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• 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]

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]

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]

Die orofazialen Funktionen stellen sich im Zuge eines langen Entwicklungs- und Reifeprozesses ein. Diese sind das Saugen, Schlucken, Kauen, die Ventilation und die Phonation. Der Artikel befasst sich mit dem physiologischen Vorgang des Schluckens. The orofacial functions emerge in the course of a long development and maturation process. These are sucking, swallowing, chewing, ventilation and phonation. This article deals with the physiological process of swallowing. [ABSTRACT FROM AUTHOR]

Poor diet can cause sleep disorders; however, this association has not been established in older populations. This study investigated the association between dietary patterns and insomnia symptoms in independent older adults. This cross-sectional study targeted independent older Japanese adults aged ≥74 years. We used insomnia symptoms classified into three domains: difficulty initiating sleep (DIS), difficulty maintaining sleep (DMS), and insomnia. These symptoms were assessed as dependent variables by a self-reported questionnaire. Dietary patterns (DP), identified by principal component analysis of a self-administered diet history questionnaire, were used as independent variables. Poisson regression analysis was used to estimate the prevalence ratios and 95% confidence intervals with adjustment for potential confounders. Among 1,311 participants (mean age = 80.1; women, 48.5%), we identified three dietary patterns: DP1 was characterized by a high intake of vegetables, soy products, and fruits and a low intake of rice; DP2 was characterized by a high intake of fish, chicken, processed meat, and noodles and a low intake of soy products; and DP3 was characterized by a lower intake of fruits and confectionaries. Higher DP1 scores were significantly associated with a lower prevalence of DIS (p-for-trend = 0.012). A higher DP2 score was significantly associated with a higher prevalence of insomnia (p-for-trend = 0.032). There was no significant association between DP3 and insomnia symptoms (p-for-trend >0.05). Our results highlighted that a dietary pattern with a high intake of vegetables, soy products, and fruits may contribute to reducing insomnia symptoms among independent older adults. • We assessed the association between dietary patterns and insomnia in older adults. • Three dietary patterns were identified by principal component analysis. • High vegetables/fruits/soy intake was associated with low insomnia prevalence. [ABSTRACT FROM AUTHOR]

Short Bowel Syndrome (SBS) is the major cause of chronic intestinal failure (IF) and requires parenteral nutrition (PN). After bowel resection, some patients develop spontaneous intestinal adaptations and hyperphagia. Since promoting oral energy intake contributes to PN weaning, this study aims to characterize hyperphagia in patients with SBS and identify its determinants. This observational retrospective study included adult patients with SBS who were followed at an expert PN center between 2006 and 2019, with at least 2 separate nutritional assessments. Exclusion criteria were: active neoplasia, alternative treatment for IF or appetite-affecting medication. Resting energy expenditure (REE) was calculated for each patient using the Harris–Benedict equation. Food Intake Ratio (FIR) was calculated by dividing the highest caloric oral intake by REE and hyperphagia was defined as FIR >1.5. Among the 59 patients with SBS included in this study, 82.6% had a FIR >1.5, including 15.5% with a FIR >3. Protein supplied approximately 16% of total energy intake while fat and carbohydrates provided 36% and 48%, respectively. The FIR was independent of gender and whether patients received oral nutrition alone (n = 28) or combined with PN (n = 31). The FIR was also not associated with residual small bowel length, nor the proportion of preserved colon. However, it was negatively correlated with the body mass index (BMI) of these patients (r = −0.533, p < 0.001), whether they had PN support or not. Patients with either a jejuno-colonic (n = 31) or a jejuno-ileal anastomosis (n = 9), had a significantly higher FIR compared to those with an end-jejunostomy (n = 18) (p < 0.05). However, no difference was found in the proportion of calories provided by protein, fat and carbohydrate between the 3 patients groups divided according to the SBS anatomical type. A large majority of patients with SBS exhibited a hyperphagia regardless of PN dependence or bowel length, which was inversely correlated with BMI. The presence of the colon in continuity, thus in contact with the nutritional flow, seems to favor a higher oral intake which is beneficial for the nutritional autonomy of patients. This raises the question of a role of colonic microbiota and hormones in this behavior. Finally, this study also revealed an unexpected discrepancy between recommended energy intakes from protein, fat and carbohydrate and the actual intake of patients with SBS. [ABSTRACT FROM AUTHOR]

Patients with SARS-CoV generally require noninvasive treatments including continuous positive airway pressure (CPAP), and appropriate nutritional therapy. Our hypothesis was that a higher body mass index (BMI) would result in greater respiratory difficulties during CPAP treatment and lead to a reduction in energy and protein intake. The study was conducted prospectively and retrospectively in a Brazilian public hospital. The sample comprised all patients (n = 70) hospitalized in COVID-19 wards and using the Elmo System (ELMO) helmet. To ensure proper nutritional support, the hospital established a standard ELMO diet and questionnaire for estimating dietary adherence. The median length of stay was 11 days (interquartile range, 9-20), and 84.3% of the patients received hospital discharge. The median duration of helmet use was 1.5 days (interquartile range, 1-4). From mid-upper arm circumference adequacy measurements, 35 patients (50%) were classified as being overweight or living with obesity and 36 adult patients (66.7%) were considered living with obesity based on their BMI. The prevalence of overweight elderly patients was 81.3%. The median energy and protein intake adequacy percentages were 65% and 72.5%, respectively. Patients with higher BMIs exhibited lower oxygen flows while wearing the ELMO helmet. Younger age and lower energy and protein intake characterized the obesity group. A correlation between oxygen therapy and food intake in COVID-19 patients undergoing CPAP treatment was observed. Patients with higher BMIs and/or mid-upper arm circumference adequacies were more susceptible to energy and protein intake declines, and patients with obesity presented the lowest intake values. This study analyzed how continuous positive airway pressure (CPAP) treatment affected COVID-19 patients' nutritional status and energy-protein intake. A standard Elmo System (ELMO) diet and monitoring protocol were used to ensure adequate nutritional support. Patients with higher body mass indexes (BMIs) used less oxygen and those living with obesity presented significantly decreased energy and protein intake. The median ELMO helmet time usage was 1.5 days. [Display omitted] [ABSTRACT FROM AUTHOR]

Ultraprocessed foods (UPF) consumption plays a critical role in the development of chronic diseases, but evidence of their effect on children's health is limited. We hypothesized that the consumption of UPF can influence blood pressure levels in 6-year-old children. This study is a secondary analysis of a randomized field trial in Brazil that is registered at clinicaltrial.gov (NCT00635453). Dietary intake was obtained using 2 multiple-pass 24-hour recalls when 305 children were 3 and 6 years old. We classified foods according to the NOVA system and determined the percentage of total energy intake derived from ultraprocessed foods. We collected anthropometric measures from and evaluated systolic and diastolic blood pressures of 6-year-old children. Linear regression analysis was used to assess the association between UPF consumption and blood pressure levels. UPF represented 40.3% (interquartile range, 34.1-48.5) of the total energy intake at 3 years and 45.2% (interquartile range, 41.5-53.2) at 6 years. The adjusted linear regression analyses showed that systolic blood pressure was associated with UPF consumption at 6 years (P =.05), birth weight (P =.02), waist circumference (P <.01), and physical activity (P =.04), whereas diastolic blood pressure was associated with UPF consumption at 3 and 6 years (P =.01 and P <.01, respectively), birth weight (P =.05), and waist circumference (P <.01). Our data suggest that UPF consumption played a role in increasing 6-year-old children's blood pressure. These results reinforce the importance of effective strategies to prevent the excessive consumption of UPF in childhood. The results of the study showed that ultraprocessed food consumption, larger waist circumference, low birth weight, and not practicing physical activity were associated with higher blood pressure among 6-year-old Brazilian children. These findings are useful for understanding the critical role that early-life factors play in cardiovascular health. [Display omitted] [ABSTRACT FROM AUTHOR]

There are three main weaknesses in the available antiobesity treatments: (i) lack of specificity and therefore harmful side effects, (ii) unknown mechanism of action in many cases, and (iii) they mainly target either intestinal absorption or feeding/appetite and not energy expenditure. Small extracellular vesicle (sEV)-based therapeutics are already undergoing clinical trials, although as yet no sEV-based therapy has been approved by the FDA. Targeting of specific sets of hypothalamic neurons with engineered sEVs would provide: (i) increased specificity and therefore reduced side effects, (ii) knowledge of the mechanism of action, and (iii) an integral targeting of energy balance, modulating both feeding and energy expenditure. Current preclinical evidence has demonstrated that specific targeting of hypothalamic cell populations using sEVs ameliorates diet-induced and genetic obesity. There are currently several pharmacological therapies available for the treatment of obesity, targeting both the central nervous system (CNS) and peripheral tissues. In recent years, small extracellular vesicles (sEVs) have been shown to be involved in many pathophysiological conditions. Because of their special nanosized structure and contents, sEVs can activate receptors and trigger intracellular pathways in recipient cells. Notably, in addition to transferring molecules between cells, sEVs can also alter their phenotypic characteristics. The purpose of this review is to discuss how sEVs can be used as a CNS-targeted strategy for treating obesity. Furthermore, we will evaluate current findings, such as the sEV-mediated targeting of hypothalamic AMP-activated protein kinase (AMPK), and discuss how they can be translated into clinical application. [ABSTRACT FROM AUTHOR]

