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Previous studies indicate that CNS administration of oxytocin (OT) reduces body weight in high fat diet-induced obese (DIO) rodents by reducing food intake and increasing energy expenditure (EE). We recently demonstrated that hindbrain (fourth ventricular [4V]) administration of OT elicits weight loss and elevates interscapular brown adipose tissue temperature (TIBAT, a surrogate measure of increased EE) in DIO mice. What remains unclear is whether OT-elicited weight loss requires increased sympathetic nervous system (SNS) outflow to IBAT. We hypothesized that OT-induced stimulation of SNS outflow to IBAT contributes to its ability to activate BAT and elicit weight loss in DIO mice. To test this hypothesis, we determined the effect of disrupting SNS activation of IBAT on the ability of 4V OT administration to increase TIBAT and elicit weight loss in DIO mice. We first determined whether bilateral surgical SNS denervation to IBAT was successful as noted by ≥ 60% reduction in IBAT norepinephrine (NE) content in DIO mice. NE content was selectively reduced in IBAT at 1-, 6- and 7-weeks post-denervation by 95.9 ± 2.0, 77.4 ± 12.7 and 93.6 ± 4.6% (P

Key points Growth differentiation factor 15 (GDF15) is a stress‐induced cytokine that suppresses food intake and causes weight loss. GDF15 also reduces voluntary physical activity and, thus, it is not clear whether combining GDF15 with exercise will be beneficial or if reductions in food intake would be offset by decreases in physical activity. We investigated how GDF15 treatment combined with voluntary wheel running (VWR) would impact weight gain, food intake, adiposity and indices of metabolic health in mice. High‐fat fed male and female mice underwent daily GDF15 treatments and were given access to voluntary running wheels, or not, for 11 days. In both sexes, VWR prevented weight gain. In males, GDF15 reduced food intake, as well as attenuated weight gain and the accumulation of adipose tissue, with no additional effect of VWR. In female mice, GDF15 did not impact body weight gain or body composition. GDF15 acutely reduced food intake in female mice but this was followed by a period of rebound hyperphagia and consequently GDF15 did not reduce total food intake in female mice. GDF15 treatment reduced wheel running distance in both sexes. There were main effects of VWR to improve glucose tolerance in female but not male mice. These findings show that GDF15 has sex‐specific effects on food intake and consequently weight gain and adiposity. There is no added benefit of combining GDF15 and voluntary physical activity for weight loss. Adaptive responses to acute caloric restriction induced by GDF15 might limit its effectiveness as a weight loss tool in females. GDF15 is a stress‐induced signalling factor that reduces food intake and voluntary physical activity. It is not known whether combining GDF15 treatment with voluntary wheel running would impart beneficial combined effects in attenuating weight gain and the accumulation of adipose tissue. In the present study, we demonstrate that GDF15 reduces food intake and prevents weight gain in male but not female mice consuming a high‐fat diet and also that combining GDF15 with voluntary wheel running (VWR) does not lead to a greater dampening of weight gain. In female mice, GDF15 acutely reduced food intake, but this was followed by a period of rebound hyperphagia resulting in no differences in total food intake. In both sexes, VWR was equivalent, or superior to GDF15 in preventing weight gain. [ABSTRACT FROM AUTHOR]

The hypothalamus is the primary center of the brain that regulates energy homeostasis. The ventromedial hypothalamus (VMH) plays a central role in maintaining energy balance by regulating food intake, energy expenditure, and glucose levels. However, the cellular and molecular mechanisms underlying its functions are still poorly understood. Cholecystokinin (CCK) is one of many genes expressed in this hypothalamic nucleus. Peripheral CCK regulates food intake, body weight, and glucose homeostasis. However, current research does not explain the function of CCK neurons in specific nuclei of the hypothalamus and their likely roles in network dynamics related to energy balance and food intake. This study uses genetic and pharmacological methods to examine the role of CCK-expressing neurons in the VMH (CCKVMH). Namely, using a previously generated BAC transgenic line expressing Cre recombinase under the CCK promoter, we performed targeted manipulations of CCKVMH neurons. Histological and transcriptomic database analysis revealed extensive distribution of these neurons in the VMH, with significant heterogeneity in gene expression related to energy balance, including co-expression with PACAP and somatostatin. Pharmacogenetic acute inhibition via Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) resulted in increased food intake and altered meal patterns, characterized by higher meal frequency and shorter intermeal intervals. Furthermore, diphtheria toxin-mediated ablation of CCKVMH neurons led to significant weight gain and hyperphagia over time, increasing meal size and duration. These mice also exhibited impaired glucose tolerance, indicative of disrupted glucose homeostasis. Our findings underscore the integral role of CCKVMH neurons in modulating feeding behavior, energy homeostasis, and glucose regulation. This study enhances our understanding of the neurohormonal mechanisms underlying obesity and metabolic disorders, providing potential targets for therapeutic interventions. [ABSTRACT FROM AUTHOR]

This functional magnetic resonance imaging (fMRI) study examined resting-state (RS) connectivity in adolescent and adult patients with anorexia nervosa (AN) using symptom provocation paradigms. Differential food reward mechanisms were investigated through separate assessments of responses to food images and low-caloric/high-caloric food consumption. Thirteen young (≤ 21 years) and seventeen adult (> 21 years) patients with AN and age-matched controls underwent two stimulus-driven fMRI sessions involving RS scans before and after the presentation of food-related stimuli and food consumption. Graph theory and machine learning were used for analyzing the fMRI and clinical data. Healthy controls (HCs) showed widespread developmental changes, while young participants with AN exhibited cerebellum differences for high-calorie food. Young individuals with AN displayed increased connectivity during the consumption of potato chips compared to zucchini, with no differences in adults with AN. Multiparametric machine learning accurately distinguished young individuals with AN from healthy controls based on RS connectivity following food visual stimulation ("anticipatory") and consumption ("consummatory"). This study highlights the differential food reward mechanisms and minimal developmental changes in RS connectivity from youth to adulthood in individuals with AN compared to healthy controls. Young individuals with AN demonstrated heightened reactivity to high-caloric foods, while adults showed decreased responsiveness, potentially due to desensitization. These findings shed light on aberrant eating behaviors in individuals with AN and contribute to our understanding of the chronicity of the disease. [ABSTRACT FROM AUTHOR]

Neuropeptide F (NPF) and short neuropeptide F (sNPF) are important neuropeptides and mainly affect feeding behaviour of insects. However, the regulation of insect feeding behaviour by NPF and sNPF appears to differ between species, and it is not clear how NPF and sNPF regulate the food intake of the brown planthopper (Nilaparvata lugens). Therefore, the functions of NPF and sNPF in regulating food intake and affecting the growth and antioxidant levels of N. lugens fed on host rice plants were investigated by knocking down NPF and sNPF respectively and simultaneously knocking down both of them by RNA interference. The results showed that NPF and sNPF were mainly expressed in the head of N. lugens, and N. lugens increased food intake after NPF and sNPF were knocked down, which was reflected in the prolonged duration of N4a and N4b waves in the electrical penetration graph (EPG) experiment after knocking down NPF and sNPF. In addition, knocking down NPF and sNPF led to the increase of body weight and mortality of N. lugens, and also led to the increase of antioxidant level of N. lugens. So it was concluded that NPF and sNPF could regulate food intake, maintain body weight stability and oxidative balance in N. lugens. Our study clarified the molecular mechanism of NPF and sNPF regulating feeding behaviour and affect the growth and antioxidant level of N. lugens. [ABSTRACT FROM AUTHOR]

Background: Developing anti-obesity interventions targeting appetite or food intake, the primary driver of obesity, remains challenging. Here, we demonstrated that dietary γ-aminobutyric acid (GABA) with GABA-degradation inhibitory drugs could be an anti-obesity intervention possessing strong food intake-suppressive and weight-loss effects. Methods: High-fat (HF)-diet-induced obese mice were divided into six groups receiving either the HF diet or the 2% GABA-HF diet with daily administration of PBS or the GABA-degradation inhibitory drugs, vigabatrin and ethanolamine-O-sulfate (EOS). In 24-h fast-induced refeeding, lean mice with a basal diet were used, and food intake was measured from 0.5 to 24 h after refeeding. Results: Coadministration of the 2% GABA-HF diet with vigabatrin or EOS significantly decreased food intake (−53%, −35%) and body weight (−22%, −16%) within 11 days in obese mice, along with a marked increase in plasma GABA levels. Mice receiving dietary GABA alone or the drugs alone exhibited no such effects. Hypothalamic GABA levels increased in drug-treated mice, regardless of diet. At 0.5 h after refeeding, food intake was similar in all groups. However, at 0.5 h, plasma GABA levels were markedly increased only in mice receiving coadministration of dietary GABA and the drugs, and their food intake was completely inhibited for over 6 h, while mice in other groups gradually increased their food intake. Conclusion: Combining dietary GABA with GABA-degradation inhibitory drugs effectively suppresses food intake and promotes weight loss in obese mice, primarily through increased plasma GABA availability. These findings may advance the development of food intake-controlling strategies for obesity management. [ABSTRACT FROM AUTHOR]

