY POINTS: The dorsal vagal complex of the rodent hindbrain possesses intrinsic circadian timekeeping mechanisms In particular, the nucleus of the solitary tract (NTS) is a robust circadian oscillator, independent of the master suprachiasmatic clock Here, we reveal that rat NTS neurons display timed daily rhythms in their neuronal activity and responsiveness to ingestive cues These daily rhythms are blunted or eliminated by a short-term high-fat diet, together with increased consumption of calories during the behaviourally quiescent day Our results help us better understand the circadian control of satiety by the brainstem and its malfunctioning under a high-fat diet.

Mathematical Modelling of Diet Planning Problem for Hypertension Patients

Hypertension or high blood pressure is also called a “silent killer” that may lead to serious damage to the heart and kidney. The worst case can result in sudden death. Unbalanced diets are one of the risk factors for hypertension. Previous studies have proven that diet plays a significant role in influencing hypertension patient condition. Proper planning on the selection of diets needs to be done to control food intake for this cardiovascular disease patient. This study aims to formulate a mathematical model of diet planning for hypertension patients. Specifically, this study attempts to determine the amount of nutrients need by hypertension patients, to find the cost of the food combination, and to identify the best model between linear programming and integer programming. The research model included 10 types of food groups with 200 variables based on Malaysian recipes and developed a mathematical model using two programming techniques; linear programming and integer programming. The finding showed that the solution provided by the entire programming method has met the constraints and requirements of the food group. The results from the integer programming approach would offer optimal and efficient alternatives to diet planning for patients with hypertension. It can serve as a guideline for hypertension patients on type of food to eat and the correct amount of serving to complete their nutritional plan.

Sugars and Sweet Taste: Addictive or Rewarding?

The notion of food “addiction” often focuses on the overconsumption of sweet tasting foods or so-called sugar “addiction”. In the extreme, some have suggested that sugar and sweet tastes elicit neural and behavioral responses analogous to those observed with drugs of abuse. These concepts are complicated by the decades long uncertainty surrounding the validity and reproducibility of functional magnetic resonance imaging (fMRI) methodologies used to characterize neurobiological pathways related to sugar and sweet taste stimuli. There are also questions of whether sweet taste or post-ingestion metabolic consequences of sugar intake would lead to addiction or excessive caloric intake. Here, we present a focused narrative review of literature related to the reward value of sweet taste which suggests that reward value can be confounded with the construct of “addictive potential”. Our review seeks to clarify some key distinctions between these constructs and questions the applicability of the addiction construct to human over-eating behaviors. To adequately frame this broad discussion requires the flexibility offered by the narrative review paradigm. We present selected literature on: techniques used to link sugar and sweet tastes to addiction neurobiology and behaviors; sugar and sweet taste “addiction”; the relationship of low calorie sweetener (LCS) intake to addictive behaviors and total calorie intake. Finally, we examined the reward value of sweet tastes and contrasted that with the literature describing addiction. The lack of reproducibility of fMRI data remains problematic for attributing a common neurobiological pathway activation of drugs and foods as conclusive evidence for sugar or sweet taste “addiction”. Moreover, the complicated hedonics of sweet taste and reward value are suggested by validated population-level data which demonstrate that the consumption of sweet taste in the absence of calories does not increase total caloric intake. We believe the neurobiologies of reward value and addiction to be distinct and disagree with application of the addiction model to sweet food overconsumption. Most hypotheses of sugar “addiction” attribute the hedonics of sweet foods as the equivalent of “addiction”. Further, when addictive behaviors and biology are critically examined in totality, they contrast dramatically from those associated with the desire for sweet taste. Finally, the evidence is strong that responses to the palatability of sweets rather than their metabolic consequences are the salient features for reward value. Thus, given the complexity of the controls of food intake in humans, we question the usefulness of the “addiction” model in dissecting the causes and effects of sweet food over-consumption.

Overfeeding during development induces temporally-dependent changes in areas controlling food intake in the brains of male Wistar rats

