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Purpose To determine the effects of dietary sugar or carbohydrate restriction on physical activity energy expenditure, energy intake, and physiological outcomes across 24 h. Methods In a randomized, open-label crossover design, twenty-five healthy men (n = 10) and women (n = 15) consumed three diets over a 24-h period: moderate carbohydrate and sugar content (MODSUG = 50% carbohydrate [20% sugars], 15% protein, 35% fat); low sugar content (LOWSUG = 50% carbohydrate [ Results The MODSUG, LOWSUG and LOWCHO diets resulted in similar mean [95%CI] rates of both physical activity energy expenditure (771 [624, 919] vs. 677 [565, 789] vs. 802 [614, 991] kcal·d−1; p = 0.29] and energy intake (2071 [1794, 2347] vs. 2195 [1918, 2473] vs. 2194 [1890, 2498] kcal·d−1; P = 0.34), respectively. The LOWCHO condition elicited the lowest glycaemic and insulinaemic responses to breakfast (P P p Conclusion When energy density is controlled for, restricting either sugar or total dietary carbohydrate does not modulate physical activity level or energy intake over a 24-h period (~ 19-h free-living) despite substantial metabolic changes. Clinical trials registration ID NCT03509610, https://clinicaltrials.gov/show/NCT03509610

In both captive and free-living birds, the emergence of the migratory phenotype is signalled by rapid and marked increases in food intake and fuelling, as well as changes in amount of nocturnality or migratory restlessness. The metabolic hormone corticosterone and, as more recently suggested, the gut-derived hormone ghrelin have been suggested to play a role in mediating such phenomenal phenotypic flexibility given that they both regulate fuel metabolism and locomotion across vertebrate taxa. Here, using the Common quail (Coturnix coturnix) as our study species, we induced autumn migration followed by a non-migratory wintering phase through controlled changes in daylight. We thus compared plasma corticosterone and ghrelin concentrations between the two sampling phases and assessed whether these hormones might reflect the migratory state. While we found no differences in plasma corticosterone between the two sampling phases and no link of this hormone with changes in body mass, levels of food intake or migratory restlessness, the migratory birds had substantially higher levels of plasma ghrelin relative to the non-migratory birds. Furthermore, while ghrelin did not correlate with the gain in body mass over the entire pre-migratory fuelling phase (over an average of nine weeks preceding blood sampling), plasma ghrelin did positively correlate with the gain in body mass observed during the final fattening stages (over an average of three weeks preceding blood sampling). Again, variation in plasma ghrelin also reflected the amount of body mass depleted over both the long- and short-time frame as birds returned to their non-migratory baseline - lower levels of plasma ghrelin consistently correlated with larger losses in body mass. Thus, while our data do not highlight a role of the hormone corticosterone in sustaining pre-migratory fattening as shown in other bird species, they do add evidence for a potential role of ghrelin in mediating migratory behaviour and further suggest that this hormone might be important in regulating the transitioning of migratory states, possibly by promoting fuel mobilisation and usage.

Purpose Taste receptors are expressed throughout the gastrointestinal tract. The activation of post-oral taste receptors using tastants could provide a non-invasive treatment option in combating the obesity epidemic. The aim of this review was to examine the effect of post-oral delivery of non-caloric tastants on eating behavior reflected by primary outcome energy intake and secondary outcomes GI symptoms and perceptions and potential underlying mechanisms. This review was conducted according to the PRISMA guidelines for systematic reviews. Methods A systematic literature search of the Cochrane, PubMed, Embase, and Medline databases was performed. This systematic review and meta-analysis was registered in the PROSPERO database on 26 February 2020 (ID: CRD42020171182). Two researchers independently screened 11,912 articles and extracted information from 19 articles. If at least two studies investigated the effect of the same taste compound on primary outcome energy intake, a meta-analysis was performed to determine pooled effect sizes. Results Nineteen papers including healthy volunteers were included. In the 19 papers analyzed, effects of various tastants were investigated in healthy volunteers. Most extensively investigated were bitter tastants. The meta-analysis of effects of bitter tastants showed a significant reduction in energy intake of 54.62 kcal (95% CI - 78.54 to - 30.69, p = 0.0014). Conclusions Bitter stimuli are most potent to influence eating behavior. Energy intake decreased after post-oral delivery of bitter tastants. This highlights the potential of a preventive role of bitter tastants in battling the obesity epidemic.

The signal mediated by leptin hormone and its receptor is a major regulator of body weight, food intake and metabolism. In mammals and many teleost fish species, leptin has an anorexigenic role and inhibits food intake by influencing the appetite centres in the hypothalamus. However, the regulatory connections between leptin and downstream genes mediating its appetite-regulating effects are still not fully explored in teleost fish. In this study, we used a loss of function leptin receptor zebrafish mutant and real-time quantitative PCR to assess brain expression patterns of several previously identified anorexigenic genes downstream of leptin signal under different feeding conditions (normal feeding, 7-day fasting, 2 and 6-h refeeding). These downstream factors include members of cart genes, crhb and gnrh2, as well as selected genes co-expressed with them based on a zebrafish co-expression database. Here, we found a potential gene expression network (GRN) comprising the abovementioned genes by a stepwise approach of identifying co-expression modules and predicting their upstream regulators. Among the transcription factors (TFs) predicted as potential upstream regulators of this GRN, we found expression pattern of sp3a to be correlated with transcriptional changes of the downstream gene network. Interestingly, the expression and transcriptional activity of Sp3 orthologous gene in mammals have already been implicated to be under the influence of leptin signal. These findings suggest a potentially conserved regulatory connection between leptin and sp3a, which is predicted to act as a transcriptional driver of a downstream gene network in the zebrafish brain.

Previous studies have suggested that human exposure to bisphenol A (BPA) and soy isoflavones (SIFs) can occur during pregnancy. The combination of these chemicals is hypothesized to have a toxic impact on the fetus. While BPA is an industrial chemical used widely in the manufacture of polycarbonate plastics and epoxy resins, SIFs are naturally occurring estrogen-like phytoestrogens. To determine the impact of the combination of BPA and SIFs on fetal development, the body weight, organ weight, anogenital distance and histopathological changes in the testes of F1 offspring were assessed in mice. Hormonal effects were determined by measuring serum levels of estrogen receptor (ESR), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T). Additionally, mitochondrial DNA copy numbers, and the serum levels of malondialdehyde and superoxide dismutase, were determined to evaluate alterations in oxidative stress and potential toxicity. Exposure to BPA increased the body weight of the pups and reduced the ratio of anogenital distance to body weight, as well as testes weight. Moreover, BPA exposure also induced testicular lesions. The seminiferous tubules of testis were denatured in varying degrees and the lumen wall structure was disordered. The levels of ESR in all offspring and the T levels in male offspring significantly increased, compared with controls. Co-exposure to BPA and SIFs exacerbated these changes in body weight, testicular lesions and hormonal levels, relative to BPA exposure alone. Additionally, oxidative damage was only induced by high-dose BPA. Collectively, these findings suggested that BPA and SIFs could have synergistic effect on the reproductive system, which could be mediated by the regulation of ESR expression and testosterone release.