Background: Rikkunshito (RKT), a traditional Japanese medicine, can relieve epigastric discomfort and anorexia in patients with functional dyspepsia. RKT enhances the orexigenic hormone, ghrelin. Ghrelin regulates food motivation by stimulating the appetite control center in the hypothalamus and the brain mesolimbic dopaminergic pathway (MDPW). However, the effect of RKT on MDPW remains unclear. Here, we aimed to investigate the central neural mechanisms underlying the orexigenic effects of RKT, focusing on the MDPW. Methods: We examined the effects of RKT on food intake and neuronal c‐Fos expression in restraint stress‐ and cholecystokinin octapeptide‐induced anorexia in male rats. Key Results: RKT treatment significantly restored stress‐ and cholecystokinin octapeptide‐induced decreased food intake. RKT increased c‐Fos expression in the ventral tegmental area (VTA), especially in tyrosine hydroxylase‐immunoreactive neurons, and nucleus accumbens (NAc). The effects of RKT were suppressed by the ghrelin receptor antagonist [D‐Lys3]‐GHRP‐6. RKT increased the number of c‐Fos/orexin‐double‐positive neurons in the lateral hypothalamus (LH), which project to the VTA. The orexin receptor antagonist, SB334867, suppressed RKT‐induced increase in food intake and c‐Fos expression in the LH, VTA, and NAc. RKT increased c‐Fos expression in the arcuate nucleus and nucleus of the solitary tract of the medulla, which was inhibited by [D‐Lys3]‐GHRP‐6. Conclusions & Inferences: RKT may restore appetite in subjects with anorexia through ghrelin‐ and orexin‐dependent activation of neurons regulating the brain appetite control network, including the hypothalamus and MDPW. [ABSTRACT FROM AUTHOR]

Summary: Numerous investigations have studied relationships between satiation, satiety, or food intake and single factors like food composition and resting metabolic rate. However, a comprehensive framework connecting food, physiological, and psychological factors together has not previously been reported. As an exploratory study with a trained panel consisting of nine participants, the contributions of twenty‐eight variables (seven food, seven psychological, and fourteen physiological factors) to satiation, satiety, and food intake of a mid‐morning snack were investigated. Both human factors and foods had contributions to perceived satiation and satiety, but with large differences in loadings, especially for metabolic factors. Food factors, including nutrient and energy contents, were major determinants of food intake, with only small contributions from human factors. Investigating diverse factors together provides a comprehensive approach linking appetite to both food and human factors. This study suggests the potential to guide manipulation of satiation, satiety, and food intake depending on individual psychological and physiological profiles. [ABSTRACT FROM AUTHOR]

Objectives: The association between ultra-processed foods (UPF) consumption and cognitive performance needs to be better characterized in adolescents, especially in lowincome settings, where the cost of human capital is high. This study investigated the association between cognitive performance and UPF in adolescents from the countryside of the Brazilian Northeast. Methods: Adolescents (15-18 years old) from three public high schools were included. Food intake was assessed using three 24-hour dietary recalls. The classification of foods as UPF was determined according to the Nova classification. Cognitive performance was evaluated using the Non-Verbal General Intelligence Test. Results: 116 adolescents were included, of which 50 (43.1%) showed low cognitive performance. The average energy intake was 1973.5 kcal, with 24.2% coming from UPF. Participants with low cognitive performance consumed 26.5% (95% CI: [22.2; 30.7]%) of daily energy intake from UPF compared to 22.5% ([18.8; 26.2]%) of those with mediumhigh cognitive performance (P = 0.17), without differences in energy and macronutrient intake. Conclusion: Despite similar UPF consumption compared to the Brazilian average, no association was found between UPF consumption and cognitive performance in this lowincome adolescent sample. [ABSTRACT FROM AUTHOR]

Background: Developing anti-obesity interventions targeting appetite or food intake, the primary driver of obesity, remains challenging. Here, we demonstrated that dietary γ-aminobutyric acid (GABA) with GABA-degradation inhibitory drugs could be an anti-obesity intervention possessing strong food intake-suppressive and weight-loss effects. Methods: High-fat (HF)-diet-induced obese mice were divided into six groups receiving either the HF diet or the 2% GABA-HF diet with daily administration of PBS or the GABA-degradation inhibitory drugs, vigabatrin and ethanolamine-Osulfate (EOS). In 24-h fast-induced refeeding, lean mice with a basal diet were used, and food intake was measured from 0.5 to 24 h after refeeding. Results: Coadministration of the 2% GABA-HF diet with vigabatrin or EOS significantly decreased food intake (-53%, -35%) and body weight (-22%, -16%) within 11 days in obese mice, along with a marked increase in plasma GABA levels. Mice receiving dietary GABA alone or the drugs alone exhibited no such effects. Hypothalamic GABA levels increased in drugtreated mice, regardless of diet. At 0.5 h after refeeding, food intake was similar in all groups. However, at 0.5 h, plasma GABA levels were markedly increased only in mice receiving coadministration of dietary GABA and the drugs, and their food intake was completely inhibited for over 6 h, while mice in other groups gradually increased their food intake. Conclusion: Combining dietary GABA with GABA-degradation inhibitory drugs effectively suppresses food intake and promotes weight loss in obese mice, primarily through increased plasma GABA availability. These findings may advance the development of food intake-controlling strategies for obesity management. [ABSTRACT FROM AUTHOR]

Objective To investigate the optimal adaptation period for mice at different developmental stages during metabolic cage experiments, aiming to provide a reference for conducting metabolic research using mice. Methods A total of 80 male C57BL/6J mice at three developmental stages (weaning period M1, adolescent M2, and adulthood M3) were subjected to a 7-day metabolic cage experiment. Data on food intake, water intake, energy expenditure, respiratory quotient, body weight, and activity levels were recorded every five minutes. The collected data were processed using time series decomposition and comprehensive cluster analysis. Statistical differences were compared using repeated measures ANOVA combined with t-test to determine the optimal adaptation period. Results Significant differences in metabolism were observed among mice in different developmental stages (P<0.01). Compared with adolescent (M2) and adult (M3) mice, weaned mice (M1) exhibited lower activity level (P<0.01) and less distinct circadian rhythm. M1 mice had higher oxygen consumption, carbon dioxide production, and energy expenditure, as well as a lower respiratory quotient (all P<0.001), indicating that they mainly relied on fat as an energy source. Analysis of food intake, water intake, and energy expenditure revealed significant differences between the first light cycle (0-12 h) and the second light cycle (24-36 h) across all developmental stages (all P<0.05) . However, there was no significant difference in daily food intake or water intake after 24 hours (both P>0.05). Comprehensive cluster analysis of multiple indicators showed that the overall indicators of mice during the first 24 hours in the metabolic cages did not cluster with those of the subsequent 6 days, demonstrating significant differences. Conclusion Metabolic cage experiment can be used to detect continuous physiological changes in mice. The results suggest that mice can adapt to new metabolic cages environment within 24 hours, providing a theoretical basis for the design of metabolic experiments using mice. [ABSTRACT FROM AUTHOR]

In parallel to the legalization of cannabis for both medicinal and recreational purposes, cannabinoid use has steadily increased over the last decade in the United States. Cannabinoids, such as tetrahydrocannabinol and anandamide, bind to the central cannabinoid‐1 (CB1) receptor to impact several physiological processes relevant for body weight regulation, including appetite and energy expenditure. The hypothalamus integrates peripheral signals related to energy balance, houses several nuclei that orchestrate eating, and expresses the CB1 receptor. Herein we review literature to date concerning cannabinergic action in the hypothalamus with a specific focus on eating behaviors. We highlight hypothalamic areas wherein researchers have focused their attention, including the lateral, arcuate, paraventricular, and ventromedial hypothalamic nuclei, and interactions with the hormone leptin. This review serves as a comprehensive analysis of what is known about cannabinoid signaling in the hypothalamus, highlights gaps in the literature, and suggests future directions. [ABSTRACT FROM AUTHOR]