Metabolic programming may be induced by reduction or enhancement of litter size, which lead to neonatal over or undernutrition, respectively. Changes in neonatal nutrition can challenge some regulatory processes in adulthood, such as the hypophagic effect of cholecystokinin (CCK). In order to investigate the effects of nutritional programming on the anorexigenic function of CCK in adulthood, pups were raised in small (SL, 3 pups per dam), normal (NL, 10 pups per dam), or large litters (LL, 16 pups per dam), and on postnatal day 60, male rats were treated with vehicle or CCK (10 µg/Kg) for the evaluation of food intake and c-Fos expression in the area postrema (AP), nucleus of solitary tract (NTS), and paraventricular (PVN), arcuate (ARC), ventromedial (VMH), and dorsomedial (DMH) nuclei of the hypothalamus. Overnourished rats showed increased body weight gain that was inversely correlated with neuronal activation of PaPo, VMH, and DMH neurons, whereas undernourished rats had lower body weight gain, inversely correlated with increased neuronal activation of PaPo only. SL rats showed no anorexigenic response and lower neuron activation in the NTS and PVN induced by CCK. LL exhibited preserved hypophagia and neuron activation in the AP, NTS, and PVN in response to CCK. CCK showed no effect in c-Fos immunoreactivity in the ARC, VMH, and DMH in any litter. These results indicate that anorexigenic actions, associated with neuron activation in the NTS and PVN, induced by CCK were impaired by neonatal overnutrition. However, these responses were not disrupted by neonatal undernutrition. Thus, data suggest that an excess or poor supply of nutrients during lactation display divergent effects on programming CCK satiation signaling in male adult rats. • Body weight is inversely correlated to neuron activity in hypothalamic nuclei. • Opposite neonatal nutrition supply has divergent effects on CCK actions in adulthood. • CCK-induced anorexigenic effect is abolished in overnourished rats. • Neonatal undernourished rats have preserved CCK satiation signaling. • SL rats have lower CCK-induced NTS and PVN neuron activation. [ABSTRACT FROM AUTHOR]

To investigate the association between the parameters used in nutritional screening assessment (body mass index [BMI], unintentional weight loss [WL] and reduced food intake) and clinical outcomes in non-critically ill, hospitalized coronavirus disease 2019 (COVID-19) patients. This was a prospective multicenter real-life study carried out during the first pandemic wave in 11 Italian Hospitals. In total, 1391 patients were included. The primary end-point was a composite of in-hospital mortality or admission to ICU, whichever came first. The key secondary end-point was in-hospital mortality. Multivariable models were based on 1183 patients with complete data. Reduced self-reported food intake before hospitalization and/or expected by physicians in the next days since admission was found to have a negative prognostic impact for both the primary and secondary end-point (P <.001 for both). No association with BMI and WL was observed. Other predictors of outcomes were age and presence of multiple comorbidities. A significant interaction between obesity and multi-morbidity (≥2) was detected. Obesity was found to be a risk factor for composite end-point (HR = 1.36 [95%CI, 1.03–1.80]; P =.031) and a protective factor against in-hospital mortality (HR = 0.32 [95%CI, 0.20–0.51]; P <.001) in patients with and without multiple comorbidities, respectively. Secondary analysis (patients, N = 829), further adjusted for high C-reactive protein (>21 mg/dL) and LDH (>430 mU/mL) levels yielded consistent findings. Reduced self-reported food intake before hospitalization and/or expected by physicians in the next days since admission was associated with negative clinical outcomes in non-critically ill, hospitalized COVID-19 patients. This simple and easily obtainable parameter may be useful to identify patients at highest risk of poor prognosis, who may benefit from prompt nutritional support. The presence of comorbidities could be the key factor, which may determine the protective or harmful role of a high body mass index in COVID-19. [ABSTRACT FROM AUTHOR]

Aims: To conduct a systematic review of the literature on the scientific evidence of the oral intake of omega-3 and omega-6 FAs and metabolic syndrome (MS) in adolescents.Data Synthesis: The study was registered in PROSPERO (number 42020185370). Studies were carried out with adolescents aged 10-19 years, who presented as intervention/exposure the oral intake of omega-3 and/or omega-6 fatty acids (FAs), in the databases PubMed, Scopus, Web of Science, LILACS, CENTRAL, and PQDT Global e BDTD. The tools used to assess the risk of bias were RoB 2.0, Agency for Healthcare Research and Quality (AHRQ), and Newcastle-Ottawa Scale. Fifteen papers retrieved published from 2010 to 2019 were included (n = 3534); nine were randomized studies and controlled clinical trials, four were cross-sectional studies, one was a retrospective cohort study, and one case-control study. No studies have evaluated the effect or association of omega-3 and/or of omega-6 FAs with actual MS, only with its components. The randomized clinical trials identified the effects of omega-3 FA on the decrease in blood pressure (n = 1 out of six), glycemia (n = 2 out of seven), and triglycerides (n = 5 out of eight), and the increase in HDL-c (n = 2 out of eight) considering the comparison between the group that received omega-3 FA and the control group.Conclusions: Scientific evidence is controversial on the association between oral intake of omega-3 FAs and MS in adolescents, due to the heterogeneity between studies and the divergence of results for the same MS component. [ABSTRACT FROM AUTHOR]

• Self-reported hunger increased at fasted and fed states and decreased self-reported fullness at fasted state in both women with and without obesity. • Dietary intake did not change throughout after 6 weeks of resistance training in both groups. • Food frequency of groups of soup and past, vegetables and eggs, and leafy and vegetables decreased pre-to-post in both groups. • There was no correlation between appetite and energy intake with body composition in both groups investigated, neither alteration in desire to eat and motivation to eat palatable foods. The aim of this study was to investigate the effect of 6-weeks resistance training (RT) on appetite, energy intake and body composition in young women with and without obesity, and to examine the relationship between these variables. Thirty-five young women were divided according to the amount of body fat [with obesity (n = 16) and without obesity (n = 19)]. Appetite was assessed through self-reported hunger, fullness, desire to eat, satiety quotient, food frequency diary and motivations to eat palatable food (power of food scale) in both fasted and fed states (after a standardized breakfast). Energy intake and body composition were evaluated at pre- and post-6 weeks of RT. Results showed that self-reported hunger increased significantly in both fasted and fed states (p = 0.007 and p = 0.029, respectively), while self-reported fullness decreased at the fasted state (p = 0.030) in both groups. There were no significant effects for desire to eat fatty, sweet, savory and salty foods, motivation to eat palatable foods, or for total energy intake. Food frequency analysis indicated a decrease in consumption of soup and past (p = 0.045), vegetables and eggs (p = 0.034), and leafy vegetables (p = 0.022) in both groups. Fat-free mass increased significantly in both groups (p = 0.011 and p = 0.003), while fat mass did not show significant changes. There were no correlations between changes in appetite/energy intake and changes in body composition. In conclusion, following the 6-week RT program, both women with and without obesity exhibited increased self-reported hunger alongside decreased fullness, suggesting an increase in orexigenic drive. However, neither group showed an increase in energy intake and fat mass, while both groups experienced an increase in fat-free mass. Registered under Brazilian Registry of Clinical Trials n°. RBR-1024f4qs. [ABSTRACT FROM AUTHOR]

• Total intake of a ranch-flavored chip snack was 77 % greater when served with dip. • Fewer g and kcal of the chip-only snack were eaten, despite higher initial liking. • Including a dip led to a faster eating rate and larger bite size of the total snack. • Consuming chips without dip may help individuals curb their snack intake. During eating, exogenous sources of oral lubrication like dips facilitate oral processing, which has been shown to influence food intake. However, few studies have directly assessed how exogenous oral lubrication (via added dip) affects acute intake, especially while snacking. In two laboratory visits, adults (n = 46, 74 % female) were served 70 g of ranch-flavored chips (2.5 servings) with or without 95 g of energy-matched ranch dip, and ad libitum intake was measured. All sessions were video recorded and annotated for number of bites and active eating time (min), which were used to calculate measures of eating microstructure, including eating rate (g/min) and bite size (g/bite). The chips + dip condition yielded 77 % greater intake (64.3 ± 16.2 g versus 36.4 ± 16.2 g; 344.6 ± 86.8 kcal versus 195.1 ± 86.8 kcal; p < 0.001) and a faster total eating rate (p < 0.001) relative to the no-dip control, despite lower initial liking of the dip condition (p = 0.002). However, there was no difference in chip intake (p = 0.83) or chip eating rate (p = 0.11) by condition. Thus, in this chips and dip snack, the greater intake in the dip condition may have been facilitated by a larger total snack bite size (p < 0.001) resulting from dip inclusion, as opposed to faster chip eating rate as a function of the lubricating dip. [ABSTRACT FROM AUTHOR]