Background and Aims To assess safety of the Exilis™ gastric electrical stimulation (GES) system and to investigate whether the settings can be adjusted for comfortable chronic use in subjects with morbid obesity. Gastric emptying and motility and meal intake were evaluated. Method In a multicenter, phase 1, open prospective cohort study, 20 morbidly obese subjects (17 female, mean BMI of 40.8 ± 0.7 kg/m2) were implanted with the Exilis™ system. Amplitude of the Exilis™ system was individually set during titration visits. Subjects underwent two blinded baseline test days (GES ON vs. OFF), after which long-term, monthly follow-up continued for up to 52 weeks. Results The procedure was safe, and electrical stimulation was well tolerated and comfortable in all subjects. No significant differences in gastric emptying halftime (203 ± 16 vs. 212 ± 14 min, p > 0.05), food intake (713 ± 68 vs. 799 ± 69 kcal, p > 0.05), insulin AUC (2448 ± 347 vs. 2186 ± 204, p > 0.05), and glucose AUC (41 ± 2 vs.41 ± 2, p > 0.05) were found between GES ON and OFF. At week 4, 13, and 26, a significant (p Conclusion Gastric electrical stimulation with the Exilis™ system can be considered as safe. No significant effect on food intake, gastric emptying, or gastric motility was observed. The reduction in weight loss with Exilis™ GES was significant but short lasting. Further electrophysiological research is needed to gain more insight in optimal stimulation parameters and lead localization.

Accurate dietary assessment in nutritional research is a huge challenge, but essential. Due to the subjective nature of self-reporting methods, the development of analytical methods for food intake and microbiota biomarkers determination is needed. This work presents an ultra-high performance liquid chromatography coupled to tandem mass spectrometry (UHPLC-MS/MS) method for the quantification and semi quantification of 20 and 201 food intake biomarkers (BFIs), respectively, as well as 7 microbiota biomarkers applied to 208 urine samples from lactating mothers (M) (N = 59). Dietary intake was assessed through a 24 h dietary recall (R24h). BFI analysis identified three distinct clusters among samples: samples from clusters 1 and 3 presented higher concentrations of most biomarkers than those from cluster 2, with dairy products and milk biomarkers being more concentrated in cluster 1, and seeds, garlic and onion in cluster 3. Significant correlations were observed between three BFIs (fruits, meat, and fish) and R24h data (r > 0.2, p-values < 0.01, Spearman correlation). Microbiota activity biomarkers were simultaneously evaluated and the subgroup patterns detected were compared to clusters from dietary assessment. These results evidence the feasibility, usefulness, and complementary nature of the determination of BFIs, R24h, and microbiota activity biomarkers in observational nutrition cohort studies.

Objective The corticotropin-releasing factor neuropeptides (corticotropin-releasing hormone [CRH] and urocortin [UCN]-1,2,3) and spexin contribute to the regulation of energy balance and inhibit food intake in mammals. However, the status of these neuropeptides in children with overweight has yet to be elucidated. This study investigated the effect of increased body weight on the circulating levels of these neuropeptides. Methods A total of 120 children with a mean age of 12 years were enrolled in the study. Blood samples were collected to assess the circulating levels of neuropeptides and were correlated with various anthropometric, clinical, and metabolic markers. Results Plasma levels of UCNs were altered in children with overweight but less so in those with obesity. Furthermore, the expression pattern of UCN1 was opposite to that of UCN2 and UCN3, which suggests a compensatory effect. However, no significant effect of overweight and obesity was observed on CRH and spexin levels. Finally, UCN3 independently associated with circulating zinc-alpha-2-glycoprotein and UCN2 levels, whereas UCN1 was strongly predicted by TNF alpha levels. Conclusions Significant changes in neuropeptide levels were primarily observed in children with overweight and were attenuated with increased obesity. This suggests the presence of a compensatory mechanism for neuropeptides to curb the progression of obesity.

The underlying cell types mediating predisposition to obesity remain largely obscure. Here, we integrated recently published single-cell RNA-sequencing (scRNA-seq) data from 727 peripheral and nervous system cell types spanning 17 mouse organs with body mass index (BMI) genome-wide association study (GWAS) data from >457,000 individuals. Developing a novel strategy for integrating scRNA-seq data with GWAS data, we identified 26, exclusively neuronal, cell types from the hypothalamus, subthalamus, midbrain, hippocampus, thalamus, cortex, pons, medulla, pallidum that were significantly enriched for BMI heritability (p−4). Using genes harboring coding mutations associated with obesity, we replicated midbrain cell types from the anterior pretectal nucleus and periaqueductal gray (p−4). Together, our results suggest that brain nuclei regulating integration of sensory stimuli, learning and memory are likely to play a key role in obesity and provide testable hypotheses for mechanistic follow-up studies.

A person can alternate between food-related mindsets, which in turn may depend on one's emotional state or situation. Being in a certain mindset can influence food-related thoughts, but interestingly it might also affect eating-related physiological responses. The current study investigates the influence of an induced 'loss of control' mindset as compared to an 'in control' mindset on hormonal, neural and behavioural responses to chocolate stimuli. Mindsets were induced by having female chocolate lovers view a short movie during two sessions in a within-subjects design. Neural responses to visual chocolate stimuli were measured using an ultra-high field (7T) scanner. Momentary ghrelin and glucagon-like peptide 1 (GLP-1) levels were determined on five moments and were simultaneously assessed with self-reports on perceptions of chocolate craving, hunger and feelings of control. Furthermore, chocolate intake was measured using a bogus chocolate taste test. It was hypothesized that the loss of control mindset would lead to hormonal, neural and behavioural responses that prepare for ongoing food intake, even after eating, while the control mindset would lead to responses reflecting satiety. Results show that neural activity in the mesocorticolimbic system was stronger for chocolate stimuli than for neutral stimuli and that ghrelin and GLP-1 levels responded to food intake, irrespective of mindset. Self-reported craving and actual chocolate intake were affected by mindset, in that cravings and intake were higher with a loss of control mindset than with a control mindset. Interestingly, these findings suggest that physiology on the one hand (hormonal and neural responses) and behavior and subjective experience (food intake and craving) on the other hand are not in sync, are not equally affected by mindset.