• Coarser oat flours reduced postprandial glycemia when consumed in a porridge. • Finer oat flour porridge reduced appetite but did not impact food intake. • Adding coarse oat flour to common foods can increase health benefits. • Processing impacts the nutritional properties of oat flours. Consumption of oats is associated with lowered risks of type 2 diabetes and obesity. However, many oat-based products (e.g., breakfast cereals) use finely milled flours but are associated with health claims based on oats of larger particle sizes. The objective of this study was to test the hypothesis that increasing oat flour particle size will result in lower postprandial glycemia and appetite. Using a randomized-controlled, crossover design, 20 participants (10 males, 10 females; age: 25.3 ± 1.0 years; body mass index: 23.2 ± 0.6 kg/m2) consumed a serving of porridge made using 40 g of coarse (675.7 ± 19.6 µm), whole (443.3 ± 36.2 µm), fine (96.0 ± 2.1 µm), or a commercial (375.9 ± 14.8 µm) oat flour unmatched in available carbohydrate, protein, and dietary fiber content. After a 12-hour overnight fast, blood glucose, insulin, and appetite were measured at 15 to 30-minute intervals over 120 minutes posttreatment consumption. Coarse and whole flours led to lower blood glucose between 30 and 60 minutes (P <.02). Blood glucose area under the curve (AUC) was lower after coarse than fine and commercial oat flours (P < 0.03), and after whole than fine oat flour (P <.002). Both coarse and whole oat flours resulted in lower insulin AUC than finer flours (P <.05). Appetite AUC was lower after the commercial than coarse flour (P <.007). Controlling milling to produce coarser oat flour to add to common foods may have health benefits. This study was registered at ClinicalTrials.gov (NCT05291351). Healthy adults consumed porridge made using coarse, whole, fine, or commercial oat flour after a 12-hour overnight fast. Postprandial glycemia and appetite were assessed every 15 to 30 minutes over 120 minutes. Food intake was assessed at an ad libitum pizza meal at 120 minutes. Coarse and whole oat flours led to lower blood glucose and insulin, but appetite was lower after the finer flours. No differences in food intake were found. Producing coarser oat flour to add to common foods may have health benefits. [Display omitted] [ABSTRACT FROM AUTHOR]

Gastrointestinal vagal afferents play an important role in communicating food related information from the gut to the brain. This information initiates vago‐vagal reflexes essential for gut functions, including gut motility and secretions. These afferents also play a role in energy homeostasis, signalling the arrival, amount and nutrient composition of a meal to the central nervous system where it is processed ultimately leading to termination of a meal. Vagal afferent responses to food related stimuli demonstrate a high degree of plasticity, responding to short term changes in nutritional demand, such as the fluctuations that occur across a 24‐hr or in response to a fast, as well as long term changes in energy demand, such as occurs during pregnancy. This plasticity is disrupted in disease states, such as obesity or chronic stress where there is hypo‐ and hypersensitivity of these afferents, respectively. Improved understanding of the plasticity of these afferents will enable identification of new treatment options for diseases associated with vagal afferent function. [ABSTRACT FROM AUTHOR]

The effects of exogenous ketones on appetite and food intake remain elusive, especially for people with type 2 diabetes (T2D). This study aimed to determine whether acute ingestion of an oral ketone monoester supplement (KME) affected appetite sensations, prospective food consumption and intake in T2D. Results showed that acute KME ingestion did not significantly alter appetite scores. However, there was a tendency for lower energy intake during an ad libitum meal 3 h following ketone ingestion compared to non-energetic placebo. Further research is warranted to understand the long-term effects of exogenous ketones for energy and macronutrient intake in T2D. [ABSTRACT FROM AUTHOR]

Kisspeptins are essential regulators of the reproductive axis, with capacity to potently activate gonadotropin‐releasing hormone neurons, acting also as central conduits for the metabolic regulation of fertility. Recent evidence suggests that kisspeptins per se may also modulate several metabolic parameters, including body weight, food intake or energy expenditure, but their actual roles and site(s) of action remain unclear. We present herein a series of studies addressing the metabolic effects of central and peripheral administration of kisspeptin‐10 (Kp‐10; 1 nmol and 3 nmol daily, respectively) for 11 days in mice of both sexes. To assess direct metabolic actions of Kp‐10 versus those derived indirectly from its capacity to modulate gonadal hormone secretion, kisspeptin effects were tested in adult male and female mice gonadectomized and supplemented with fixed, physiological doses of testosterone or 17β‐estradiol, respectively. Central administration of Kp‐10 decreased food intake in male mice, especially during the dark phase (~50%), which was accompanied by a reduction in total and nocturnal energy expenditure (~16%) and locomotor activity (~70%). In contrast, opposite patterns were detected in female mice, with an increase in total and nocturnal locomotor activity (>65%), despite no changes in food intake or energy expenditure. These changes were independent of body weight, as no differences were detected in mice of both sexes at the end of Kp‐10 treatments. Peripheral administration of Kp‐10 failed to alter any of the metabolic parameters analyzed, except for a decrease in locomotor activity in male mice and a subtle increase in 24 h food intake in female mice, denoting a predominant central role of kisspeptins in the control of energy metabolism. Finally, glucose tolerance and insulin sensitivity were not significantly affected by central or peripheral treatment with Kp‐10. In conclusion, our data reveal a potential role of kisspeptins in the control of key metabolic parameters, including food intake, energy expenditure and locomotor activity, with a preferential action at central level, which is sex steroid‐independent but sexually dimorphic. [ABSTRACT FROM AUTHOR]

Aim: Liver‐expressed antimicrobial peptide 2 (LEAP2) dynamics in human plasma and its association with feeding behaviour remain poorly understood. Therefore, this study aims: (a) to investigate fasting LEAP2 in participants with normal weight or with overweight or mild obesity (OW/OB); (b) to study the association between fasting LEAP2 and anthropometric and metabolic traits, feeding behaviour, LEAP2 genetic variants and blood cell DNA methylation status; and (c) to ascertain postprandial changes in LEAP2 after high protein intake and the association with feeding behaviour and food intake. Methods: Anthropometric and behavioural measures, genotyping, methylation profiling, plasma glucose and LEAP2 concentrations were assessed in 327 females and males. A subgroup of 123 participants received an ad libitum high‐protein meal, and postprandial LEAP2 concentration and behavioural measures were assessed. Results: LEAP2 concentration was higher in participants with OW/OB (p < 0.001) and in females (p < 0.001), and was associated with LEAP2 single nucleotide polymorphisms rs765760 (p = 0.012) and rs803223 (p = 0.019), but not with LEAP2 methylation status. LEAP2 concentration was directly related to glycaemia (p = 0.001) and fullness (p = 0.003) in participants with normal weight, whereas it was associated with body mass index (p = 0.018), waist circumference (p = 0.014) and motor impulsivity in participants with OW/OB (p = 0.005). A negative association with reward responsiveness was observed in participants with OW/OB (p = 0.023). LEAP2 concentration was inversely associated with food intake (p = 0.034) and decreased after a high‐protein meal (p < 0.001), particularly in women (p = 0.002). Conclusion: Increased LEAP2 in participants with OW/OB is associated with behavioural characteristics of obesity. Our results show sexual dimorphism in LEAP2 concentration before and after food intake and highlight the role of LEAP2 in feeding regulation. [ABSTRACT FROM AUTHOR]

Copyright of Pamukkale Medical Journal is the property of Pamukkale Journal of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Gynäkologische Endokrinologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To evaluate an association between eating patterns and sleep quality in Chilean university students. A cross-sectional analytical study was conducted. Participants included students from 4 Chilean universities. Each student was administered survey Questionnaire on the frequency of healthy and unhealthy eating habits and Pittsburgh Sleep Quality Index and their weight and height were taken to obtain the Body Mass Index (BMI). A total of 1,079 young university students, 80.26 % were women and the average age was 21.7 years. The 73.68 % have inadequate sleep quality. There is a significant differences in frequency between sleep quality and the intake of breakfast (p<0.001), fish (p<0.05) and dinner (p<0.05), that is, university students who reported optimal sleep consume breakfast and dinner on a daily basis and their fish intake is in line with nutritional recommendations. With respect to the association between sleep quality and healthy dietary patterns, it is observed a significant association (p<0.01) between optimal sleep and daily breakfast consumption in model 3 (Odds Ratio (OR): 0.61 (0.46–0.82)). Regarding unhealthy dietary patterns, a significant association (p<0.05) is observed in model 3 between sleep quality and alcohol consumption (OR: 1.42 (1.02–1.96)). Furthermore, a significant association between optimal sleep and salt consumption is observed in both model 2 (OR: 0.73 (0.54–0.99)) and model 3 (OR: 0.72 (0.53–0.97)). Finally, a significant relationship between not tobacco use and optimal sleep is observed (OR: 0.68 (0.48–0.96)). A positive relationship between healthy diet and sleep quality was observed in university students, which certain dietary patterns, such as the consumption of breakfast and low salt consumption and alcohol, are crucial to talk about a good sleep quality in this population group. [ABSTRACT FROM AUTHOR]