An imbalance between energy intake and energy expenditure predisposes obesity and its related metabolic diseases. Soluble dietary fiber has been shown to improve metabolic homeostasis mainly via microbiota reshaping. However, the application and metabolic effects of insoluble fiber are less understood. Herein, we employed nanotechnology to design citric acid-crosslinked carboxymethyl cellulose nanofibers (CL-CNF) with a robust capacity of expansion upon swelling. Supplementation with CL-CNF reduced food intake and delayed digestion rate in mice by occupying stomach. Besides, CL-CNF treatment mitigated diet-induced obesity and insulin resistance in mice with enhanced energy expenditure, as well as ameliorated inflammation in adipose tissue, intestine and liver and reduced hepatic steatosis, without any discernible signs of toxicity. Additionally, CL-CNF supplementation resulted in enrichment of probiotics such as Bifidobacterium and decreased in the relative abundances of deleterious microbiota expressing bile salt hydrolase, which led to increased levels of conjugated bile acids and inhibited intestinal FXR signaling to stimulate the release of GLP-1. Taken together, our findings demonstrate that CL-CNF administration protects mice from diet-induced obesity and metabolic dysfunction by reducing food intake, enhancing energy expenditure and remodeling gut microbiota, making it a potential therapeutic strategy against metabolic diseases. [ABSTRACT FROM AUTHOR]

Transcranial direct stimulation (tDCS) targeted to the dorsolateral prefrontal cortex (DLPFC) reduces food intake and hunger, but its effects on circulating factors are unclear. We assessed the effect of repeated administration of tDCS to the left DLPFC (L-DLPFC) on concentrations of pro/anti-inflammatory and appetitive hormone concentrations. Twenty-nine healthy adults with obesity (12 M; 42±11 y; BMI=39±8 kg/m2) received 3 consecutive inpatient sessions of either anodal or sham tDCS targeted to the L-DLPFC during a period of ad libitum food intake. Fasting plasma concentrations of IL-6, orexin, cortisol, TNF-α, IL-1β, ghrelin, PYY, and GLP-1 were measured before the initial and after the final tDCS sessions. IL-6 (β=-0.92 pg/ml p=0.03) decreased in the anodal group compared with sham, even after adjusting for kcal intake; there were no changes in other hormones. Mean kcal intake was associated with higher IL-1β and ghrelin concentrations after the ad libitum period (β=0.00018 pg/ml/kcal, p=0.03; β=0.00011 pg/ml/kcal, p=0.02; respectively), but not differ by intervention groups. IL-6 concentrations were reduced following anodal tDCS to the L-DLPFC independent of ad libitum intake. IL-6 concentrations reflect the inflammatory state of adiposity and may affect eating behavior and weight gain. These findings provide evidence of therapeutic benefit of tDCS. • Anodal tDCS to the L-DLPFC diminished IL-6, a chronic inflammatory marker in obesity. • Reduction of IL-6 following tDCS was independent of ad libitum food intake. • tDCS affects IL-6 levels by modulating brain and sympathetic nervous system activity. • Study pioneers tDCS as a potential obesity intervention by influencing cytokines. [ABSTRACT FROM AUTHOR]

The pond loach (Misgurnus anguillicaudatus) is an important aquaculture freshwater species, used as an ornamental fish, food source for humans and angling bait. Pond loaches are resistant to fasting and extreme environmental conditions, including temperature and low oxygen levels. Little is known about how these factors affect the feeding physiology and the endocrine regulation of feeding of loaches. In this study, we examined the effects of fasting, as well as increased temperature and decreased oxygen levels on food intake and transcript levels of appetite regulators. Fasted fish had lower blood glucose levels, and lower expression levels of intestine CCK and PYY, and brain CART1, but had higher levels of brain orexin and ghrelin than fed fish. Fish held at 30 °C had higher food intake, glucose levels, and mRNA levels of intestine CCK and PYY, and brain CART2, but lower brain orexin levels than fish at 20 °C. Fish held at low oxygen levels had a lower food intake, higher intestine CCKa and ghrelin, and brain orexin, CART2 and ghrelin mRNA expression levels than fish held at high O 2 levels. Our results suggest that fasting and high temperatures increase the expression of orexigenic and anorexigenic factors respectively, whereas the increase in expression of both orexigenic and anorexigenic factors in low O 2 environments might not be related to their role in feeding, but possibly to protection from tissue damage. The results of our study might shed new light on how pond loaches are able to cope with extreme environmental conditions such as low food availability, extreme temperatures and hypoxia. [Display omitted] • Pond loaches are tolerant of fasting, high temperatures and low oxygen levels. • Fasting increased expression of orexigenic factors and decreased anorexigenic factors. • High temperatures increased food intake and brain CART and intestine CCK and PYY. • Low oxygen decreased food intake and increased orexin, CART and CCK expressions. • This study might help understand how pond loaches cope with extreme environments. [ABSTRACT FROM AUTHOR]

• Substance use is associated with altered or elevated food consumption. • Breadth (variety) of drug use is associated with larger food portion size. • The association was fully mediated by impulsivity, in particular, sensation seeking. • Breadth of drug use may lead to more eating independent of substance use disorder. Substance use is associated with altered or elevated food consumption and disordered eating. In the present study we examined whether breadth (variety) of drug use was associated with elevated portion size in a general population sample as it was in persons in recovery from substance use disorder. Furthermore, measures of emotional eating, impulsivity, food misuse, food craving were taken as possible mediators and reward responsiveness was examined as a potential moderator of this association. 444 adults (48.6 % women, mean age of 47.8 years) completed an online study in which they were asked to make judgements of ideal portion size for 6 different foods using a validated online tool that allowed participants to adjust the portion size of images of foods. Ideal portion size has been identified as a strong predictor of actual consumption. Participants were also asked to report the number of substances used in the past and provide anthropometric information. The results confirmed that breadth of drug use was associated with selection of higher portion size. Reward responsiveness was not a moderator of this relationship. Of the tested mediators, only impulsivity mediated the association between breadth of drug use and portion size. The results show that impulsivity may underlie the association between eating and substance use. [ABSTRACT FROM AUTHOR]

The molecular control of feeding after fasting is essential for maintaining energy homeostasis, while overfeeding usually leads to obesity. Identifying non-coding microRNAs (miRNAs) that control food intake could reveal new oligonucleotide-based therapeutic targets for treating obesity and its associated diseases. This study aims to identify a miRNA modulating food intake and its mechanism in neuronal regulation of food intake and energy homeostasis. A comprehensive genome-wide miRNA screening in the arcuate nucleus of the hypothalamus (ARC) of fasted mice and ad libitum mice was performed. Through stereotactic virus injections, intracerebroventricular injections, and miRNA sponge technology, miR-7a-5p was inhibited specifically in AgRP neurons and the central nervous system, and metabolic phenotypes were monitored. Quantitative real-time PCR, Western blotting, immunofluorescence, whole-cell patch-clamp recording, and luciferase reporter assay were used to investigate the mechanisms underlying miR-7a-5p's regulation of food intake. We found a significant increase in miR-7a-5p levels after fasting. miR-7a-5p was highly expressed in the ARC, and inhibition of miR-7a-5p specifically in AgRP neurons reduced food intake and body weight gain. miR-7a-5p inhibited S6K1 gene expression by binding to its 3'-UTR. Furthermore, the knockdown of ribosomal S6 kinase 1 (S6K1) in AgRP neurons can partially reverse the effects caused by miR-7a-5p inhibition. Importantly, intracerebroventricular administration of the miR-7a-5p inhibitor could also reduce food intake and body weight gain. Our findings suggest that miR-7a-5p responds to energy deficit and regulates food intake by fine-tuning mTOR1/S6K1 signaling in the AgRP neurons, which could be a promising oligonucleotide-based therapeutic target for treating obesity and its associated diseases. • Fasting induces microRNAomic changes in the arcuate nucleus of the hypothalamus. • miR-7a-5p regulates orexigenic neuropeptide expression and food intake by targeting mTOR1/S6K1 signaling. • Intracerebroventricular administration of the miR-7a-5p inhibitor reduces food intake and body weight. [ABSTRACT FROM AUTHOR]

Reducing salt intake is considered one of the most cost-effective interventions to decrease morbidity and mortality resulting from noncommunicable diseases. This study aimed to describe changes in sodium intake in the Brazilian population using data from the National Dietary Surveys (NDS) conducted in 2008-2009 and 2017-2018. We hypothesized that over the 10-year period evaluated, sodium intake has remained high in Brazil. Nationwide representative samples of 34,003 and 46,164 individuals (aged ≥10 years) from NDS 2008-2009 and 2017-2018, respectively, were evaluated. Food consumption data were obtained from 2 nonconsecutive food records (NDS 2008-2009) and two 24-hour food recalls (NDS 2017-2018). Trends, percentiles of distribution, and proportions of the population exceeding the age-specific tolerable upper intake level for sodium were estimated. Dietary sodium intake was also estimated as a function of energy intake (mg/1000 kcal). Overall, mean crude daily sodium intake was slightly lower in 2017-2018 than in 2008-2009 (2489 mg/d vs. 2529 mg/d). The decrease in sodium intake (mg/day) was statistically significant (P <.05) only among female adolescents and subjects in the highest income level. Additionally, an overall statistically significant increase in dietary sodium density was observed independent of age, sex, and income level for energy-adjusted data (P <.05). Our findings indicate that sodium intake has not significantly changed over time in the Brazilian population; thus, policies aimed at reducing sodium intake in Brazil are necessary. Sodium intake has not changed over time in the Brazilian population. An overall significant increase in dietary sodium density was observed independent of age, sex, and income level. Beans and legumes, breads, rice and rice dishes, meat and meat dishes, and sandwiches were the leading contributors of dietary sodium intake. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: When children choose amounts of food to eat, it is unclear what influences the portions they select and whether their selections are related to the amounts they consume.Objectives: Using a computer survey, we investigated the effect of food liking on portion selection in middle childhood and examined how children's selections were related to measured intake at meals in which portions of all foods were varied across 4 test days.Methods: Fifty-one children aged 7-10 y completed a computer survey of 20 common foods with a range of energy density. For each food, the survey presented sliding scales with 5 images varying in portion size and children indicated their liking and the amount they would eat at a specified meal or snack. On 4 test days in a randomized crossover design, children were served a meal of 6 foods from the survey with portions of 100%, 133%, 167%, or 200% of baseline amounts. Data were analyzed using random coefficients models.Results: Across the 20 foods used in the survey, portion selection ratings were predicted by food liking ratings (P < 0.0001). After accounting for liking, portion selection ratings did not vary by food energy density (P = 0.50). At the meals, intake of all 6 foods increased when larger portions were served (P = 0.002). Furthermore, the selected portion of a food on the survey was positively related both to intake of that food at the 100%-portion meal (P = 0.014) and to increased intake as larger portions were served (P < 0.0001).Conclusions: Children aged 7-10 y were able to use a computer survey to choose food portions that predicted their measured intake in response to increased portions. The relation of liking to selection and intake indicates that to promote children's consumption of larger portions of low-energy-dense foods such as fruits and vegetables, these foods must be well liked by the children. This trial was registered at clinicaltrials.gov as NCT02759523. [ABSTRACT FROM AUTHOR]