Purpose of Review We aimed to accrue recent evidence exploring effects of modern online activities (e.g., Internet use) on feeding and eating disorder symptoms, and related traits. We examined available evidence to ascertain any direct influences from online activities on feeding and eating disorders, thereby shedding light on putative mechanisms by which those influences may occur. Recent Findings Many facets of problematic usage of the Internet correlate cross sectionally with eating disorder and related psychopathology. There is evidence to suggest that significant effects do exist in the direction of specific Internet activities contributing to eating disorder symptoms, viewed dimensionally. Putative mechanisms are discussed. However, a significant number of eating disorder phenotypes and Internet-related activities remain under-researched. Specific facets of engagement with the online environment appear to confer risk for feeding and eating problems, evidence being strongest for non-clinical studies using dimensional measures. More research is required to rigorously confirm causal effects, including in patients meeting formal diagnostic criteria for eating disorders. We also highlight the need for high-quality evidence to explore how eating disorder phenotypes are commonly as well as uniquely affected by different online activities. Such research is needed in order that scientific understanding in this area can be translated to protect those most at risk of disordered eating, including through changes in public health approaches and clinical practice.

Background/Objectives Seasonal variation in body mass is a model for the study of body mass regulation. Here a long-term study is presented on body mass, body composition, and activity-induced energy expenditure in a subject with a large seasonal variation in body mass of about 3.0 kg. Subject/Methods Body mass was assessed daily over >20 consecutive years. Daily assessment of activity-induced energy expenditure was performed over the last 10 years. Body composition was assessed monthly for 1 year in the middle and at the end of the observation interval. Additionally, data were compared with data on body composition, resting energy expenditure, and total daily energy expenditure of the same subject as a participant in published studies. Results Body mass showed a pronounced seasonal variation, associated with a synchronous variation in physical activity. Body mass peaked in the cold winter months when physical activity reached the lowest annual value and decreased to the lowest value in mid-summer when daily physical activity peaked. The seasonal variation in body mass consisted mainly of body fat. Longitudinally, over the past 8 years of the observation interval, average fat-free mass showed a decrease of 1.0 kg and fat mass increased 0.8 kg. Conclusions In a subject with a pronounced seasonal variation in physical activity, activity-induced variation in energy requirement was covered by an annual variation in body mass, mainly as fat. Maintenance of activity-induced energy expenditure did not protect against loss of fat-free body mass with advancing age.

Significance Gonadotropin Releasing Hormone (GnRH) acts as a key regulator of sexual maturation in vertebrates, and is required for the integration of environmental stimuli to orchestrate breeding cycles. Whether this integrative function is conserved across phyla remains unclear. We characterized GnRH-type signaling systems in the marine worm Platynereis dumerilii, in which both metabolic state and lunar cycle regulate reproduction. We find gnrh-like (gnrhl) genes upregulated in sexually mature animals, after feeding, and in specific lunar phases. Animals in which the corazonin1/gnrhl1 gene has been disabled exhibit delays in growth, regeneration, and maturation. Molecular analyses reveal glycoprotein turnover/energy homeostasis as targets of CRZ1/GnRHL1. These findings point at an ancestral role of GnRH superfamily signaling in coordinating energy demands dictated by environmental and developmental cues., The molecular mechanisms by which animals integrate external stimuli with internal energy balance to regulate major developmental and reproductive events still remain enigmatic. We investigated this aspect in the marine bristleworm, Platynereis dumerilii, a species where sexual maturation is tightly regulated by both metabolic state and lunar cycle. Our specific focus was on ligands and receptors of the gonadotropin-releasing hormone (GnRH) superfamily. Members of this superfamily are key in triggering sexual maturation in vertebrates but also regulate reproductive processes and energy homeostasis in invertebrates. Here we show that 3 of the 4 gnrh-like (gnrhl) preprohormone genes are expressed in specific and distinct neuronal clusters in the Platynereis brain. Moreover, ligand–receptor interaction analyses reveal a single Platynereis corazonin receptor (CrzR) to be activated by CRZ1/GnRHL1, CRZ2/GnRHL2, and GnRHL3 (previously classified as AKH1), whereas 2 AKH-type hormone receptors (GnRHR1/AKHR1 and GnRHR2/AKHR2) respond only to a single ligand (GnRH2/GnRHL4). Crz1/gnrhl1 exhibits a particularly strong up-regulation in sexually mature animals, after feeding, and in specific lunar phases. Homozygous crz1/gnrhl1 knockout animals exhibit a significant delay in maturation, reduced growth, and attenuated regeneration. Through a combination of proteomics and gene expression analysis, we identify enzymes involved in carbohydrate metabolism as transcriptional targets of CRZ1/GnRHL1 signaling. Our data suggest that Platynereis CRZ1/GnRHL1 coordinates glycoprotein turnover and energy homeostasis with growth and sexual maturation, integrating both metabolic and developmental demands with the worm’s monthly cycle.

Integrating research on elementary eating behaviors, savoring, mental imagery, mindfulness, cooking, and dinner rituals, a psychological theory of moderate eating is formulated that does not require effortful self-control and giving up on the pleasures of eating. The theory proposes that taste and pleasure can be combined with a relatively objective attitude toward food, resulting in a relatively slow, gentle, and thoughtful manner of eating that enhances satiation. The objective food attitude is thought to result from (a) the accumulation of multiple sensorimotor expectancies and perspectives and (b) a motivational mechanism underlying prosocial behavior, food sharing, and aggression-inhibiting dinner rituals.

Objectives: Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are two syndromes that are caused by the same chromosomal deletion on 15q11.2-q13. Due to methylation patterns, different genes are responsible for the two distinct phenotypes resulting in the disorders. Patients of both disorders exhibit hypotonia in neonatal stage, delay in development and hypopigmentation. Typical features for PWS include hyperphagia, which leads to obesity, the major cause of mortality, and hypogonadism. In AS, patients suffer from a more severe developmental delay, they have a distinctive behaviour that is often described as unnaturally happy, and a tendency for epileptic seizures. For both syndromes, we identified and visualised molecular downstream pathways of the deleted genes that could give insight on the development of the clinical features. Methods: This was done by consulting literature, genome browsers and pathway databases to identify molecular interactions and to construct downstream pathways. Results: A pathway visualisation was created and uploaded to the open pathway database WikiPathways covering all molecular pathways that were found. Conclusions: The visualisation of the downstream pathways of PWS- and AS-deleted genes shows that some of the typical symptoms are caused by multiple genes and reveals critical gaps in the current knowledge.