Aims Methods Results Conclusion Researchers were invited by Aboriginal leaders to collaborate on this study which aimed to assess food intake in the Walgett Aboriginal community to inform long‐term community‐led efforts to improve food and water security and nutrition.Aboriginal adults living in or near Walgett, a remote community in north‐west NSW, Australia, completed an adapted Menzies Remote Short‐item Dietary Assessment Tool, which was administered verbally and face‐to‐face in early 2022. Aboriginal people were involved in the survey design, training and collection, and analysis of data. Descriptive statistics were tabulated, overall and by gender, age, and location. Differences by sex, age group (18‐44 years versus ≥45 years), and location (Walgett town or other) were determined using a chi‐square test.A total of 242 participants completed the survey; 55% were female. Three‐quarters of participants reported meeting the recommendations for discretionary foods (73%); however, more than half (56%) exceeded the recommended maximum serves of sugar‐sweetened beverages. The proportion of participants meeting core food group guidelines was 72% for meat, 36% for fruit, 20% for bread and cereals, 6% for dairy, and 3% for vegetables. Overall, none of the participants met the recommended serves of all food groups outlined in the Australian Dietary Guidelines.Findings show that Walgett Aboriginal community members surveyed were consuming a healthier diet than national data reported for Aboriginal and Torres Strait Islander people in Australia. However, none of the participants were meeting all of the national dietary guidelines, placing them at increased risk of diet‐related chronic disease. Local Aboriginal community‐led efforts to improve food and water security should include specific strategies to improve nutrition. [ABSTRACT FROM AUTHOR]

Chalcones constitute an important group of natural compounds abundant in fruits and comestible plants. They are a subject of increasing interest because of their biological activities, including anti-diabetic and anti-obesity effects. The simple chalcone structural scaffold can be modified at multiple sites with different chemical moieties. Here, we generated an artificial chalcone, i.e., 3,5-dimethyl-2,4,6-trimethoxychalcone (TriMetChalc), derived from 2′,4′-Dihydroxy-6′-methoxy-3′,5′-dimethylchalcone (DMC). DMC is a major compound of Cleistocalyx operculatus, a plant widely used in Asia for its anti-hyperglycemic activity. Using ob/ob mice as an obesity model, we report that, after 3 weeks of per os administration, TriMetChalc modified food intake through the specific activation of brain structures dedicated to the regulation of energy balance. TriMetChalc also decreased weight gain, glucose intolerance, and hepatic steatosis. Moreover, through extensive liver lipidomic analysis, we identified TriMetChalc-induced modifications that could contribute to improving the liver status of the animals. Hence, TriMetChalc is a chalcone derivative capable of reducing food intake and the addition of glucose intolerance and hepatic steatosis in a mouse model of obesity. In light of these results, we believe that TriMetChalc action deserves to be more deeply evaluated over longer treatment periods and/or in combination with other chalcones with protective effects on the liver. [ABSTRACT FROM AUTHOR]

Background: The part played by oxytocin and oxytocin neurons in the regulation of food intake is controversial. There is much pharmacological data to support a role for oxytocin notably in regulating sugar consumption, however, several recent experiments have questioned the importance of oxytocin neurons themselves. Methods: Here we use a combination of histological and chemogenetic techniques to investigate the selective activation or inhibition of oxytocin neurons in the hypothalamic paraventricular nucleus (OxtPVH). We then identify a pathway from OxtPVH neurons to the bed nucleus of the stria terminalis using the cell-selective expression of channel rhodopsin. Results: OxtPVH neurons increase their expression of cFos after both physiological (fast-induced re-feeding or oral lipid) and pharmacological (systemic administration of cholecystokinin or lithium chloride) anorectic signals. Chemogenetic activation of OxtPVH neurons is sufficient to decrease free-feeding in OxtCre:hM3Dq mice, while inhibition in OxtCre:hM4Di mice attenuates the response to administration of cholecystokinin. Activation of OxtPVH neurons also increases energy expenditure and core-body temperature, without a significant effect on locomotor activity. Finally, the selective, optogenetic stimulation of a pathway from OxtPVH neurons to the bed nucleus of the stria terminalis reduces the consumption of sucrose. Conclusion: Our results support a role for oxytocin neurons in the regulation of whole-body metabolism, including a modulatory action on food intake and energy expenditure. Furthermore, we demonstrate that the pathway from OxtPVH neurons to the bed nucleus of the stria terminalis can regulate sugar consumption. [ABSTRACT FROM AUTHOR]

Food intake regulation is a complex mechanism involving the interaction between central and peripheral structures. Among the latter, the gastrointestinal tract represents one of the main sources of both nervous and hormonal signals, which reach the central nervous system that integrates them and sends the resulting information downstream to effector organs involved in energy homeostasis. Gut hormones released by nutrient-sensing enteroendocrine cells can send signals to central structures involved in the regulation of food intake through more than one mechanism. One of these is through the modulation of gastric motor phenomena known to be a source of peripheral satiety signals. In the present review, our attention will be focused on the ability of the glucagon-like peptide 2 (GLP-2) hormone to modulate gastrointestinal motor activity and discuss how its effects could be related to peripheral satiety signals generated in the stomach and involved in the regulation of food intake through the gut–brain axis. A better understanding of the possible role of GLP-2 in regulating food intake through the gut–brain axis could represent a starting point for the development of new strategies to treat some pathological conditions, such as obesity. [ABSTRACT FROM AUTHOR]

The aim of this article was to study the quality of hospital-provided nutrition in Algeria, to understand possible deficiencies and weaknesses and then propose appropriate recommendations based on the recommendations of The ESPEN, the AFDN, and the SFNCM guidelines. The energetic and nutritional value of served meals throughout the week in four public hospitals in east Algeria was calculated. The menus proposed by the dietician of each hospital were used. Energy and nutrient values for each food item were calculated using "CIQUAL Table, 2016". The energy average per day was 9759 ± 1111.6 kJ (2332 kcal), and the macronutrients averages per day were: 106 ± 9.2 g, 65 ± 20.5 g, and 326 ± 39.3 g for proteins, lipids and carbohydrates respectively. Results showed imbalance in macronutrients, severe deficiency in healthy fats and micronutrients. Several types of food are absent or insufficient, or proposed in inaccurate types and quantities in hospital menus. The absence and shortage of some types of food and the inaccuracy of types and quantities were the main reasons for the imbalance of the proposed menus in hospitals. We propose a series of evidence-based recommendations tailored to the Algerian healthcare context especially by offering multiple meal choices, addressing macronutrient proportions, and ensuring that diets are responsive to individual patient needs. Nutrition approach in the hospitals concerned with the study is to reconsider, taking into account hospital menus and all the factors of reduced food intake, to prevent and treat hospital malnutrition and minimize its clinical and economic outcomes. [ABSTRACT FROM AUTHOR]

Purpose: Previous research has established that food intake is a biological regulator of the human sleep–wake cycle. As such, the timing of eating relative to sleep may influence the quality of sleep, including daytime naps. Here, we examine whether the timing of lunch (1 h vs. 2 h interval between lunch and a napping opportunity) impacts the quality of an afternoon nap. Methods: Using a randomized within-subject design over two separate experimental sessions (7 days apart), participants (n = 40, mean age = 25.8 years) consumed lunch 1 h and 2 h prior to an afternoon nap opportunity. Polysomnography and subjective self-reports were used to assess sleep architecture, sleepiness levels, and nap quality. Results: Results revealed no significant differences in subjective ratings of sleep quality and sleepiness, or in sleep architecture (total sleep time, sleep efficiency, sleep onset latency, sleep stages) between the 1 h and 2-h lunch conditions. Conclusions: All sleep measures were similar when napping followed eating by either 1 h or 2 h, suggesting that eating closer to nap onset may not negatively impact sleep architecture and quality. Future research should continue to identify conditions that improve nap quality, given the well-documented benefits of naps to reduce sleep pressure and improve human performance. [ABSTRACT FROM AUTHOR]