Adiponectin (AdipoQ) as an adipocytokine has the potential to regulate feeding behavior, but the information about adipoq in fish is limited. In this study, Siberian sturgeon adiponectin (Ssadipoq) gene was cloned encoding 264 amino acids. The amino acid identity of SsAdipoQ was low compared with that of mammals, birds, amphibians and teleost fishes. The expression of Ssadipoq in the hypothalamus was significantly decreased at 1 h and 3 h post feeding, and increased after 15-day fasting. The mature domain of AdipoQ (fAd) was inserted into expression vector pET32a and successfully expressed in Escherichia coli BL21 (DE3) after stimulated by isopropyl-β-d-thiogalactoside. Food intake at 1 h and 3 h post treatment with SsfAd protein decreased significantly (P < 0.05). The mRNA expression of pyy and cck in the valvula intestine was promoted and hypothalamic npy , agrp and pomc mRNA expression were inhibited after treatment with SsfAd protein. Furthermore, hypothalamic ampk subunits expression was associated with peripheral SsfAd treatment. In summary, present study indicate that SsfAd plays an important role in the regulation of food intake and appetite signals in Siberian sturgeon, which provides a basis for further study application of prokaryotic AdipoQ in feeding behavior regulation. • In the hypothalamus, adiponectin expression responded quickly to short-term and long-term changes of feeding status. • Intraperitoneal administration of SsfAd inhibited food intake at 1 h and 3 h post injection in Siberian sturgeon. • Peripheral SsfAd administration affected appetite factors mRNA expression in the hypothalamus and valvula intestine. • Hypothalamic ampkα2 was significantly up-regulated when treated with peripheral SsfAd protein. [ABSTRACT FROM AUTHOR]

Hypothalamic AMP-activated protein kinase (AMPK) is a canonical regulator of energy balance and metabolism at the whole-body level. This makes this enzyme an attractive target for treating energy balance-related diseases. However, targeting AMPK within the hypothalamus presents a challenge related to the specific cellular biodistribution of the enzyme and the need to use clinically safe methods of administration. Current evidence has shown that targeting based on small extracellular vesicles (sEVs) might offer a realistic approach for regulating hypothalamic AMPK. This would allow modulation of both sides of the energy-balance equation, namely food intake and energy expenditure, and therefore of overall metabolism. Moreover, this strategy could provide treatment options not only for obesity but also for catabolic/wasting diseases such as hyperthyroidism, rheumatoid arthritis, and even cancer cachexia. Hypothalamic AMP-activated protein kinase (AMPK) is a canonical regulator of energy balance that regulates food intake (both homeostatic and hedonic), brown adipose tissue thermogenesis, and peripheral glucose and lipid metabolism. Genetic evidence, using conditional mouse models and virogenetic approaches, shows that nucleus- and/or neuron-specific targeting of hypothalamic AMPK can be a useful strategy for targeting both positive (e.g., obesity) and negative (e.g., hyperthyroidism and rheumatoid arthritis) energy balance-related diseases. Targeting hypothalamic AMPK faces three major challenges: (i) cell-specificity, (ii) the need to cross the blood–brain barrier, and (iii) delivery via a clinically safe mode of administration. Targeting hypothalamic AMPK in steroidogenic factor 1 (SF1) neurons with small extracellular vesicles (sEVs) is an effective strategy for treating obesity in preclinical rodent models. [ABSTRACT FROM AUTHOR]

Despite their reliability- and validity-related challenges, self-reports remain the most common data collection method in nutrition research, food-related consumer and marketing research. The rapid development of technology has nevertheless inspired attempts to overcome the challenges of self-reports by applying technological solutions capable of capturing objective data. We reviewed objective measurement technologies applicable in nutrition research, food-related consumer and marketing research, spanning the continuum from food-evoked emotions to food choice and dietary intake. Focusing on non-invasive solutions, we categorised identified technologies according to five study domains: 1) detecting food-related emotions, 2) monitoring food choices, 3) detecting eating actions, 4) identifying the type of food consumed, and 5) estimating the amount of food consumed. Additionally, we considered technologies not yet applied in the targeted research disciplines but worth considering in future research. Within each domain, several variables have been measured using diverse technologies or combinations of technologies. These technologies cover wearable and remotely applied solutions that collect data on the individual or provide indirect information on consumers' food choices or dietary intake. The key challenges of the reviewed technologies concern their applicability in real-world settings; capabilities to produce accurate, reliable, and meaningful data with reasonable resources; participant burden, and privacy protection. We provide recommendations for researchers and practitioners in nutrition research, food-related consumer and marketing research to work around the key challenges. For fruitful use of available technologies, we encourage collaboration between technology developers and experts in nutrition, consumer, and marketing sciences. • Nutrition, food-related consumer and marketing research rely on self-reports. • A review explored technologies for objective data collection. • The work spans study domains from food-evoked emotions to food choice and intake. • Narrative description covers capabilities and challenges of existing technologies. • Recommendations suggest ways to overcome key challenges. [ABSTRACT FROM AUTHOR]

Adiponectin (AdipoQ) is a hormone that regulates food intake and energy homeostasis in mammals. The globular adiponectin (gAd) has been reported involved in the regulation of appetite, but the regulatory role and mechanism in fish remains unelucidated. Using Siberian sturgeon as a model of Chondrostei, the recombinant gAd protein of Siberian sturgeon (SsgAd) was produced by Escherichia coli expression system and verified using western blotting. Intraperitoneal injection of recombinant SsgAd protein at 100 ng/g BW suppressed food intake 1 h after administration. Peripheral injection of SsgAd protein caused the upregulation of anorexigenic pyy expression in the valvula intestine, but did not affect cck expression in the valvula intestine and orexigenic ghrelin expression in the stomach. The SsgAd administration significantly increased the hypothalamic expressions of pomc and decreased npy , agrp , and cart expression. In addition, SsgAd recombinant protein promoted adipor1 , ampkα2 , akt , and mtor mRNA expressions within the hypothalamus, whereas inhibited ampkβ1 , ampkβ2 and ampkγ2 mRNA expression, suggesting AMPK and mTOR signaling pathways might be related to SsgAd protein-mediated anorexia activity. Furthermore, the injection of an mTOR antagonist (rapamycin) reversed the reduced food intake and npy , agrp , and cart expression due to the peripheral injection of SsgAd, as well as the increased pomc expression induced by SsgAd, which were not observed after AMPK antagonist (dorsomorphin) treatment. In summary, the current study, for the first time, suggest that the anorexigenic function of SsgAd might bind with AdipoR1 and activate the mTOR signal pathway to affect the expression of hypothalamic appetite factors in Siberian sturgeon. This study provides new insight into the molecular mechanism of AdipoQ in feeding regulation in fish, and a basis for further exploration on physiological function of AdipoQ. • This study for the fist time demonstrated that SsgAd effectively inhibited food intake of Siberian sturgeon. • Peripheral SsgAd affected appetite factors expression in the hypothalamus and valvula intestine of Siberian sturgeon. • AdipoR1 rather than AdipoR2 was implicated in activation of hypothalamic appetite signals by SsgAd. • The inhibitory effect on food intake induced by peripheral SsgAd was reversed by mTOR antagonist in Siberian sturgeon. [ABSTRACT FROM AUTHOR]

Cocaine- and amphetamine-regulated transcript (CART) peptide is a brain-gut neuropeptide that has been implicated in a range of physiological functions including appetite, which is disturbed during chemotherapy. The aims of the present study were to identify the distribution and expression of CART mRNA and CART peptide, and to examine the potential of CART (55–102) to attenuate cisplatin-induced emesis in Suncus murinus. CART mRNA and peptide were detected throughout the entire brain, including the forebrain, hypothalamus, and brainstem, and also in the gut wall and stomach. In conscious, freely moving animals, intracerebroventricular administration of CART (55–102) did not modulate food and water intake or alter locomotor activity when administered alone. Cisplatin induced emesis and upregulated the expression of CART mRNA in the brainstem. However, CART (55–102) reduced the number of cisplatin-induced retches. Both CART (55–102) and cisplatin increased the number of c-Fos positive cells in the nucleus tractus solitarius, lateral hypothalamus, paraventricular hypothalamus, and bed nucleus of the stria terminalis (BNST), compared to saline-treated animals, whereas cisplatin also induced c-Fos expression in the area postrema (AP), arcuate nucleus, and central nucleus of the amygdala. Pre-treatment with CART (55–102) significantly attenuated the increased c-Fos positive cells in the BNST and AP. These data indicate that CART mRNA and peptide were localized to regions involved in reward/enforcement, emotion, feeding and emesis. The anti-emetic effect of CART (55–102) against cisplatin-induced emesis may involve both the forebrain limbic system and the brainstem. [ABSTRACT FROM AUTHOR]