Aim To assess 1) the prevalence of children and adolescents with type 1 diabetes (T1D) changing from low-risk into borderline-high-risk lipid levels or from borderline-high-risk into high-risk lipid levels (‘lose track of lipids’) and 2) the power of a risk score including the determinants HbA1c, body mass index (BMI), gender, age, diabetes duration and ethnicity in predicting which patients lose track of lipids. Methods 651 children and adolescents with T1D were included in this longitudinal retrospective cohort study. Lipid dynamics and the impact of the risk score on losing track of lipids were evaluated. Kaplan-Meier analysis was used to estimate screening intervals. Results 31–43% percent of the patients had lost track of one or more lipids at the next lipid measurement. This happened more frequently in patients with a low-risk lipid level at start. Depending on the lipid parameter, 5% of patients with low-risk lipid levels lost track of lipids after 13–23 months. The risk score based on concomitant information on the determinants was moderately able to predict which patients would lose track of lipids on the short term. Conclusions A considerable number of children and adolescents with T1D loses track of lipids and does so within a 2-year screening interval. The predictive power of a risk score including age, BMI, gender, HbA1c, diabetes duration and ethnicity is only moderate. Future research should focus on another approach to the determinants used in this study or other determinants predictive of losing track of lipids on the short term.

Summary Background Many patients with type 2 diabetes do not achieve sustained diabetes remission after metabolic (bariatric) surgery for the treatment of obesity. Liraglutide, a glucagon-like peptide-1 analogue, improves glycaemic control and reduces bodyweight in patients with type 2 diabetes. Our aim was to assess the safety and efficacy of liraglutide 1·8 mg in patients with persistent or recurrent type 2 diabetes after metabolic surgery. Methods In the GRAVITAS randomised double-blind, placebo-controlled trial, we enrolled adults who had undergone Roux-en-Y gastric bypass or vertical sleeve gastrectomy and had persistent or recurrent type 2 diabetes with HbA1c levels higher than 48 mmol/mol (6·5%) at least 1 year after surgery from five hospitals in London, UK. Participants were randomly assigned (2:1) via a computer-generated sequence to either subcutaneous liraglutide 1·8 mg once daily or placebo, both given together with a reduced-calorie diet, aiming for a 500 kcal per day deficit from baseline energy intake, and increased physical activity. The primary outcome was the change in HbA1c from baseline to the end of the study period at 26 weeks, assessed in patients who completed the trial. Safety was assessed in the safety analysis population, consisting of all participants who received either liraglutide or placebo. This trial is registered with EudraCT, number 2014-003923-23, and the ISRCTN registry, number ISRCTN13643081. Findings Between Jan 29, 2016, and May 2, 2018, we assigned 80 patients to receive either liraglutide (n=53) or placebo (n=27). 71 (89%) participants completed the study and were included in the principal complete-cases analysis. In a multivariable linear regression analysis, with baseline HbA1c levels and surgery type as covariates, liraglutide treatment was associated with a difference of −13·3 mmol/mol (−1·22%, 95% CI −19·7 to −7·0; p=0·0001) in HbA1c change from baseline to 26 weeks, compared with placebo. Type of surgery had no significant effect on the outcome. 24 (45%) of 53 patients assigned to liraglutide and 11 (41%) of 27 assigned to placebo reported adverse effects: these were mainly gastrointestinal and in line with previous experience with liraglutide. There was one death during the study in a patient assigned to the placebo group, which was considered unrelated to study treatment. Interpretation These findings support the use of adjunctive liraglutide treatment in patients with persistent or recurrent type 2 diabetes after metabolic surgery. Funding JP Moulton Foundation.

Aim: Urbanized environments may stimulate unhealthy food choices and stress. Several theories explain that exposure to green nature can counter these stress effects. Since we spend most time indoors, integrating nature in the interior could be a promising health promotion tool. Hence, we tested whether the beneficial effect of nature for stress recovery is also present in indoor settings via the use of plants or green colors, and whether it is applicable on eating behavior as a new outcome. Methods: The 92 participants (18-30y, 16% men) were divided into four groups. Each viewed a 6-min slideshow with room pictures containing either green plants, green objects, greyscale plants or greyscale objects to allow distinction between color- and plant-effects. Group differences were tested for the perceived restorativeness scale, psychological recovery and eating behavior. To allow psychological recovery testing, participants were exposed to a stressor before the picture slideshow via the Trier Social Stress Test. The change of self-reports (stress, positive and negative affect) and psychophysiology (heart rate and vagal-induced heart rate variability RMSSD) post-slideshow versus pre-slideshow was checked. Eating behavior outcomes included change in hunger, craving, and food choice (for fruits, vegetables and snacks). Results: From the four picture sets, the green plants pictures were reported as most mentally restorative and appeared most beneficial for post-stressor recovery of positive affect, but not for negative affect or stress recovery. The green plants group also had higher preference for vegetables and lower preference or craving for (unhealthy) snacks. Those significant group differences were mainly due to the presence of plants and only occasionally due to the green color. Conclusion: Indoor green plant pictures were associated with higher mental restorativeness and healthier food choices. Integrating plants in the interior seems to be a relevant health promotion approach, while applying green colors seems less relevant.