Ghrelin is an appetite-stimulating hormone secreted from the gastric mucosa in the fasting state, and secretion decreases in response to food intake. After sleeve gastrectomy (SG), plasma concentrations of ghrelin decrease markedly. Whether this affects appetite and glucose tolerance postoperatively is unknown. We investigated the effects of ghrelin infusion on appetite and glucose tolerance in individuals with obesity before and 3 mo after SG. Twelve participants scheduled for SG were included. Before and 3 mo after surgery, a mixed-meal test followed by an ad libitum meal test was performed with concomitant infusions of acyl-ghrelin (1 pmol/kg/min) or placebo. Infusions began 60 min before meal intake to reach a steady state before the mixed-meal and were continued throughout the study day. Two additional experimental days with 0.25 pmol/kg/min and 10 pmol/kg/min of acyl-ghrelin infusions were conducted 3 mo after surgery. Both before and after SG, postprandial glucose concentrations increased dose dependently during ghrelin infusions compared with placebo. Ghrelin infusions inhibited basal and postprandial insulin secretion rates, resulting in lowered measures of β-cell function, but no effect on insulin sensitivity was seen. Ad libitum meal intake was unaffected by the administration of ghrelin. In conclusion, ghrelin infusion increases postprandial plasma glucose concentrations and impairs β-cell function before and after SG but has no effect on ad libitum meal intake. We speculate that the lower concentration of ghrelin after SG may impact glucose metabolism following this procedure. NEW & NOTEWORTHY: Ghrelin's effect on glucose tolerance and food intake following sleeve gastrectomy (SG) was evaluated. Acyl-ghrelin was infused during a mixed-meal and ad libitum meals before and 3 mo after surgery. Postprandial glucose concentrations increased during ghrelin infusions, both before and after surgery, while insulin production was inhibited. However, ad libitum meal intake did not differ during ghrelin administration compared with placebo. The decreased ghrelin concentration following SG may contribute to the glycemic control after surgery. [ABSTRACT FROM AUTHOR]

Evaluate the validity of the PortionSize application. In this pilot study, 14 adults used PortionSize to record their free-living food intake over 3 consecutive days. Digital photography was the criterion measure, and the main outcomes were estimated intake of food (grams), energy (kilocalories), and food groups. Equivalence tests with ±25% equivalence bounds and Bland-Altman analysis were performed. Estimated gram intake from PortionSize was equivalent (P < 0.001) to digital photography estimates. PortionSize and digital photography estimated energy intake, however, were not equivalent (P = 0.08), with larger estimates from PortionSize. In addition, PortionSize and digital photography were equivalent for vegetable intake (P = 0.01), but PortionSize had larger estimates of fruits, grains, dairy, and protein intake (P >0.07; error range 11% to 23%). Compared with digital photography, PortionSize accurately estimated food intake and had reasonable error rates for other nutrients; however, it overestimated energy intake, indicating further application improvements are needed for free-living conditions. [ABSTRACT FROM AUTHOR]

Research shows that features of food packaging can help to promote healthy food choices. Laboratory‐based studies demonstrate that smart design of packaging facilitates portion control. However, the extent to which consumers notice packaging features for portion control is not known. Therefore, this study investigated how individuals interact with food packaging, how they utilise the on‐pack serving‐size guidelines and how they make portion decisions. To do this, 25 adult participants were recruited to participate in an online semi‐structured interview. Data were analysed using thematic analysis until saturation was achieved. Participants reported that they rarely attend to on‐pack serving recommendations and indicated some resistance to them. Some structural features (small/single serving, pre‐portioned and resealable packaging) were identified as facilitators of portion control. In contrast, the healthiness evaluation of the product from packaging cues was described as a permissive cue to eat more of the product. Participants in this study value their autonomy and control, preferring convenient behavioural choices over recommended portion servings. They also reported future concerns about the effects of their diet on health, but that current context (hunger, convenience) sometimes presented a barrier to healthy eating. Packaging does more than protect its contents, packaging can affect eating decisions to support portion control, and for some, offers permission to overconsume. This study identified ways that participants use packaging to make portion decisions, revealing the role of habits, current context and future health considerations. The interviews revealed the importance of consumer values on food choice in general and portion control in particular. In conclusion, smart food packaging design could use these findings to nudge healthy portion decisions by incorporating consumer values and by recognising consumer needs for habitual, current and future concerns. [ABSTRACT FROM AUTHOR]

Background: Studies investigating the quality of the diet and dietary intake of children with Down syndrome (DS) are required because the features attributed to the syndrome can affect growth, development and quality of life. Methods: This cross‐sectional study was conducted with 77 Brazilian children with DS between 5 and 36 months of age receiving care at the multidisciplinary outpatient clinic of the University Hospital. Participants' sociodemographic, dietary and anthropometric data were collected from the care protocols. Dietary data were collected from 24‐h recalls and dietary practices were assessed according to the WHO dietary guidelines. Associations between inadequate feeding practices and demographic variables were assessed using logistic regression models. Results: Fruits, milk or infant formula, vegetables, beans and meat were among the five most consumed foods by the children investigated. Overall, we observed a high number of cases of early weaning (50.6%), low minimum dietary diversity (MDD; 40.3%), inadequate consistency for age (64.9%), early presence of ultra‐processed foods (76.6%), sugars and sweets (33.8%) in the diet of the children with DS. In the associations of inadequate feeding practices by age group, low MDD [odds ratio (OR): 18.6; 95% confidence interval (CI): 3.4; 57.1] and inadequate consistency (OR: 6.65; 95% CI: 1.8; 24.7) were more frequent among children aged below 12 months while this relationship was inverse for early introduction of sugar and sweets (OR: 0.04; 95% CI: 0.01; 0.29). Conclusion: Our findings showed a high number of cases of inadequate dietary practices in children with DS investigated, which could adversely affect the long‐term health of this population. [ABSTRACT FROM AUTHOR]

Neuroactive steroids are a type of steroid hormones produced within the nervous system or in peripheral glands and then transported to the brain to exert their neuromodulatory effects. Neuroactive steroids have pleiotropic effects, that include promoting myelination, neuroplasticity, and brain development. They also regulate important physiological functions, such as metabolism, feeding, reproduction, and stress response. The homoeostatic processes of metabolism and reproduction are closely linked and mutually dependent. Reproductive events, such as pregnancy, bring about significant changes in metabolism, and metabolic status may affect reproductive function in mammals. In females, the regulation of reproduction and energy balance is controlled by the fluctuations of oestradiol and progesterone throughout the menstrual cycle. Neurosteroids play a key role in the neuroendocrine control of reproduction. The synthesis of neuroestradiol and neuroprogesterone within the brain is a crucial process that facilitates the release of GnRH and LH, which in turn, regulate the transition from oestrogen-negative to oestrogen-positive feedback. In addition to their function in the reproductive system, oestrogen has a key role in the regulation of energy homoeostasis by acting at central and peripheral levels. The oestrogenic effects on body weight homoeostasis are primarily mediated by oestrogen receptors-α (ERα), which are abundantly expressed in multiple brain regions that are implicated in the regulation of food intake, basal metabolism, thermogenesis, and brown tissue distribution. The tight interplay between energy balance and reproductive physiology is facilitated by shared regulatory pathways, namely POMC, NPY and kisspeptin neurons, which are targets of oestrogen regulation and likely participate in different aspects of the joint control of energy balance and reproductive function. The aim of this review is to present a summary of the progress made in uncovering shared regulatory pathways that facilitate the tight coupling between energy balance and reproductive physiology, as well as their reciprocal interactions and the modulation induced by neurosteroids. [ABSTRACT FROM AUTHOR]

Introduction There is increasing interest in food biomarkers to address the shortcomings of self-reported dietary assessments. Berries are regarded as important fruits worldwide; however, there are no well-validated biomarkers of berry intake. Thus, the objective of this study is to identify urinary biomarkers of berry intake. Methods For the discovery study, participants consumed 192 g strawberries with 150 g blueberries, and urine samples were collected at 2, 4, 6, and 24 h post-consumption. A dose–response study was performed, whereby participants consumed three portions (78 g, 278 g, and 428 g) of mixed strawberries and blueberries. The urine samples were profiled by an untargeted LC-MS metabolomics approach in the positive and negative modes. Results Statistical analysis of the data revealed that 39 features in the negative mode and 15 in the positive mode significantly increased between fasting and 4 h following mixed berry intake. Following the analysis of the dose–response data, 21 biomarkers showed overall significance across the portions of berry intake. Identification of the biomarkers was performed using fragmentation matches in the METLIN, HMDB, and MoNA databases and in published papers, confirmed where possible with authentic standards. Conclusions The ability of the panel of biomarkers to assess intake was examined, and the predictability was good, laying the foundations for the development of biomarker panels. [ABSTRACT FROM AUTHOR]