Though μ and δ opioid receptors are reported to regulate energy homeostasis, any role for κ opioid receptors in these processes remains unclear. The present study investigated the role of κ opioid receptors in regulation of feeding behavior and plasma glucose levels using nalfurafine, a κ opioid receptor agonist used clinically. Systemic injection of nalfurafine increased food intake under non-fasted conditions, but not after food deprivation, and this effect was inhibited by the κ opioid receptor antagonist norbinaltorphimine. In contrast, nalfurafine did not affect plasma glucose levels. I.c.v. injection of nalfurafine increased food intake, whereas systemic injection of nalfurafine methiodide, which does not penetrate the blood brain barrier, was without effect. In addition, nalfurafine tended to increase preproorexin mRNA in the hypothalamus. However, neither the orexin OX1 receptor antagonist YNT-1310 nor the non-selective orexin receptor antagonist suvorexant inhibited the increase in food intake induced by nalfurafine. While nalfurafine injected into the lateral hypothalamus did not affect food intake, nalfurafine injected into the nucleus accumbens increased food intake, which was inhibited by norbinaltorphimine. Finally, we examined the effect of nalfurafine on anorexia induced by the anti-cancer agent 5-fluorouracil. Reduced food intake at 2 days following 5-fluorouracil administration was alleviated across the first 3 h following daily injection of nalfurafine, though daily food intake was not influenced. These results indicate that nalfurafine promotes feeding behavior through stimulation of κ opioid receptors in the nucleus accumbens and may be a candidate for reducing anorexia due to anti-cancer agents. • The role of κ opioid receptors (KOR) in regulating feeding behavior was examined. • The KOR agonist nalfurafine increased food intake but not plasma glucose. • Stimulation of KOR in the nucleus accumbens (NAcc) increased food intake. • Repeated injection of nalfurafine acutely reversed 5-fluorouracil-induced anorexia. • Stimulation of KOR in NAcc promotes feeding and may alleviate such anorexia. [ABSTRACT FROM AUTHOR]

• Protein beverages varying in lubricity and coating properties on satiety was tested • Changes in salivary lubricity and gut peptides post beverage ingestion were tested • Sporadic effect of high coating versus low coating on fullness was observed • Food intake and gut peptides did not differ between conditions We investigated the effects of complex textural attributes of food i.e. lubricity and oral coating, on appetite ratings, food intake, salivary and gut peptides for the first time. Milk protein-rich beverages (whey and casein) were instrumentally analyzed (tribology, viscosity and adsorption, latter representing oral coating) using in vitro measurements. Then these protein beverage preloads differing in their coating properties (low coating, medium coating and high coating) were assessed in two cross-over satiety trials (Study 1, n=37; Study 2, n=15; Total n= 52). Fullness ratings increased in the high coating beverage condition (p <.05) only after 20 min with limited effects on other time points, suggesting a sporadic effect of oral coating on appetite ratings (n=37). There was a correlation between concentration of protein in saliva and appetite ratings; the higher the concentration of protein in saliva the lower the desire to eat (r = - 0.963; p < 0.05) and prospective food consumption ratings (r =- 0.980; p < 0.05). Human saliva was more lubricating after ingesting preload with high coating properties, thus explaining the results on appetite ratings. There was no effect of oral coating on energy intake and gut peptides (n=15), suggesting that complex textural attributes having influence on oral processing might not have any effect on the later parts of the satiety cascade. Oral coating/ lubricity appears to have a subtle and sporadic effect on appetite suppression, which needs further investigation with changing macronutrients/energy load and degree of coating/ lubricity. [ABSTRACT FROM AUTHOR]

The central nucleus of the amygdala (CeA) is part of the dopaminergic reward system and controls energy balance. Recently, a cluster of neurons was identified as responsive to the orexigenic effect of ghrelin and fasting. However, the signaling pathway by which ghrelin and fasting induce feeding is unknown. AMP-activated protein kinase (AMPK) is a cellular energy sensor, and its Thr172 phosphorylation (AMPKThr172) in the mediobasal hypothalamus regulates food intake. However, whether the expression and activation of AMPK in CeA could be one of the intracellular signaling activated in response to ghrelin and fasting eliciting food intake is unknown. To evaluate the activation of AMPK into CeA in response to ghrelin, fasting, and 2-deoxy-D-glucose (2DG) and whether feeding accompanied these changes. In addition, to investigate whether the inhibition of AMPK into CeA could decrease food intake. On a chow diet, eight-week-old Wistar male rats were stereotaxically implanted with a cannula in the CeA to inject several modulators of AMPKα1/2Thr172 phosphorylation, and we performed physiological and molecular assays. Fasting increased, and refeeding reduced AMPKThr172 in the CeA. Intra-CeA glucose injection decreased feeding, whereas injection of 2DG, a glucoprivation inductor, in the CeA, increased food intake and blood glucose, despite faint increases in AMPKThr172. Intra-CeA ghrelin injection increased food intake and AMPKThr172. To further confirm the role of AMPK in the CeA, chronic injection of Melanotan II (MTII) in CeA reduced body mass and food intake over seven days together with a slight decrease in AMPKThr172. Our findings identified that AMPK might be part of the signaling machinery in the CeA, which responds to nutrients and hormones contributing to feeding control. The results can contribute to understanding the pathophysiological mechanisms of altered feeding behavior/consumption, such as binge eating of caloric-dense, palatable food. • Fasting increases and refeeding decreases AMPK phosphorylation in the CeA. • Ghrelin in the CeA activates AMPK, increasing feeding. • Glucose in the CeA decreases feeding contrary to neuroglycopenia (2-DG), which increases food intake and glycemia. • CeA AMPK pharmacological inhibition (MTII) decreases feeding and body weight. • AMPK might be part of the machinery in the CeA, which responds to nutrients and hormones contributing to feeding control. [ABSTRACT FROM AUTHOR]

Adrenomedullin has various physiological roles including appetite regulation. The objective of present study was to determine the effects of ICV injection of adrenomedullin and its interaction with NPY and CCK receptors on food intake regulation. In experiment 1, chickens received ICV injection of saline and adrenomedullin (1, 2, and 3 nmol). In experiment 2, birds injected with saline, B5063 (NPY 1 receptor antagonist, 1.25 µg), adrenomedullin (3 nmol) and co-injection of B5063+adrenomedullin. Experiments 3 to 5 were similar to experiment 2 and only SF22 (NPY 2 receptor antagonist, 1.25 µg), SML0891 (NPY 5 receptor antagonist, 1.25 µg) and CCK 4 (1 nmol) were injected instead of B5063. In experiment 6, ICV injection of saline and CCK 8s (0.125, 0.25, and 0.5 nmol) were done. In experiment 7, chickens injected with saline, CCK 8s (0.125 nmol), adrenomedullin (3 nmol) and co-injection of CCK 8s +adrenomedullin. After ICV injection, birds were returned to their individual cages immediately and cumulative food intake was measured at 30, 60, and 120 min after injection. Adrenomedullin (2 and 3 nmol) decreased food intake compared to control group (P < 0.05). Coinjection of B5063+adrenomedullin amplified hypophagic effect of adrenomedullin (P < 0.05). The ICV injection of the CCK 8s (0.25 and 0.5 nmol) reduced food intake (P < 0.05). Co-injection of the CCK 8s +adrenomedullin significantly potentiated adrenomedullin-induced hypophagia (P < 0.05). Administration of the SF22, SML0891 and CCK 4 had no effect on the anorexigenic response evoked by adrenomedullin (P > 0.05). These results suggested that the hypophagic effect of the adrenomedullin is mediated by NPY 1 and CCK 8s receptors. However, our novel results should form the basis for future experiments. [ABSTRACT FROM AUTHOR]

Glyphosate (GLY)-based herbicide (GBH) formulations are widely used pesticides in agriculture. The European Union recently decided to extend the use of GLY in Europe until 2034. Previously, we showed that chronic dietary GBH exposure in adult hens resulted in a reversible increase in early mortality in chicken embryos. In this present study, we investigated the GBH effects on metabolism and ovarian functions by using a transcriptomic approach in vivo in young female broilers and in vitro in ovarian explant cultures. We exposed 11-day-old female broilers to 13 mg GLY equivalent/kg body weight/d (GBH13, n = 20), 34 mg GLY equivalent/kg body weight/d (GBH34, n = 20), or a standard diet (control [CT], n = 20) for 25 d. These 2 GBH concentrations correspond to approximatively one-eighth and one-third of the no observed adverse effect level (NOAEL) as defined by European Food Safety Authority in birds. During this period, we evaluated body weight, fattening, food intake, and the weight of organs (including the ovaries). Chronic dietary GBH exposure dose dependently reduced food intake, body weight, and fattening, but increased oxidative stress and relative ovary weight. We analyzed the ovarian gene expression profile in CT, GBH13, and GBH34 broilers with RNA sequencing and showed that differentially expressed genes are mainly enriched in pathways related to cholesterol metabolism, steroidogenesis, and RNA processing. With quantitative polymerase chain reaction and western blotting, we confirmed that GBH decreased ovarian STAR and CYP19A1 messenger RNA and protein expression, respectively. Furthermore, we confirmed that GBH altered steroid production in ovarian explants. We have identified potential regulatory networks associated with GBH. These data provide valuable support for understanding the ovarian transcriptional regulatory mechanism of GBH in growing broilers. [ABSTRACT FROM AUTHOR]