BackgroundThere is a growing consensus that sugar consumption should be reduced and the naturally occurring, low-calorie sweeteners xylitol and erythritol are gaining popularity as substitutes, but their effect on brain circuitry regulating appetite is unknown.AimThe study’s objective was to examine the effects of the two sweeteners on cerebral blood flow (rCBF) and resting functional connectivity in brain networks involved in appetite regulation, and test whether these effects are related to gut hormone release.MethodsThe study was performed as a randomized, double-blind, placebo-controlled, cross-over trial. Twenty volunteers received intragastric (ig) loads of 50g xylitol, 75g erythritol, 75g glucose dissolved in 300mL tap water or 300mL tap water. Resting perfusion and blood oxygenation level-dependent data were acquired to assess rCBF and functional connectivity. Blood samples were collected for determination of CCK, PYY, insulin and glucose.ResultsWe found: (i) xylitol, but not erythritol, increased rCBF in the hypothalamus, whereas glucose had the opposite effect; (ii) graph analysis of resting functional connectivity revealed a complex pattern of similarities and differences in brain network properties following xylitol, erythritol, and glucose; (iii) erythritol and xylitol induced a rise in CCK and PYY, (iv) erythritol had no and xylitol only minimal effects on glucose and insulin.ConclusionXylitol and erythritol have a unique combination of properties: no calories, virtually no effect on glucose and insulin while promoting the release of gut hormones, and impacting appetite-regulating neurocircuitry consisting of both similarities and differences with glucose. Background: There is a growing consensus that sugar consumption should be reduced and the naturally occurring, low-calorie sweeteners xylitol and erythritol are gaining popularity as substitutes, but their effect on brain circuitry regulating appetite is unknown. Aim: The study’s objective was to examine the effects of the two sweeteners on cerebral blood flow (rCBF) and resting functional connectivity in brain networks involved in appetite regulation, and test whether these effects are related to gut hormone release. Methods: The study was performed as a randomized, double-blind, placebo-controlled, cross-over trial. Twenty volunteers received intragastric (ig) loads of 50g xylitol, 75g erythritol, 75g glucose dissolved in 300mL tap water or 300mL tap water. Resting perfusion and blood oxygenation level-dependent data were acquired to assess rCBF and functional connectivity. Blood samples were collected for determination of CCK, PYY, insulin and glucose. Results: We found: (i) xylitol, but not erythritol, increased rCBF in the hypothalamus, whereas glucose had the opposite effect; (ii) graph analysis of resting functional connectivity revealed a complex pattern of similarities and differences in brain network properties following xylitol, erythritol, and glucose; (iii) erythritol and xylitol induced a rise in CCK and PYY, (iv) erythritol had no and xylitol only minimal effects on glucose and insulin. Conclusion: Xylitol and erythritol have a unique combination of properties: no calories, virtually no effect on glucose and insulin while promoting the release of gut hormones, and impacting appetite-regulating neurocircuitry consisting of both similarities and differences with glucose.

Caenorhabditiselegans (C. elegans) has gained importance as a model for studying host-microbiota interactions and bacterial infections related to human pathogens. Assessing the fate of ingested bacteria in the worm’s intestine is therefore of great interest, in particular with respect to normal bacterial digestion or intestinal colonization by pathogens. Here, we report an in vivo study of bacteria in the gut of C. elegans. We take advantage of a polydimethylsiloxane (PDMS) microfluidic device enabling passive immobilization of adult worms under physiological conditions. Non-pathogenic Escherichia coli (E. coli) bacteria expressing either pH-sensitive or pH-insensitive fluorescence reporters as well as fluorescently marked indigestible microbeads were used for the different assays. Dynamic fluorescence patterns of the bacterial load in the worm gut were conveniently monitored by time-lapse imaging. Cyclic motion of the bacterial load due to peristaltic activity of the gut was observed and biochemical digestion of E. coli was characterized by high-resolution fluorescence imaging of the worm’s intestine. We could discriminate between individual intact bacteria and diffuse signals related to disrupted bacteria that can be digested. From the decay of the diffuse fluorescent signal, we determined a digestion time constant of 14 ± 4 s. In order to evaluate the possibility to perform infection assays with our platform, immobilized C. elegans worms were fed pathogenic Mycobacterium marinum (M. marinum) bacteria. We analyzed bacterial fate and accumulation in the gut of N2 worms and mitochondrial stress response in a hsp-6::gfp mutant.

This systematic review examined the impact of exercise training interventions on energy intake (EI) and appetite control in adults with overweight/obesity (>= 18 years including older adults). Articles were searched up to October 2019. Changes in EI, fasting appetite sensations, and eating behavior traits were examined with random effects meta-analysis, and other outcomes were synthesized qualitatively. Forty-eight articles were included (median [range] BMI = 30.6 [27.0-38.4] kg/m(2)). Study quality was rated as poor, fair, and good in 39, seven, and two studies, respectively. Daily EI was assessed objectively (N = 4), by self-report (N = 22), with a combination of the two (N = 4) or calculated from doubly labeled water (N = 1). In studies rated fair/good, no significant changes in pre-post daily EI were found and a small but negligible (SMD < 0.20) postintervention difference when compared with no-exercise control groups was observed (five study arms; MD = 102 [1, 203] kcal). There were negligible-to-small pre-post increases in fasting hunger and dietary restraint, decrease in disinhibition, and some positive changes in satiety and food reward/preferences. Within the limitations imposed by the quality of the included studies, exercise training (median duration of 12 weeks) leads to a small increase in fasting hunger and a small change in average EI only in studies rated fair/good. Exercise training may also reduce the susceptibility to overconsumption (PROSPERO: CRD42019157823).

Macronutrients in the gastrointestinal (GI) lumen are able to activate "intestinal brakes", feedback mechanisms on proximal GI motility and secretion including appetite and energy intake. In this review, we provide a detailed overview of the current evidence with respect to four questions: (1) are regional differences (duodenum, jejunum, ileum) present in the intestinal luminal nutrient modulation of appetite and energy intake? (2) is this "intestinal brake" effect macronutrient specific? (3) is this "intestinal brake" effect maintained during repetitive activation? (4) can the "intestinal brake" effect be activated via non-caloric tastants? Recent evidence indicates that: (1) regional differences exist in the intestinal modulation of appetite and energy intake with a proximal to distal gradient for inhibition of energy intake: ileum and jejunum > duodenum at low but not at high caloric infusion rates. (2) the "intestinal brake" effect on appetite and energy appears not to be macronutrient specific. At equi-caloric amounts, the inhibition on energy intake and appetite is in the same range for fat, protein and carbohydrate. (3) data on repetitive ileal brake activation are scarce because of the need for prolonged intestinal intubation. During repetitive activation of the ileal brake for up to 4 days, no adaptation was observed but overall the inhibitory effect on energy intake was small. (4) the concept of influencing energy intake by intra-intestinal delivery of non-caloric tastants is intriguing. Among tastants, the bitter compounds appear to be more effective in influencing energy intake. Energy intake decreases modestly after post-oral delivery of bitter tastants or a combination of tastants (bitter, sweet and umami). Intestinal brake activation provides an interesting concept for preventive and therapeutic approaches in weight management strategies.