ObjectiveDespite great advances in obesity therapeutics in recent years, there is still a need to identify additional therapeutic targets for the treatment of this disease. We previously discovered a signature of genes, including Chloride intracellular channel 1 (Clic1), whose expression was associated with drug-induced weight gain, and in these studies, we assess the effect of Clic1 inhibition on food intake and body weight in mice.MethodsWe studied the impact of Clic1 inhibition in mouse models of binge-eating, diet-induced obese mice and genetic models of obesity (Magel2 KO mice).ResultsClic1 knockout (KO) mice ate significantly less and had a lower body weight than WT littermates when either fed chow or high fat diet. Furthermore, pharmacological inhibition of Clic1 in diet-induced obese mice resulted in suppression of food intake and promoted highly efficacious weight loss. Clic1 inhibition also reduced food intake in binge-eating models and hyperphagic Magel2 KO mice. We observed that chronic obesity resulted in a significant change in subcellular localization of Clic1 with an increased ratio of Clic1 in the membrane in the obese state. These observations provide a novel therapeutic strategy to block Clic1 translocation as a potential mechanism to reduce food intake and lower body weight.ConclusionsThese studies attribute a novel role of Clic1 as a driver of food intake and overconsumption. In summary, we have identified hypothalamic expression of Clic1 plays a key role in food intake, providing a novel therapeutic target to treat overconsumption that is the root cause of modern obesity.

Summary: Background & Aims: Perioperative nutritional status is critical during the postoperative recovery process in patients undergoing cardiac surgery. Several studies on patients undergoing cardiac surgery have reported low energy intake in early postoperative food intake via oral nutrition; however, no study has shown an association of low energy intake with postoperative hospital length of stay (LOS). This study aimed to determine whether early postoperative low food intake was associated with prolonged postoperative hospital LOS in patients undergoing cardiac surgery. Methods: This was a retrospective, observational, singlecenter study conducted in patients aged ≥18 years undergoing elective cardiac surgery from January 1, 2020, to May 31, 2023. Patients were categorized by food intake as food intake < 50% (low food intake group) and ≥ 50% (adequate food intake group) at lunch on postoperative day (POD) 3. The primary outcome of this study was the postoperative hospital LOS. A generalized linear model was used to examine the association between food intake and postoperative hospital LOS using the following explanatory variables: age, European System for Cardiac Operative Risk Evaluation (EuroSCORE) II value, preoperative risk of malnutrition, activities of daily living status, Sequential Organ Failure Assessment score, and C-reactive protein level. Results: Of the 315 patients, 104 (33.0%) had a food intake of

Purpose: Previous research has established that food intake is a biological regulator of the human sleep–wake cycle. As such, the timing of eating relative to sleep may influence the quality of sleep, including daytime naps. Here, we examine whether the timing of lunch (1 h vs. 2 h interval between lunch and a napping opportunity) impacts the quality of an afternoon nap. Methods: Using a randomized within-subject design over two separate experimental sessions (7 days apart), participants (n = 40, mean age = 25.8 years) consumed lunch 1 h and 2 h prior to an afternoon nap opportunity. Polysomnography and subjective self-reports were used to assess sleep architecture, sleepiness levels, and nap quality. Results: Results revealed no significant differences in subjective ratings of sleep quality and sleepiness, or in sleep architecture (total sleep time, sleep efficiency, sleep onset latency, sleep stages) between the 1 h and 2-h lunch conditions. Conclusions: All sleep measures were similar when napping followed eating by either 1 h or 2 h, suggesting that eating closer to nap onset may not negatively impact sleep architecture and quality. Future research should continue to identify conditions that improve nap quality, given the well-documented benefits of naps to reduce sleep pressure and improve human performance.

Abstract Background A food environment intervention using nudge tactics was implemented at a hospital convenience store (CVS) in Tokyo to improve employees’ eating habits. The objective of this study was to evaluate its effects on the urinary sodium-to-potassium ratio (Na/K), food intake, eating attitude, and behavior. Methods Using a pre–post design; the intervention incorporated nudge tactics, healthier options, easy-to-pick food placement, and eye-catching information. We also used price incentives. The primary outcomes included changes in Na/K and sodium and potassium excretion assessed using spot urine samples at health checkups. Secondary outcomes were changes in staff food intake, eating attitude, and behavior which were assessed using questionnaire surveys. All outcomes were evaluated statistically. Furthermore, we investigated how the intervention led to outcomes using path analysis. Results A total of 140 participant (52men and 88women) were analyzed. Significant changes were observed in Na/K (3.16 to 2.98 in median, p = 0.02) and potassium excretion (43.4 to 45.2 mmol/day in mean, p = 0.03). However, sodium excretion did not change significantly. The intake of fruits and dairy products increased with improved self-efficacy. The most influential factor for lowering Na/K and increasing potassium excretion was information from the CVS; purchasing “balanced meals” to lower Na/K and salads to increase potassium excretion were second. Conclusions Food environment intervention using nudge tactics can improve staff’s food intake and lower Na/K. Trial registration Registration number: UMIN000049444 (UMIN-CTR). Date of registration: November. 7. 2022.

Abstract Background Eating is fundamental not only to survival and health, but also to how humans organise their social lives. Eating together with others is often seen as the healthy ideal, while eating alone is highlighted as a risk factor for negative health outcomes, especially among older adults. This paper, therefore, investigates the relationship between the frequency and subjective experience of eating alone and food-related outcomes among 70- to 75-year-olds in Sweden. Methods A survey was distributed to a nationally representative random sample of 1500 community-living in Sweden, aged 70–75 years. Two different constructs of eating alone (objective and subjective) were measured, along with the following food-related outcomes: a food index, intake of food groups, consumption of ready-made meals, number of main meals per day, and body mass index (BMI). Results In total, 695 respondents were included in the final sample. A quarter of the respondents were categorised as eating alone, of which a small proportion reported that doing so bothered them. There were no associations between eating alone and food index scores, BMI, or intake frequencies of fruits and berries, or fish and shellfish. However, people eating alone were less likely to report eating three meals per day (OR: 0.53, CI: 0.37–0.76, p = 0.006), less likely to report higher intake frequencies of vegetables and snacks, sugary foods, and sweet drinks (adjusted OR: 0.68, CI: 0.48–0.95, p = 0.023 resp. OR: 0.59, CI: 0.43–0.81, p = 0.001), and more likely to report higher intake frequencies of ready-made meals (adjusted OR: 3.71, CI: 2.02–6.84, p

Introduction: Palatable foods have potent reinforcing effects that are mediated, partly, by an abrupt augmentation of dopaminergic neurotransmitters in the brain’s reward pathways. Food addiction to highly palatable foods contributes to the increasing prevalence of obesity. Aim: To evaluate the effect of food addiction on neurobehavioural parameters and the Behavioral Satiety Sequence (BSS) during restriction to a highly palatable diet in a food addiction rat model. Materials and Methods: The experimental study was conducted in the Pharmacology Department at PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India from April 2018 to January 2019. The study included six animals out of 28 female Sprague Dawley rats aged approximately 10 weeks and weighing 180-220 g were allocated to the control group and were fed a Standard Chow diet (SC) throughout the study. Twenty-two animals (induction group) were exposed to free choice between SC and a highly palatable Cafeteria Diet (CD), a mix of equal amounts of Bounty®, Snickers®, Mars®, and Milka® chocolate made into homogenous food pellets. After six weeks, 12 animals were randomly selected to have restricted access to the CD diet with free access to SC, while the rest continued to receive a free choice between the two diets for two weeks. Central Nervous System (CNS) parameters, BSS, 24-hour food intake, and body weight were recorded. Results: A significant decrease of 25.4 seconds (18.27%) in the mean time the CD restricted group stayed on the rotarod (113.6±8.31) seconds. and a reduced locomotor activity score of 46.92 (20.94%) in the CD access group in the actophotometer (177.08±5.29) compared to SC was noted. In the open field test, the CD restricted group demonstrated a 47.33% increase in grooming (12.0±1.11) and a 30% lower number of central squares crossed (2.80±0.57). In the Elevated Plus Maze (EPM), the time spent in the open arm (15.00±8.10) was statistically lower (p=0.045). No statistically significant difference between groups was recorded in the forced swim or tail suspension tests. Disruption of the BSS in varying dimensions was apparent in both CD groups. Conclusion: The study has shown that anxiety and altered feeding behaviour were evident in the CD restricted rats in the food addiction model.