The A allele of rs9939609 polymorphism at the FTO gene has been consistently associated with higher body mass index in different populations, but conflicting results have been found regarding its contribution to food intake variability. This study aimed to investigate the association between this genetic variant and nutrient and food intake in an urban Argentinian population. A cross-sectional, analytic investigation was performed between October 2018 and February 2020. Adults of both sexes residing in La Plata, Argentina, were recruited through social networks (Instagram and Facebook). Of 179 eligible adults, a total of 173 adults were included in the final analyses. Nutrient and food group intake data were obtained by an interview-administered food frequency questionnaire. Height and weight were measured, and genotypes were obtained by real-time polymerase chain reaction. The per-allele effect on nutrient and food group intake was assessed by general linear models, adjusting for age, sex, educational level, total energy intake, and body mass index. Dietary patterns were derived by principal component analysis. The association of the A allele with adherence to each dietary pattern was also evaluated by the general linear model. The frequency of the risk allele was 27%. A-carriers showed a higher total fat (1.88 [0.55, 3.21] % of total energy intake), saturated fatty acids (0.82 [0.25–1.39] % of total energy intake), and monounsaturated fatty acids (0.66 [0.08, 1.24] % of total energy intake), and a lower carbohydrate (−1.99 [−3.48, −0.50] % of total energy intake) intake than TT homozygous. A-carriers also reported a higher "milk and yogurt" (1.08 [0.24, 1.91] % of total energy intake), "animal fats" (1.09 [0.14–2.03] % of total energy intake), and fat-rich ultraprocessed foods (2.10 [0.52, 3.67] % of total energy intake) intake in comparison with TT homozygous. Furthermore, A-carriers showed higher adherence to the Western dietary pattern. The A allele contributed to nutrient and food intake variability in the studied population and was associated with the consumption of saturated fatty acids–enriched foods. [ABSTRACT FROM AUTHOR]

• The shape of bread (bun vs. slice) influenced both bread and topping intake. • Total breakfast food intake was not different for buns vs. slices. • Ratio bread:topping intake was higher for buns compared to slices. The size and shape of foods are geometrical textural properties that have been shown to influence food intake. Changing shapes and sizes of carrier food such as bread influences the spreadable surface area and this may affect the amount of toppings used. In a cross-over study, 37 participants (11 males, 24 ± 7 years old, BMI of 23 ± 3 kg/m2) consumed three times an ad libitum breakfast consisting of either small buns (SB: 34 g per unit), large buns (LB: 47 g), or squared sandwich slices (SA: 36 g), similar in nutritional composition. Participants were free to use four kinds of toppings similar in energy density (2.3–2.4 kcal/g): apple syrup, jam, cream cheese, and egg salad. The ratio bread(g):topping(g) differed considerably (1:0.49 for SB; 1:0.53 for LB; and 1:0.63 for SA, p < 0.001), but total meal intake did not differ (g or kcal) p = 0.27. In sum, the meal with SA leads to relatively higher intake of toppings and lower intake of bread, whereas the meal with small buns (SB) leads to relatively lower intake of toppings and higher intake of bread. Changing surface areas by shapes of carrier foods can be used to manipulate the amount of toppings, condiments or sauces and thereby modulate the macronutrient and energy intakes within a meal or snack. [ABSTRACT FROM AUTHOR]

[Display omitted] • The associations of urinary Te level (uTeL) with blood pressure (BP) was analyzed. • A positive association of uTeL with BP was found in humans. • A positive association between uTeL and hypertension (HT) was also found in humans. • Intake of cereals/beans was positively associated with the Te-mediated risk of HT. • Oral exposure to Te significantly increased BP with elevated uTeL in mice. People worldwide are routinely exposed to tellurium mainly via dietary ingestion. There has been no study to clarify the contribution of tellurium to blood pressure in humans or animals. In this cross-sectional study conducted in a general population of 2592 residents in Japan, the associations of urinary tellurium levels with blood pressure and prevalence of hypertension were investigated. The potential sources of tellurium were also investigated. An interventional study in mice confirmed the effect of tellurium exposure on blood pressure. Linear and logistic regression analyses with consideration of confounders including urinary sodium–potassium ratio showed significant positive associations of urinary tellurium level with prevalence of hypertension and blood pressure. Cereals/beans and vegetables/fruits were determined to be potential dietary sources of tellurium exposure. Intermediary analysis suggested that increased intake of cereals/beans, but not that of vegetables/fruits, is positively associated with the tellurium-mediated risk of hypertension. Correspondingly, the mouse study showed that exposure to a putative human-equivalent dose of tellurium via drinking water increased blood pressure with an elevated level of urinary tellurium. The temporally increased blood pressure was decreased to the normal level by a break of tellurium exposure with a reduced level of urinary tellurium. The interdisciplinary approach provided the first evidence that tellurium exposure is a potential risk for increase of blood pressure. Since the human urinary tellurium level in this study is comparable with the levels in general populations in other Asian and European countries in previous studies, exposure to tellurium may be a latent universal risk for hypertension. [ABSTRACT FROM AUTHOR]

[Display omitted] • Structure of konjac glucomannan - recrystallized resistant starch (KRS3) was studied. • KRS3 samples kept peak temperature values above 110 °C. • KRS3 slowed gastric emptying and intestinal propulsion rate. • KRS3, with 0.5% konjac glucomannan, reduced food intaking and improved satiety. The effects of the structure and digestibility of konjac glucomannan (KGM)-recrystallized resistant starch complex (KRS3) on the glycemic response and short-term satiety in mice were investigated. KRS3 samples were prepared by recrystallized debranched starch (RS3) at 50 °C, and then combined with KGM. The RS3 and KRS3 samples displayed an A-type pattern and maintained peak temperature values above 110 °C. With an increase in KGM, the swelling power and apparent viscosity of KRS3 increased. The results of in vitro and in vivo digestion revealed that KRS3 with a resistant starch content ranging from 69.4 % to 78.8 % could effectively maintain postprandial blood glucose levels. KRS3, particularly with 0.5 % KGM, slowed gastric emptying of mice from 82.7 % to 36.6 % and intestinal propulsion rate from 60.9 % to 35.3 %, resulting in strong satiety. RS3 combined with KGM could serve as a new approach to develop RS3 based foods with low glycemic responses and high-satiety. [ABSTRACT FROM AUTHOR]

Thirty-five participants completed the study. Two ad libitum food intake sessions were conducted, one using conventional chopsticks (Normal) and the other with user-friendly chopsticks supported by an adapter (Supported). All participants reported that Supported chopsticks were easier to use compared to the Normal ones. The results revealed a statistically significant 22.5% reduction in the volume of food consumed in a single bite with Supported chopsticks compared to Normal chopsticks (p < 0.05). Furthermore, a significant 12.0% decrease in the overall volume of food intake was observed when using Supported chopsticks compared to the Normal chopsticks (p < 0.05). These findings suggest that the easy of using cutlery can induce influence both bite size and overall food intake. [ABSTRACT FROM AUTHOR]

Le tractus gastro-intestinal produit une très grande diversité de peptides et peut être considéré comme la plus grande et la plus complexe des glandes endocrines. Depuis la découverte de la sécrétine, plus de 30 gènes codant pour des pro-hormones ont été identifiés et, du fait d'épissages alternatifs et/ou de maturations post-traductionnelles, ils permettent la production et la sécrétion de plus de 100 peptides actifs différents. Ces hormones intestinales, appelées également entérohormones, exercent de nombreux effets sur le tractus gastro-intestinal lui-même mais également à distance (cerveau, pancréas, foie...) participant au contrôle de l'entrée des nutriments dans l'organisme, de la prise alimentaire, de l'homéostasie glucidique. Les entérohormones sont produites par les cellules entéroendocrines dispersées le long du tractus gastro-intestinal et sécrétées en réponse à des signaux luminaux mais également endocrines, paracrines, et neuronaux. La fonction entéroendocrine est altérée au cours de la dénutrition ou de l'obésité. La chirurgie bariatrique, principal traitement des obésités sévères, et la résection étendue de l'intestin grêle menant au syndrome de grêle court, principale cause d'insuffisance intestinale, induisent des modifications importantes des secrétions de plusieurs entérohormones. Cette revue résume les dernières connaissances en physiologie de la fonction endocrine intestinale (les cellules entéroendocrines, les signaux les stimulant, les principaux rôles des entérohormones) mais aussi lors de pathologies nutritionnelles (obésité, dénutrition) et les possibles approches pour cibler cette fonction à des fins thérapeutiques. The gastrointestinal tract produces a very wide variety of peptides and is considered as the largest and most complex endocrine glands. Since the discovery of secretin, more than 30 genes encoding pro-hormones have been identified and, due to alternative splicing and/or regulated post-translational maturation, these genes allow the production and secretion of more than 100 different peptides. These intestinal hormones, also called enterohormones, exert numerous effects on the gastrointestinal tract itself but also at distance (brain, pancreas, liver...) participating in the control of the entry of nutrients into the body, the food intake, carbohydrate homeostasis. Enterohormones are produced by enteroendocrine cells scattered along the gastrointestinal tract and secreted in response to luminal, but also endocrine, paracrine, and neuronal signals. Enteroendocrine function is impaired during undernutrition or obesity. Bariatric surgery, the main treatment for severe obesity, and extensive resection of the small intestine leading to short bowel syndrome (the main cause of intestinal failure) induce significant changes in the secretions of several enterohormones. This review summarizes the latest knowledge in the physiology of intestinal endocrine function (enteroendocrine cells, the signals stimulating them, the main roles of enterohormones) but also during nutritional pathologies (obesity, undernutrition) and the possible approaches to target this function for specific therapeutic purposes. [ABSTRACT FROM AUTHOR]