Food variety, complexity, and portion size each influence food choice and consumption, but their relative importance is poorly understood. In an online discrete choice-experiment, we investigated the relative importance of variety, complexity, and portion size in consumer preferences by systematically varying ice cream offerings. Complexity was defined as the presence of different components within a scoop (e.g., chunks or flavors), while variety was defined as combinations of ice cream scoops that differ in flavor and/or texture. A choice-based conjoint questionnaire with two sections was presented to 498 Dutch (50.8% females) and 502 American (52.6% females) consumers aged between 18 and 65 years. Section 1 tested the relative importance of complexity and variety in consumer preferences, while Section 2 tested the relative importance of variety and portion size in preferences. Participants chose their preferred option when presented with various ice cream options showing different levels of variety and complexity (Section 1), or different levels of variety and portion sizes (Section 2). Across countries, variety was a stronger driver of ice cream preference than complexity, but the most preferred ice cream options were both varied and complex. Further, across countries, flavor was more important than portion size, and again a variety of flavors was the most preferred. Finally, American participants overall preferred larger portion sizes than did Dutch participants. These data indicate variety is a key determinant of food preference, at least within the context of this study, for consumers in both the Netherlands and the United States.

The interplay between external auditory cues in the eating environment and cognitive processes, such as distraction, may influence food intake, but how and the degree to which they do is unclear. We report an experiment designed to investigate the effects of different sonic atmospheres on meal duration, food intake and evaluations, and responses to the sonic eating environment. In a quasi-naturalistic cafeteria setting, participants (N = 248) were eating a lunch meal whilst being in one of four conditions: slow music, fast music, cafeteria noise, and silence. The results revealed that participants eating their lunch while exposed to some kind of background sound spent more time on their meal than those eating in silence. In terms of music tempo, slow music prolonged meal duration compared to fast music, but did not lead to increased intake. The appropriateness and liking of the sonic atmosphere were positively correlated with the overall pleasantness of the eating experience and liking of the food. The findings provide support for existing evidence documenting the importance of ambient sound in relation to food experiences and provide further insights into how individuals perceive and respond to sonic meal environments. Results are discussed in terms of recommendations for future design of eating environments in different contexts.

Glutaric aciduria type I (GA-I, OMIM # 231670) is an inborn error of metabolism caused by a deficiency of glutaryl-CoA dehydrogenase (GCDH). Patients develop acute encephalopathic crises (AEC) with striatal injury most often triggered by catabolic stress. The pathophysiology of GA-I, particularly in brain, is still not fully understood. We generated the first knock-in rat model for GA-I by introduction of the mutation p.R411W, the rat sequence homologue of the most common Caucasian mutation p.R402W, into the Gcdh gene of Sprague Dawley rats by CRISPR/CAS9 technology. Homozygous Gcdhki/ki rats revealed a high excretor phenotype, but did not present any signs of AEC under normal diet (ND). Exposure to a high lysine diet (HLD, 4.7%) after weaning resulted in clinical and biochemical signs of AEC. A significant increase of plasmatic ammonium concentrations was found in Gcdhki/ki rats under HLD, accompanied by a decrease of urea concentrations and a concomitant increase of arginine excretion. This might indicate an inhibition of the urea cycle. Gcdhki/ki rats exposed to HLD showed highly diminished food intake resulting in severely decreased weight gain and moderate reduction of body mass index (BMI). This constellation suggests a loss of appetite. Under HLD, pipecolic acid increased significantly in cerebral and extra-cerebral liquids and tissues of Gcdhki/ki rats, but not in WT rats. It seems that Gcdhki/ki rats under HLD activate the pipecolate pathway for lysine degradation. Gcdhki/ki rat brains revealed depletion of free carnitine, microglial activation, astroglyosis, astrocytic death by apoptosis, increased vacuole numbers, impaired OXPHOS activities and neuronal damage. Under HLD, Gcdhki/ki rats showed imbalance of intra-and extracellular creatine concentrations and indirect signs of an intracerebral ammonium accumulation. We successfully created the first rat model for GA-I. Characterization of this Gcdhki/ki strain confirmed that it is a suitable model not only for the study of pathophysiological processes, but also for the development of new ther-apeutic interventions. We further brought up interesting new insights into the pathophysiology of GA-I in brain and periphery., (c) 2021 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/).

Objective To determine the acute effect of fasted and fed exercise on energy intake, energy expenditure, subjective hunger and gastrointestinal hormone release. Methods CENTRAL, Embase, MEDLINE, PsycInfo, PubMed, Scopus and Web of Science databases were searched to identify randomised, crossover studies in healthy individuals that compared the following interventions: (i) fasted exercise with a standardised post-exercise meal [FastEx + Meal], (ii) fasted exercise without a standardised post-exercise meal [FastEx + NoMeal], (iii) fed exercise with a standardised post-exercise meal [FedEx + Meal], (iv) fed exercise without a standardised post-exercise meal [FedEx + NoMeal]. Studies must have measured ad libitum meal energy intake, within-lab energy intake, 24-h energy intake, energy expenditure, subjective hunger, acyl-ghrelin, peptide YY, and/or glucagon-like peptide 1. Random-effect network meta-analyses were performed for outcomes containing ≥5 studies. Results 17 published articles (23 studies) were identified. Ad libitum meal energy intake was significantly lower during FedEx + Meal compared to FedEx + NoMeal (MD: −489 kJ; 95% CI, −898 to −80 kJ; P = 0.019). Within-lab energy intake was significantly lower during FastEx + NoMeal compared to FedEx + NoMeal (MD: −1326 kJ; 95% CI, −2102 to −550 kJ; P = 0.001). Similarly, 24-h energy intake following FastEx + NoMeal was significantly lower than FedEx + NoMeal (MD: −2095 kJ; 95% CI, −3910 kJ to −280 kJ; P = 0.024). Energy expenditure was however significantly lower during FastEx + NoMeal compared to FedEx+NoMeal (MD: −0.67 kJ/min; 95% CI, −1.10 to −0.23 kJ/min; P = 0.003). Subjective hunger was significantly higher during FastEx + Meal (MD: 13 mm; 95% CI, 5–21 mm; P = 0.001) and FastEx + NoMeal (MD: 23 mm; 95% CI, 16–30 mm; P Conclusion FastEx + NoMeal appears to be the most effective strategy to produce a short-term decrease in energy intake, but also results in increased hunger and lowered energy expenditure. Concerns regarding experimental design however lower the confidence in these findings, necessitating future research to rectify these issues when investigating exercise meal timing and energy balance. PROSPERO registration number CRD42020208041. Key points Fed exercise with a standardised post-exercise meal resulted in the lowest energy intake at the ad libitum meal served following exercise completion. Fasted exercise without a standardised post-exercise meal resulted in the lowest within-lab and 24-h energy intake, but also produced the lowest energy expenditure and highest hunger. Methodological issues lower the confidence in these findings and necessitate future work to address identified problems