Abstract Background COVID-19 is a pandemic caused by nCoV-2019, a new beta-coronavirus from Wuhan, China, that mainly affects the respiratory system and can be modulated by nutrition. Methods This review aims to summarize the current literature on the association between dietary intake and serum levels of micronutrients, malnutrition, and dietary patterns and respiratory infections, including flu, pneumonia, and acute respiratory syndrome, with a focus on COVID-19. We searched for relevant articles in various databases and selected those that met our inclusion criteria. Results Some studies suggest that dietary patterns, malnutrition, and certain nutrients such as vitamins D, E, A, iron, zinc, selenium, magnesium, omega-3 fatty acids, and fiber may have a significant role in preventing respiratory diseases, alleviating symptoms, and lowering mortality rates. However, the evidence is not consistent and conclusive, and more research is needed to clarify the mechanisms and the optimal doses of these dietary components. The impact of omega-3 and fiber on respiratory diseases has been mainly studied in children and adults, respectively, and few studies have examined the effect of dietary components on COVID-19 prevention, with a greater focus on vitamin D. Conclusion This review highlights the potential of nutrition as a modifiable factor in the prevention and management of respiratory infections and suggests some directions for future research. However, it also acknowledges the limitations of the existing literature, such as the heterogeneity of the study designs, populations, interventions, and outcomes, and the difficulty of isolating the effects of single nutrients from the complex interactions of the whole diet.

Complex homeostatic control mechanisms are tools to adjust the food birds eat and their appetite. Birds and mammals differ in several ways considering food intake regulation. Therefore, this study aimed to investigate the special effects of the intracerebroventricular (ICV) injection of spexin and its interaction with nitric oxide, serotonin and corticotropin receptors on central food intake regulation in broilers. In the test 1, Broilers received ICV injection of saline, PCPA (p-chlorophenylalanine,1.25 µg), spexin (10 nmol) and PCPA+spexin. In test 2–7, 8-OH-DPAT, SB-242084 (5-HT2C, 1.5 µg), L-arginine (Precursor of nitric oxide, 200 nmol), L-NAME (nitric oxide synthetize inhibitor, 100 nmol), Astressin-B (30 µg) and Astressin2-B (30 µg) were injected to Broilers instead of the PCPA. Then, the amount of food received was measured up to 2 h after the injection. The food consumption was significantly decreased by Spexin (10 nmol) (P

Background Traditional dietary assessments are often inaccurate and prone to self-reporting biases. Tracking the physiological responses associated with eating and digestion events via wearable technologies may provide an effective approach for continuously monitoring food intake and estimating energy consumption. Eating and digestion are accompanied by a series of changes in the heart rate, skin temperature, blood oxygen saturation, and blood pressure. These changes can be tracked by wearable devices, such as smartwatches, which have been widely accepted in the market. This systematic review is the first to evaluate the effectiveness of tracking such physiological biomarkers in differentiating between high- and low-calorie meals, potentially paving the way for more accurate dietary monitoring. Methods Following the PRISMA-P guidelines, we will conduct a systematic literature search through MEDLINE, EMBASE, and PubMed for clinical trials that investigated physiological responses following meal intake in healthy subjects. Two independent reviewers will screen and select articles based on pre-defined eligibility criteria, with a third review to resolve any discrepancies. This will be followed by data extraction and quality assessment of the included studies. Statistical analyses, including meta-analyses, will be performed using R Studio software. Our primary outcome will be the comparison of physiological biomarkers before and after meal intake, while secondary outcomes will include comparisons of physiological biomarkers between high- and low-calorie meal consumption and the correlation between the caloric content of consumed meals and postprandial physiological changes. Discussion This systematic review and meta-analysis will identify physiological indicators for eating events and inform the design of wearable sensors that estimate food intake in healthy subjects. Systematic Review Registration PROSPERO Registration ID: CRD42024544353

Foods consumed at lower eating rates (ER) lead to reductions in energy intake. Previous research has shown that texture-based differences in eating rateER can reduce meal size. The effect size and consistency of these effects across a wide range of composite and complex meals differing considerably in texture and varying in meal occasion have not been reported. We determined how consistently texture-based differences in ER can influence food and energy intake across a wide variety of meals. In a crossover design, healthy participants consumed twelve breakfast and twelve lunch meals that differed in texture to produce a fast or slow ER. A breakfast group (n = 15) and lunch group (n = 15) completed twelve ad libitum meal sessions each (six 'fast' and six 'slow' meals), where intake was measured and behavioural video annotation was used to characterise eating behaviour. Liking did not differ significantly between fast and slow breakfasts (P = 0·44) or lunches (P = 0·76). The slow meals were consumed on average 39 % ± 9 % (breakfast) and 45 % ± 7 % (lunch) slower than the fast meals (both P < 0·001). Participants consumed on average 22 % ± 5 % less food (84 g) and 13 % ± 6 % less energy (71 kcal) from slow compared with fast meals (mean ± SE; P < 0·001). Consuming meals with a slower ER led to a reduction in food intake, where an average decrease of 20 % in ER produced an 11 % ± 1 % decrease in food intake (mean ± SE). These findings add to the growing body of evidence showing that ER can be manipulated using food texture and that this has aits consistent effect on food and energy intake across a wide variety of Hedonically equivalent meals. [ABSTRACT FROM AUTHOR]

SH2B1 mutations are associated with obesity, type 2 diabetes, and metabolic dysfunction‐associated steatotic liver disease (MASLD) in humans. Global deletion of Sh2b1 results in severe obesity, type 2 diabetes, and MASLD in mice. Neuron‐specific restoration of SH2B1 rescues the obesity phenotype of Sh2b1‐null mice, indicating that the brain is a main SH2B1 target. However, SH2B1 neurocircuits remain elusive. SH2B1‐expressing neurons in the paraventricular hypothalamus (PVHSH2B1) and a PVHSH2B1→dorsal raphe nucleus (DRN) neurocircuit are identified here. PVHSH2B1 axons monosynaptically innervate DRN neurons. Optogenetic stimulation of PVHSH2B1 axonal fibers in the DRN suppresses food intake. Chronic inhibition of PVHSH2B1 neurons causes obesity. In male and female mice, either embryonic‐onset or adult‐onset deletion of Sh2b1 in PVH neurons causes energy imbalance, obesity, insulin resistance, glucose intolerance, and MASLD. Ablation of Sh2b1 in the DRN‐projecting PVHSH2B1 subpopulation also causes energy imbalance, obesity, and metabolic disorders. Conversely, SH2B1 overexpression in either total or DRN‐projecting PVHSH2B1 neurons protects against diet‐induced obesity. SH2B1 binds to TrkB and enhances brain‐derived neurotrophic factor (BDNF) signaling. Ablation of Sh2b1 in PVHSH2B1 neurons induces BDNF resistance in the PVH, contributing to obesity. In conclusion, these results unveil a previously unrecognized PVHSH2B1→DRN neurocircuit through which SH2B1 defends against obesity by enhancing BDNF/TrkB signaling. [ABSTRACT FROM AUTHOR]

Background: Eating is fundamental not only to survival and health, but also to how humans organise their social lives. Eating together with others is often seen as the healthy ideal, while eating alone is highlighted as a risk factor for negative health outcomes, especially among older adults. This paper, therefore, investigates the relationship between the frequency and subjective experience of eating alone and food-related outcomes among 70- to 75-year-olds in Sweden. Methods: A survey was distributed to a nationally representative random sample of 1500 community-living in Sweden, aged 70–75 years. Two different constructs of eating alone (objective and subjective) were measured, along with the following food-related outcomes: a food index, intake of food groups, consumption of ready-made meals, number of main meals per day, and body mass index (BMI). Results: In total, 695 respondents were included in the final sample. A quarter of the respondents were categorised as eating alone, of which a small proportion reported that doing so bothered them. There were no associations between eating alone and food index scores, BMI, or intake frequencies of fruits and berries, or fish and shellfish. However, people eating alone were less likely to report eating three meals per day (OR: 0.53, CI: 0.37–0.76, p = 0.006), less likely to report higher intake frequencies of vegetables and snacks, sugary foods, and sweet drinks (adjusted OR: 0.68, CI: 0.48–0.95, p = 0.023 resp. OR: 0.59, CI: 0.43–0.81, p = 0.001), and more likely to report higher intake frequencies of ready-made meals (adjusted OR: 3.71, CI: 2.02–6.84, p < 0.001) compared to those eating together with others. The subjective experience of eating alone did not have an impact on food-related outcomes. Conclusion: Eating alone or with others played a role in participants' food intake, and seemed to influence aspects of the organisation of everyday eating routines rather than overall dietary healthiness or weight status. Our findings add to the previous body of research on commensality, eating alone, and health among the older population, providing insights into the development of future health policies and research. [ABSTRACT FROM AUTHOR]