A recent Perspective article described the "carbohydrate-insulin model (CIM)" of obesity, asserting that it "better reflects knowledge on the biology of weight control" as compared with what was described as the "dominant energy balance model (EBM)," which fails to consider "biological mechanisms that promote weight gain." Unfortunately, the Perspective conflated and confused the principle of energy balance, a law of physics that is agnostic as to obesity mechanisms, with the EBM as a theoretical model of obesity that is firmly based on biology. In doing so, the authors presented a false choice between the CIM and a caricature of the EBM that does not reflect modern obesity science. Here, we present a more accurate description of the EBM where the brain is the primary organ responsible for body weight regulation operating mainly below our conscious awareness via complex endocrine, metabolic, and nervous system signals to control food intake in response to the body's dynamic energy needs as well as environmental influences. We also describe the recent history of the CIM and show how the latest "most comprehensive formulation" abandons a formerly central feature that required fat accumulation in adipose tissue to be the primary driver of positive energy balance. As such, the new CIM can be considered a special case of the more comprehensive EBM but with a narrower focus on diets high in glycemic load as the primary factor responsible for common obesity. We review data from a wide variety of studies that address the validity of each model and demonstrate that the EBM is a more robust theory of obesity than the CIM. [ABSTRACT FROM AUTHOR]

Controlling mechanisms of appetite and food intake is an important issue for a variety of different types of athletes. Previous studies showed omega-3 fatty acid increased appetite in patients, but results in healthy individuals are inconclusive. This study assessed the effect of omega-3 fatty acid supplements on food intake and appetite in young male athletes with normal body fat percentage. In a three-week double-blind placebo-controlled RCT in Tabriz, Iran (2019), 72 male athletes, age 22.2 (±2.5) y with 13.9 (8.5) body fat percent were randomized to either an omega-3 (2000 mg/day; EPA: 360 mg, DHA: 240 mg) or placebo (2000 mg/day paraffin) group. 3-day food diaries were completed before and after the intervention. Body composition was measured by bioelectrical impedance analysis. Appetite was assessed by visual analog scale (VAS) before and after each week of intervention. Results showed carbohydrate intake increased in the omega-3 group (MD = 65.8 g; 95% CI = 9.1, 70.1; P = 0.03). VAS score for satiety decreased. Hunger sensation, desire to eat, and desire to eat sweet foods increased in each of the three weeks. In conclusion, our findings showed that omega-3 supplementation increased appetite in healthy athletes without significant change in body fat percentage. Further research is needed to generalize the results to other populations. [ABSTRACT FROM AUTHOR]

Objective: To evaluate in postmenopausal women the association between menopause symptom intensity and the quality of life and clinical, anthropometric, and lifestyle factors, focusing on food consumption by degree of processing.Study Design: A cross-sectional study of 288 postmenopausal women using interviews.Main Outcome Measures: The Kupperman-Blatt Menopausal Index and the Women's Health Questionnaire were used to evaluate the main outcomes of menopausal symptom intensity and quality of life, respectively. Data on socioeconomic, clinical, anthropometric, and lifestyle variables (smoking, alcohol intake, physical activity, and food consumption) were collected.Results: Most women had moderate to severe intensity of menopausal symptoms. The highest tertile of ultra-processed food consumption was associated with a greater intensity of vasomotor symptoms (prevalence ratio [PR] 0.73, 95% confidence intervals [CI] 0.55-0.96) and sexual behavior (PR 1.22, CI 1.01-1.49). Higher intakes of sugar-sweetened beverages and sausages were associated with somatic symptoms (PR 1.23, CI 1.01-1.49) and poorer memory/concentration (PR 1.22, CI 1.02-1.47/ PR 1.22, CI 1.01-1.48). The highest tertile of vegetable intake was associated with greater protection against depressive mood (PR 0.64, CI 0.43-0.96), vasomotor symptoms (PR 0.79, CI 0.63-0, 99), and sleep disorders (PR 0.83, CI 0.69-0.99), and better quality of life (PR 0.79, CI 0.62-0.99).Conclusion: More intense vasomotor, sexual, somatic, and memory and concentration symptoms are associated with a higher consumption of ultra-processed foods, whereas those with a higher consumption of vegetables reported lower menopause symptom intensity and a better quality of life. [ABSTRACT FROM AUTHOR]

Background: Optimum functioning of the central nervous system is dependent on a wide range of nutrients, so mental illness can be impacted by diet via several mechanisms. We aimed to investigate the associations of antioxidants (vitamin A, C and E, and selenium and zinc) and vitamin B complex (B6, folate and B12) intake with depression in 14,737 subjects of the Brazilian Longitudinal Study of Adult Health.Methods: Baseline cross-sectional data was analyzed. Micronutrients intake was measured using the Food Frequency Questionnaire, and depression was assessed using the Clinical Interview Schedule Revised. Logistic regression models were built using daily intake quintiles of micronutrients.Results: A significant inverse relationship was observed between depression and higher intake of selenium, zinc, vitamins B6 and B12 for the total sample. Among women, a similar pattern of associations was observed, in addition to the higher intake of vitamins A and C. Among men, a significant inverse relationship between depression was observed only with the intake of vitamins B12 and B6. Higher total antioxidant intake was significantly associated with lower odds of depression and an inverse dose-response effect between total antioxidant intake and clinical severity of depression was observed among women, in adjusted models.Limitations: Recall bias in assessing diet. Misclassification bias regarding current depression.Conclusions: Depression is associated with lower intake of antioxidants and B vitamins. Higher intake of selected micronutrients may contribute to reduce depression occurrence and severity. [ABSTRACT FROM AUTHOR]

• Meal-related memory inhibits eating in humans. • Amnesia is associated with overeating and impaired interoception in humans. • Research in rodents and humans implicates the hippocampus in these effects. • Obesity disrupts memory and hippocampal functioning in rodents and humans. • These effects of obesity may create a vicious cycle that perpetuates obesity. This paper reviews evidence demonstrating a bidirectional relationship between memory and eating in humans and rodents. In humans, amnesia is associated with impaired processing of hunger and satiety cues, disrupted memory of recent meals, and overconsumption. In healthy participants, meal-related memory limits subsequent ingestive behavior and obesity is associated with impaired memory and disturbances in the hippocampus. Evidence from rodents suggests that dorsal hippocampal neural activity contributes to the ability of meal-related memory to control future intake, that endocrine and neuropeptide systems act in the ventral hippocampus to provide cues regarding energy status and regulate learned aspects of eating, and that consumption of hypercaloric diets and obesity disrupt these processes. Collectively, this evidence indicates that diet-induced obesity may be caused and/or maintained, at least in part, by a vicious cycle wherein excess intake disrupts hippocampal functioning, which further increases intake. This perspective may advance our understanding of how the brain controls eating, the neural mechanisms that contribute to eating-related disorders, and identify how to treat diet-induced obesity. [ABSTRACT FROM AUTHOR]

In captive facilities, odontocetes are subject to daily training/feeding sessions which often create close relationships between animals and their caretakers. Therefore, such sessions are thought to provide information that can be useful for welfare assessment. Recent studies on bottlenose dolphins (Tursiops truncatus) validated caretakers' ratings of dolphins' participation during training sessions as a welfare indicator. Even though their behavior, adaptation to captive settings or relationship with humans may differ from bottlenose dolphins, many other odontocete species remain much less studied. In the present study, animals from three groups including Yangtze finless porpoises (Neophocaena asiaeorientalis asiaeorientalis), East-Asian finless porpoises (Neophocaena asiaeorientalis sunameri), and bottlenose dolphins were monitored during training sessions. Four variables were recorded: a participation score rated by caretakers, the leaving rate, the amount of food eaten, and the propensity to finish the attributed food. Bottlenose dolphins participated better in sessions: they were attributed higher participation scores, departed less and finished their food more often than finless porpoises. The context of the sessions, including time of the day, season, type of session, social grouping, occurrence of unusual events or presence of visitors affected the parameters recorded during sessions in the three groups. The inter-species differences and the context-related variations of the four measured parameters should be used to adapt the schedules and techniques of training sessions for each group. Such adaptation could improve training effectiveness and the human-animal relationship. In addition, the associations among the four measured parameters and between these parameters and the animals' displayed activity revealed the most informative parameter for each group: participation score for Yangtze finless porpoises, food intake for East-Asian finless porpoises and leaving rate for bottlenose dolphins. These parameters best reflect the motivation of the animals during sessions, and may therefore be beneficial to integrate into welfare monitoring tools. [ABSTRACT FROM AUTHOR]