Natural abundances of stable nitrogen and carbon isotopes (δ15N and δ13C) can vary with both dietary intake and metabolic (specifically catabolic) state. In low-income countries, weaning is a period of dietary transition from milk to plant-based foods and a high-risk period for malnutrition. We explored how diet and malnutrition impact hair δ15N and δ13C in young children by an observational, cross-sectional study in Cox’s Bazar District, Bangladesh [255 children, 6–59 months with 19.6% wasted (7.1% severely) and 36% stunted (9.8% severely)]. Hair δ15N and δ13C exhibited exponential decreases with age, with the loss of one trophic level (3.3‰ and 0.8‰, respectively) from 6 to 48 months, which we associate with the shift from exclusive breastfeeding to complete weaning. After adjustment for age and breastfeeding status, hair isotopic values were unaffected by wasting but lower in severe stunting (−0.45‰ to −0.6‰, P 15N and δ13C values in severely stunted children that likely indicate chronic exposure to diets low in animal products.

Understanding the mechanisms of hunger, satiety and how nutrients affect appetite control is important for successful weight management across the lifecourse. The primary aim of this study was to describe acute appetite control across the lifecourse, comparing age groups (children, adolescents, adults, elderly), weight categories, genders and European sites (Scotland and Greece). Participants (n = 391) consumed four test drinks, varying in composition (15% (normal protein, NP) and 30% (high protein, HP) of energy from protein) and quantity (based on 100% basal metabolic rate (BMR) and 140% BMR), on four separate days in a double-blind randomized controlled study. Ad libitum energy intake (EI), subjective appetite and biomarkers of appetite and metabolism (adults and elderly only) were measured. The adults&rsquo, appetite was significantly greater than that of the elderly across all drink types (p &lt, 0.004) and in response to drink quantities (p &lt, 0.001). There were no significant differences in EI between age groups, weight categories, genders or sites. Concentrations of glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) were significantly greater in the elderly than the adults (p &lt, 0.001). Ghrelin and fasting leptin concentrations differed significantly between weight categories, genders and sites (p &lt, 0.05), while GLP-1 and PYY concentrations differed significantly between genders only (p &lt, 0.05). Compared to NP drinks, HP drinks significantly increased postprandial GLP-1 and PYY (p &lt, 0.001). Advanced age was concomitant with reduced appetite and elevated anorectic hormone release, which may contribute to the development of malnutrition. In addition, appetite hormone concentrations differed between weight categories, genders and geographical locations.

BACKGROUND: Different peripheral pathways are implicated in the regulation of the food ingestion-digestion cycle. METHODS: Narrative review on gastrointestinal mechanisms involved in satiety and hunger signalling. RESULTS: Combined mechano- and chemoreceptors, peripherally released peptide hormones and neural pathways provide feedback to the brain to determine sensations of hunger (increase energy intake) or satiation (cessation of energy intake) and regulate the human metabolism. The gastric accommodation reflex, which consists of a transient relaxation of the proximal stomach during food intake, has been identified as a major determinant of meal volume, through activation of tension-sensitive gastric mechanoreceptors. Motilin, whose release is the trigger of gastric Phase 3, has been identified as the major determinant of return of hunger after a meal. In addition, the release of several peptide hormones such as glucagon-like peptide 1 (GLP-1), cholecystokinin as well as motilin and ghrelin contributes to gut-brain signalling with relevance to control of hunger and satiety. A number of nutrients, such as bitter tastants, as well as pharmacological agents, such as endocannabinoid receptor antagonists and GLP-1 analogues act on these pathways to influence hunger, satiation and food intake. CONCLUSION: Gastrointestinal mechanisms such as gastric accommodation and motilin release are key determinants of satiety and hunger. ispartof: UNITED EUROPEAN GASTROENTEROLOGY JOURNAL vol:9 issue:6 pages:727-734 ispartof: location:England status: published

The bioactive peptides galanin, spexin and kisspeptin have a common ancestral origin and their pathophysiological roles are increasingly the subject of investigation. Evidence suggests that these bioactive peptides play a role in the regulation of metabolism, pancreatic β-cell function, energy homeostasis, mood and behaviour in several species, including zebrafish, rodents and humans. Galanin signalling suppresses insulin secretion in animal models (but not in humans), is potently obesogenic and plays putative roles governing certain evolutionary behaviours and mood modulation. Spexin decreases insulin secretion and has potent anorectic, analgesic, anxiolytic and antidepressive-like effects in animal models. Kisspeptin modulates glucose-stimulated insulin secretion, food intake and/or energy expenditure in animal models and humans. Furthermore, kisspeptin is implicated in the control of reproductive behaviour in animals, modulation of human sexual and emotional brain processing, and has antidepressive and fear-suppressing effects. In addition, galanin-like peptide is a further member of the galaninergic family that plays emerging key roles in metabolism and behaviour. Therapeutic interventions targeting galanin, spexin and/or kisspeptin signalling pathways could therefore contribute to the treatment of conditions ranging from obesity to mood disorders. However, many gaps and controversies exist, which must be addressed before the therapeutic potential of these bioactive peptides can be established. The bioactive peptides galanin, spexin and kisspeptin have a common ancestral origin. This Review summarizes the available evidence on the role of these peptides in the regulation of metabolism, pancreatic β-cell function, energy homeostasis, mood and behaviour.