AimsWe sought to evaluate the effects of overfeeding during lactation on the feeding behavior and expression of specific regulatory genes in brain areas associated with food intake in 22- and 60-day old male rats. MethodsWe evaluated body weight, food intake of standard and palatable diet, and mRNA expression of dopamine receptor D1 (DDR1), dopamine receptor (DDR2), melanocortin 4 receptor (MC4R), the μ-opioid receptor (MOR), neuropeptide Y (NPY), agouti-related protein (AGRP), proopiomelanocortin (POMC), cocaine-and amphetamine-regulated transcript (CART), serotonin (5-hydroxytryptamine; 5-HT) transporter (SERT), 5-hydroxytryptamine receptor 1B (5-HT1B), 5-hydroxytryptamine receptor 2C receptor (5-HT2C), Clock (CLOK), cryptochrome protein 1 (Cry1) and period circadian protein homolog 2 (Per2) in the striatum, hypothalamus and brainstem of male rats at post-natal days (PND) 22 and 60. Key findingsOverfeeding resulted in significantly increased body weight through PND60, and a 2-fold increase in palatable food intake at PND22, but not at PND60. We observed significant increases in DDR1, DDR2, and MC4R gene expression in the striatum and brainstem and POMC/CART in the hypothalamus of the OF group at PND22 that were reversed by PND60. Hypothalamic levels of 5-HT1B, 5-HT2C and NPY/AGRP on the other hand were decreased at PND22 and increased at PND60 in OF animals. Clock genes were unaffected by OF at PND22, but were significantly elevated at PND60. SignificanceOverfeeding during early development of the rat brain results in obesity and altered feeding behavior in early adulthood. The altered behavior might be the consequence of the changes in food intake and reward gene expression.

Living Environment Considerations on Obesity Prevention Behaviors and Self-Efficacy among Chinese Americans.

The aim of this study is to ascertain if the living environment (type of residential neighborhood and number of household members) will elucidate differences in obesity risk reduction behaviors and self-efficacy in Chinese Americans. A cross-sectional survey design was used to recruit participants from Los Angeles County and New York City metropolitan areas. A total of 650 adults were recruited from diverse socioeconomic backgrounds. Descriptive statistics were measured for 19 behaviors reflecting food intake and portion size control and items measuring self-efficacy and attitudes. T-tests were applied for the two categories of living environment. The mean age of the sample was 36.3 years. The ‘high income’ neighborhood group indicated a greater frequency of behaviors, including choosing steamed over fried foods (p < 0.01) and using small amounts of oil (p < 0.05). In general, this group exhibited more favorable attitudes and stronger self-efficacy to perform health behaviors. Multiple regression analyses point to the impact of self-efficacy in predicting behaviors. Nutrition professionals must assess client’s living environments in the adoption of obesity prevention behaviors and the fostering of behavioral confidence.

Associations of physical activity and sedentary behavior with appetite sensations and eating regulation behaviors before and during the initial year following bariatric surgery.

BackgroundBariatric surgery produces weight loss in part by impacting appetite and eating behavior. Research suggests physical activity (PA) assists with regulation of appetite and eating during non‐surgical weight loss, although whether PA carries similar benefits in the context of bariatric surgery is unknown.ObjectiveEvaluate associations of moderate‐to‐vigorous intensity PA (MVPA) and sedentary time (ST) with appetite sensations (hunger [homeostatic/hedonic], satiety) and eating regulation behaviors (restraint, disinhibition) before and during the initial year following bariatric surgery.MethodAdult bariatric patients received an accelerometer to measure MVPA/ST and a smartphone to complete appetite/eating ratings at four semi‐random times daily for 10 days at pre‐ and 3‐, 6‐, and 12‐months post‐surgery. Data were analyzed using generalized linear mixed models.ResultsHigher MVPA levels related to more satiety across time (p = 0.045) and more restraint at 3‐months post‐surgery (p < 0.001). At pre‐surgery, higher MVPA levels also related to more disinhibition (p's < 0.01), although participants reported more disinhibition on days they performed less MVPA than usual (p = 0.017). MVPA did not relate to hunger. Lower ST levels related to more hedonic hunger (p = 0.003), especially at 12‐months post‐surgery (p < 0.001), and participants reported more homeostatic hunger on days they accumulated more ST than usual (p = 0.044). Additionally, higher ST levels related to more disinhibition at 3‐months post‐surgery (p's < 0.01) and lower restraint at pre‐surgery (p's < 0.05). ST did not relate to satiety.ConclusionsThis study is the first to show that MVPA and ST each associate with appetite and eating regulation in daily life before and during post‐surgical weight loss. Results, while preliminary and requiring experimental confirmation, highlight potential for targeting bariatric patients' activity behaviors to enhance modulation of appetite, control of food intake, and resistance to overeating.

Beneficial effects of Pleurotus albidus supplementation on body weight and food intake in healthy C57BL/6 mice

The current investigation intended to check the influence of Pleurotus albidus extract supplementation on body weight, food intake, glycemia, serum lipids, and oxidative stress parameters. Healthy male C57BL/6 mice were partitioned into two experimental groups: control and P. albidus. The supplementation was performed by gavage (500 mg/kg) for 20 uninterrupted days. During this period, all animals received water and food ad libitum and they had their food ingestion and body weight monitored weekly. After, mice underwent an insulin sensitivity test, followed by euthanasia and biochemical analyses. P. albidus supplementation decreased the body weight and food intake, but it did not change other parameters in healthy mice. This work showed for the first time that the P. albidus extract supplementation presents a promising potential on body weight and food intake control.