Previous studies indicate that CNS administration of oxytocin (OT) reduces body weight in high fat diet-induced obese (DIO) rodents by reducing food intake and increasing energy expenditure (EE). We recently demonstrated that hindbrain (fourth ventricular [4V]) administration of OT elicits weight loss and elevates interscapular brown adipose tissue temperature (TIBAT, a surrogate measure of increased EE) in DIO mice. What remains unclear is whether OT-elicited weight loss requires increased sympathetic nervous system (SNS) outflow to IBAT. We hypothesized that OT-induced stimulation of SNS outflow to IBAT contributes to its ability to activate BAT and elicit weight loss in DIO mice. To test this hypothesis, we determined the effect of disrupting SNS activation of IBAT on the ability of 4V OT administration to increase TIBAT and elicit weight loss in DIO mice. We first determined whether bilateral surgical SNS denervation to IBAT was successful as noted by ≥ 60% reduction in IBAT norepinephrine (NE) content in DIO mice. NE content was selectively reduced in IBAT at 1-, 6- and 7-weeks post-denervation by 95.9 ± 2.0, 77.4 ± 12.7 and 93.6 ± 4.6% (P<0.05), respectively and was unchanged in inguinal white adipose tissue, pancreas or liver. We subsequently measured the effects of acute 4V OT (1, 5 µg ≈ 0.99, 4.96 nmol) on TIBAT in DIO mice following sham or bilateral surgical SNS denervation to IBAT. We found that the high dose of 4V OT (5 µg ≈ 4.96 nmol) elevated TIBAT similarly in sham mice as in denervated mice. We subsequently measured the effects of chronic 4V OT (16 nmol/day over 29 days) or vehicle infusions on body weight, adiposity and food intake in DIO mice following sham or bilateral surgical denervation of IBAT. Chronic 4V OT reduced body weight by 5.7 ± 2.23% and 6.6 ± 1.4% in sham and denervated mice (P<0.05), respectively, and this effect was similar between groups (P=NS). OT produced corresponding reductions in whole body fat mass (P<0.05). Together, these findings support the hypothesis that sympathetic innervation of IBAT is not necessary for OT-elicited increases in BAT thermogenesis and reductions of body weight and adiposity in male DIO mice. [ABSTRACT FROM AUTHOR]

It is well established that high-protein diets (i.e. ~25-30% of energy intake from protein) provide benefits for achieving weight loss, and subsequent weight maintenance, in individuals with obesity, and improve glycemic control in type 2 diabetes (T2D). These effects may be attributable to the superior satiating property of protein, at least in part, through stimulation of both gastrointestinal (GI) mechanisms by protein, involving GI hormone release and slowing of gastric emptying, as well as post-absorptive mechanisms facilitated by circulating amino acids. In contrast, there is evidence that the beneficial effects of greater protein intake on body weight and glycemia may only be sustained for 6-12 months. While both suboptimal dietary compliance and metabolic adaptation, as well as substantial limitations in the design of longer-term studies are all likely to contribute to this contradiction, the source of dietary protein (i.e. animal vs. plant) has received inappropriately little attention. This issue has been highlighted by outcomes of recent epidemiological studies indicating that long-term consumption of animal-based protein may have adverse effects in relation to the development of obesity and T2D, while plant-based protein showed either protective or neutral effects. This review examines information relating to the effects of dietary protein on appetite, energy intake and postprandial glycemia, and the relevant GI functions, as reported in acute, intermediate- and long-term studies in humans. We also evaluate knowledge relating to the relevance of the dietary protein source, specifically animal or plant, to the prevention, and management, of obesity and T2D. [ABSTRACT FROM AUTHOR]

Background: A food environment intervention using nudge tactics was implemented at a hospital convenience store (CVS) in Tokyo to improve employees' eating habits. The objective of this study was to evaluate its effects on the urinary sodium-to-potassium ratio (Na/K), food intake, eating attitude, and behavior. Methods: Using a pre–post design; the intervention incorporated nudge tactics, healthier options, easy-to-pick food placement, and eye-catching information. We also used price incentives. The primary outcomes included changes in Na/K and sodium and potassium excretion assessed using spot urine samples at health checkups. Secondary outcomes were changes in staff food intake, eating attitude, and behavior which were assessed using questionnaire surveys. All outcomes were evaluated statistically. Furthermore, we investigated how the intervention led to outcomes using path analysis. Results: A total of 140 participant (52men and 88women) were analyzed. Significant changes were observed in Na/K (3.16 to 2.98 in median, p = 0.02) and potassium excretion (43.4 to 45.2 mmol/day in mean, p = 0.03). However, sodium excretion did not change significantly. The intake of fruits and dairy products increased with improved self-efficacy. The most influential factor for lowering Na/K and increasing potassium excretion was information from the CVS; purchasing "balanced meals" to lower Na/K and salads to increase potassium excretion were second. Conclusions: Food environment intervention using nudge tactics can improve staff's food intake and lower Na/K. Trial registration: Registration number: UMIN000049444 (UMIN-CTR). Date of registration: November. 7. 2022. [ABSTRACT FROM AUTHOR]

Feeding behavior is a complex physiological process regulated by the interplay between homeostatic and hedonic feeding circuits. Among the neural structures involved, the nucleus accumbens (NAc) has emerged as a pivotal region at the interface of these two circuits. The NAc comprises distinct subregions and in this review, we focus mainly on the NAc shell (NAcSh). Homeostatic feeding circuits, primarily found in the hypothalamus, ensure the organism's balance in energy and nutrient requirements. These circuits monitor peripheral signals, such as insulin, leptin, and ghrelin, and modulate satiety and hunger states. The NAcSh receives input from these homeostatic circuits, integrating information regarding the organism's metabolic needs. Conversely, so-called hedonic feeding circuits involve all other non-hunger and -satiety processes, i.e., the sensory information, associative learning, reward, motivation and pleasure associated with food consumption. The NAcSh is interconnected with hedonics-related structures like the ventral tegmental area and prefrontal cortex and plays a key role in encoding hedonic information related to palatable food seeking or consumption. In sum, the NAcSh acts as a crucial hub in feeding behavior, integrating signals from both homeostatic and hedonic circuits, to facilitate behavioral output via its downstream projections. Moreover, the NAcSh's involvement extends beyond simple integration, as it directly impacts actions related to food consumption. In this review, we first focus on delineating the inputs targeting the NAcSh; we then present NAcSh output projections to downstream structures. Finally we discuss how the NAcSh regulates feeding behavior and can be seen as a neural hub integrating homeostatic and hedonic feeding signals, via a functionally diverse set of projection neuron subpopulations. [ABSTRACT FROM AUTHOR]

Irisin was identified as a peptide hormone in 2012. The most important known physiological effect of irisin is that it activates uncoupling protein 1 and converts white adipose tissue to brown adipose tissue. Due to this effect of irisin on adipose tissue, it was thought that it may be closely related to obesity, feeding behavior and energy expenditure, and interest in research in this direction has increased. Later studies revealed that irisin, beyond its known effects, also influences the reproductive, nervous, cardiovascular, and excretory systems. Recent studies have determined that irisin has anti-oxidant, anti-inflammatory and anti-apoptotic properties, and it has been reported that pathologies such as obesity, endocrine and metabolic diseases, Alzheimer's disease, chronic kidney disease, cardiovascular diseases, atherosclerosis and cancer may be associated with changes irisin levels. The fact that irisin is expressed in different tissues other than muscle and fat tissue and exhibits autocrine and endocrine functions, as well as being expressed in different regions of the brain and participating in neuroendocrine processes in these regions, brings to mind that irisin may be a new neuroendocrine factor. In this review, we present information that will constitute evidence that irisin is a real neuroendocrine factor. [ABSTRACT FROM AUTHOR]