Purpose Taste receptors are expressed throughout the gastrointestinal tract. The activation of post-oral taste receptors using tastants could provide a non-invasive treatment option in combating the obesity epidemic. The aim of this review was to examine the effect of post-oral delivery of non-caloric tastants on eating behavior reflected by primary outcome energy intake and secondary outcomes GI symptoms and perceptions and potential underlying mechanisms. This review was conducted according to the PRISMA guidelines for systematic reviews. Methods A systematic literature search of the Cochrane, PubMed, Embase, and Medline databases was performed. This systematic review and meta-analysis was registered in the PROSPERO database on 26 February 2020 (ID: CRD42020171182). Two researchers independently screened 11,912 articles and extracted information from 19 articles. If at least two studies investigated the effect of the same taste compound on primary outcome energy intake, a meta-analysis was performed to determine pooled effect sizes. Results Nineteen papers including healthy volunteers were included. In the 19 papers analyzed, effects of various tastants were investigated in healthy volunteers. Most extensively investigated were bitter tastants. The meta-analysis of effects of bitter tastants showed a significant reduction in energy intake of 54.62 kcal (95% CI − 78.54 to − 30.69, p = 0.0014). Conclusions Bitter stimuli are most potent to influence eating behavior. Energy intake decreased after post-oral delivery of bitter tastants. This highlights the potential of a preventive role of bitter tastants in battling the obesity epidemic.

Purpose To compare endocrine responses to intermittent vs continuous enteral nutrition provision during short-term bed rest. Methods Twenty healthy men underwent 7 days of bed rest, during which they were randomized to receive enteral nutrition (47%E as carbohydrate, 34%E as fat, 16%E as protein and 3%E as fibre) in a continuous (CONTINUOUS; n = 10; 24 h day−1 at a constant rate) or intermittent (INTERMITTENT; n = 10; as 4 meals per day separated by 5 h) pattern. Daily plasma samples were taken every morning to assess metabolite/hormone concentrations. Results During bed rest, plasma leptin concentrations were elevated to a lesser extent with INTERMITTENT vs CONTINUOUS (iAUC: 0.42 ± 0.38 vs 0.95 ± 0.48 nmol L−1, respectively; P = 0.014) as were insulin concentrations (interaction effect, P −1 in CONTINUOUS, compared to 94 ± 38 pmol L−1 in INTERMITTENT (P = 0.001). Changes in glucose infusion rate were positively correlated with changes in fasting plasma GLP-1 concentrations (r = 0.44, P = 0.049). Conclusion Intermittent enteral nutrition attenuates the progressive rise in plasma leptin and insulinemia seen with continuous feeding during bed rest, suggesting that continuous feeding increases insulin requirements to maintain euglycemia. This raises the possibility that hepatic insulin sensitivity is impaired to a greater extent with continuous versus intermittent feeding during bed rest. To attenuate endocrine and metabolic changes with enteral feeding, an intermittent feeding strategy may, therefore, be preferable to continuous provision of nutrition. This trial was registered on clinicaltrials.gov as NCT02521025.

Hydroxysteroid 17-beta dehydrogenase 12 (HSD17B12) is suggested to be involved in the elongation of very long chain fatty acids. Previously, we have shown a pivotal role for the enzyme during mouse development. In the present study we generated a conditional Hsd17b12 knockout (HSD17B12cKO) mouse model by breeding mice homozygous for a floxed Hsd17b12 allele with mice expressing the tamoxifen-inducible Cre recombinase at the ROSA26 locus. Gene inactivation was induced by administering tamoxifen to adult mice. The gene inactivation led to a 20% loss of body weight within six days, associated with drastic reduction in both white (83% males, 75% females) and brown (65% males, 60% females) fat, likely due to markedly reduced food and water intake. Furthermore, the knockout mice showed sickness behavior and signs of liver toxicity, specifically microvesicular hepatic steatosis and increased serum alanine aminotransferase (4.6-fold in males, 7.7-fold in females). The hepatic changes were more pronounced in females than males. Pro-inflammatory cytokines, such as interleukin 6 (IL-6), IL-17 and granulocyte-colony stimulating factor were increased in the HSD17B12cKO mice indicating inflammatory response. Serum lipidomics study showed an increase in the amount of dihydroceramides, despite the dramatic overall loss of lipids. In line with the proposed role for HSD17B12 in the fatty acid elongation, we observed accumulation of ceramides, dihydroceramides, hexosylceramides and lactosylceramides with shorter than 18-carbon fatty acid side chains in the serum. The results indicate that HSD17B12 is essential for proper lipid homeostasis, and HSD17B12 deficiency rapidly results in fatal systemic inflammation and lipolysis in adult mice.

Background and AimsThere is this intriguing but not yet well-explored suggestion that highly absorbable sucrose-sweetened drinks might exacerbate hunger by promoting temporal hypoglycemia-like responses already in non-diabetic healthy individuals. This might provide a possible additional explanatory mechanism for previous reported associations between consumption of sugar-sweetened drinks and body weight gain. The current study involves two separate and independently conducted human experiments exploring the effects of two different single-doses of sugar-sweetened beverages on temporal blood glucose nadir and possible related behavioral hypoglycemic-like symptoms in healthy participants.MethodsBy way of two separately conducted between-subjects experiments, effects of 1) a low (29 g) sugar-containing beverage compared to a sweetened zero-energy drink and a milk drink (experiment-1) or 2) a high (80 g) sugar-sweetened beverage compared to a zero-energy and a non-sweetened colored water drink (experiment-2) were measured on changes in blood glucose, behavioral hypoglycemia, appetite and mood.ResultsExperiment-1: The 29 g sucrose containing beverage caused a high (37%) glycemic increase and a smaller response (15%) to the milk drink, which both peaked 30 min after consumption, whereas the sweetened zero-energy drink had very little effect on blood glucose. Regardless of the different magnitude of peak glycemic responses, both the sugar and milk drinks rather equally caused blood glucose concentrations to return to normal and stable baseline values 90 min later. There were no (different) effects of the beverages on behavioral hypoglycemic-like symptoms, appetite or mood. Experiment-2: the 80 g sucrose containing beverage caused a large (72%) glycemic peak response at +30 min after consumption, whereas neither the sweetened zero-energy nor the non-sweetened colored water drink had any meaningful effect on blood glucose. After intake of the 80 g sugar beverage, blood glucose concentrations remained elevated (13%) at +120 min and returned to lower baseline values in the direction of hypoglycemia levels at +165 min. There were no (differential) effects of the beverages on behavioral hypoglycemic symptoms, appetite or mood.ConclusionsThe current findings indicate that instead of a low (29 g) sugar-containing beverage, a high (80 g) sugar-containing beverage caused blood glucose concentrations to fall below baseline values almost reaching hypoglycemia levels at the end of measurements. There were no hypoglycemic-like behavioral symptoms including changes in appetite or mood: at least not at end of measurements +165 min after consumption. Since this might include that in particular consumption of high-glycemic index drinks could still promote symptoms in the longer run, further research is needed to explore possible hypoglycemic-like effects of high dosages of sugar-sweetened beverages across more extended/delayed time measurements.