• LDX is the only approved drug to treat Binge Eating Disorder. • The neuropsychopharmacological mechanisms underlying treatment efficacy remain unclear. • LDX reduces homeostatic and hedonic food intake in rodents and humans. • LDX likely improves BED through catecholaminergic and serotoninergic actions on appetite/satiety, reward, and cognitive processes. Binge-Eating Disorder (BED) is the most common eating disorder in the United States. Lisdexamfetamine (LDX) was approved in 2015 by the FDA for treatment of BED and is the only drug approved for treating the disorder. There has been no systematic evaluation of the published clinical and preclinical evidence for efficacy of LDX in treating BED and the mechanisms responsible for the therapeutic action of the drug. To address this gap, we conducted a systematic review and meta-analysis using PRISMA guidelines. Fourteen clinical and seven preclinical articles were included. There is consistent evidence from clinical studies that LDX is an effective treatment for BED and that the drug reduces the BED symptoms and body weight of patients with the disorder. There is also consistent evidence from preclinical studies that LDX reduces food intake but no consistent evidence for a preferential reduction of palatable food consumption by the drug in rodents. The evidence on mechanism of action is more limited and suggests LDX may reduce binge eating by a combination of effects on appetite/satiety, reward, and cognitive processes, including attention and impulsivity/inhibition, that are mediated by catecholamine and serotonin mechanisms in the brain. There is an urgent need for adequately powered, placebo-controlled, behavioural and neuroimaging studies with LDX (recruiting patients and/or individuals with subclinical BED symptoms) to further investigate the mechanism of action of the drug in treating BED. An improved understanding of the behavioural and neurochemical mechanisms of action of LDX could lead to the development of improved drug therapies to treat BED. [ABSTRACT FROM AUTHOR]

Energy balance is orchestrated by an extended network of highly interconnected nuclei across the central nervous system. While much is known about the hypothalamic circuits regulating energy homeostasis, the 'extra-hypothalamic' circuits involved are relatively poorly understood. In this review, we focus on the brainstem's dorsal raphe nucleus (DRN), integrating decades of research linking this structure to the physiologic and behavioral responses that maintain proper energy stores. DRN neurons sense and respond to interoceptive and exteroceptive cues related to energy imbalance and in turn induce appropriate alterations in energy intake and expenditure. The DRN is also molecularly differentiable, with different populations playing distinct and often opposing roles in controlling energy balance. These populations are integrated into the extended circuit known to regulate energy balance. Overall, this review summarizes the key evidence demonstrating an important role for the DRN in regulating energy balance. The dorsal raphe nucleus (DRN) has extensive afferent and efferent connections with forebrain loci regulating feeding and thermogenesis; the DRN also polysynaptically innervates brown adipose tissue (BAT). Modulating these DRN projections can augment or suppress food intake and/or thermogenesis. DRN subpopulations expressing specific neuropeptides and/or their receptors have been functionally implicated in energy balance. Reduced serotonin (5-HT) release from the DRN increases food intake, and 5-HT release from the DRN is necessary for maintaining normal thermogenesis. Excitatory and inhibitory DRN neurons respond to energy deficit or surfeit and exert bidirectional control over energy balance. Inhibitory DRN neurons are responsive to thermal challenge; these neurons regulate BAT thermogenesis and overall energy expenditure. [ABSTRACT FROM AUTHOR]

In hospitals through Europe and worldwide, the practices regarding hospital diets are very heterogeneous. Hospital diets are rarely prescribed by physicians, and sometimes the choices of diets are based on arbitrary reasons. Often prescriptions are made independently from the evaluation of nutritional status, and without taking into account the nutritional status. Therapeutic diets (low salt, gluten-free, texture and consistency modified, ...) are associated with decreased energy delivery (i.e. underfeeding) and increased risk of malnutrition. The European Society for Clinical Nutrition and Metabolism (ESPEN) proposes here evidence-based recommendations regarding the organization of food catering, the prescriptions and indications of diets, as well as monitoring of food intake at hospital, rehabilitation center, and nursing home, all of these by taking into account the patient perspectives. We propose a systematic approach to adapt the hospital food to the nutritional status and potential food allergy or intolerances. Particular conditions such as patients with dysphagia, older patients, gastrointestinal diseases, abdominal surgery, diabetes, and obesity, are discussed to guide the practitioner toward the best evidence based therapy. The terminology of the different useful diets is defined. The general objectives are to increase the awareness of physicians, dietitians, nurses, kitchen managers, and stakeholders towards the pivotal role of hospital food in hospital care, to contribute to patient safety within nutritional care, to improve coverage of nutritional needs by hospital food, and reduce the risk of malnutrition and its related complications. [ABSTRACT FROM AUTHOR]

Background Both diet and familial factors have a major role in the development of cardiovascular disease (CVD). However, it remains unclear whether familial predisposition to CVD modifies the association between dietary factors and CVD. Objectives The aim was to assess whether the association between diet and CVD varies with familial predisposition to CVD. Methods In this prospective cohort of the UK Biobank, 462,155 CVD-free participants were included in 2006–2010 and followed for CVD incidence until 2020. Food intake was measured using a short food-frequency questionnaire. Familial predisposition was measured by self-reported family history of CVD and by polygenic risk score (PRS) for CVD based on summary statistics of independent genome-wide association studies. Results During a median follow-up of 11.2 y, 46,164 incident CVD cases were identified. A moderately higher risk of CVD was associated with more frequent processed-meat consumption, with an adjusted HR of 1.07 (95% CI: 1.03, 1.11; highest vs. lowest level). Conversely, intakes of fish, cheese, vegetables, and fruit were each associated with reduced CVD risk [HR (95% CI): 0.92 (0.89, 0.96), 0.90 (0.86, 0.94), 0.98 (0.95, 1.00), and 0.93 (0.89, 0.96), respectively]. Stratification analyses by family history of CVD and by PRS for CVD revealed an inverse association between CVD and intakes of fish and cheese, for both subgroups with and without a familial predisposition to CVD. Notably, while the association between processed-meat intake and CVD was restricted to individuals with a familial predisposition to CVD [e.g. HR: 1.11 (1.05, 1.16) and 1.03 (0.97, 1.10) for with and without a family history, respectively, P- interaction < 0.001], the risk reduction of CVD associated with vegetable and fruit intake was only noted among participants without a CVD familial predisposition [e.g. HR for fruit consumption: 1.00 (0.97, 1.03) and 0.91 (0.87, 0.95), respectively, P  < 0.001]. Conclusions Familial factors modify the association between diet and CVD, underscoring the need for personalized dietary guidelines for CVD prevention. [ABSTRACT FROM AUTHOR]

Background: l-Tryptophan reduces energy intake in healthy men. The underlying mechanisms, including appetite, plasma cholecystokinin (CCK), tryptophan (Trp), and the ratio of Trp to large neutral amino acids (Trp:LNAAs ratio), and whether responses differ in lean and obese individuals, are uncertain.Objectives: We evaluated the effects of intragastric Trp on energy intake (primary outcome) and their potential mechanisms, pre- and postmeal, in lean men and those with obesity.Methods: Twelve lean men [mean ± SD age: 30 ± 3 y; BMI (in kg/m2): 23 ± 1] and 13 men with obesity (mean ± SD age: 31 ± 3 y; BMI: 33 ± 1) received, on 3 separate occasions, in double-blind, randomized order, 3 g ("Trp-3") or 1.5 g ("Trp-1.5") Trp, or control ("C"), intragastrically, 30 min before a buffet-meal. Energy intake from the buffet-meal, hunger, fullness, and plasma CCK and amino acid concentrations were measured in response to Trp alone and for 2 h postmeal. Data were analyzed using maximum likelihood mixed-effects models, with treatment, group, and treatment-by-group interaction as fixed effects.Results: Trp alone increased plasma CCK, Trp, and the Trp:LNAAs ratio (all P < 0.001), with no difference between groups. Trp suppressed energy intake (P < 0.001), with no difference between groups (lean, C: 1085 ± 102 kcal, Trp-1.5: 1009 ± 92 kcal, Trp-3: 868 ± 104 kcal; obese, C: 1249 ± 98 kcal, Trp-1.5: 1217 ± 90 kcal, Trp-3: 1012 ± 100 kcal). Postmeal, fullness was greater after Trp-3 than after C and Trp-1.5 (all P < 0.05), and in men with obesity than in lean men (P < 0.05). Plasma Trp and the Trp:LNAAs ratio were greater after Trp-3 and Trp-1.5 than after C (all P < 0.001), and tended to be less in men with obesity than in the lean (P = 0.07) (Trp:LNAAs ratio: lean, C: 1.5 ± 0.2, Trp-1.5: 6.9 ± 0.7, Trp-3: 10.7 ± 1.4; obese, C: 1.4 ± 0.1, Trp-1.5: 4.6 ± 0.7, Trp-3: 7.8 ± 1.3). There were inverse correlations of energy intake with plasma Trp and the Trp:LNAAs ratio in both groups (lean, both r = -0.50, P < 0.01; obese, both r = -0.40, P < 0.05).Conclusions: Intragastric Trp has potent energy intake-suppressant effects, in both lean men and those with obesity, apparently related to the Trp:LNAAs ratio. [ABSTRACT FROM AUTHOR]