Nutritional Neuroscience最新文献

Objectives: Obesity is a common public health problem, affecting 2.5 billion adults. Chronic high-fat diet (HFD) exposure, an experimental obesity model, strongly impacts the hypothalamic arcuate nucleus (ARC), a structure vulnerable to dietary-induced inflammation. Extra-virgin olive oil (EVOO) supplementation can be an interesting nutritional strategy to understand and/or treat obesity: EVOO has high nutritional quality, and acts on multiple molecular targets. We investigated EVOO supplementation's impact on metabolic parameters, satiety and hypothalamic inflammation in adult rats exposed to HFD from weaning, considering sex-specific outcomes.

Methods: 21-day-old Wistar rats were allocated into groups: (1) standard chow (SC); (2) SC+EVOO; (3) HFD; (4) HFD + EVOO. EVOO was administered daily by gavage. In adulthood, the behavioral satiety sequence was evaluated. Plasma leptin and ARC inflammatory markers levels were measured by ELISA technique. The immunofluorescence intensity of Toll-like receptor-4 (TLR-4) and ionized calcium-binding adaptor molecule-1 (IBA-1) were measured in the ARC.

Results: Chronic HFD-induced obesity was evidenced in both sexes, with increased body weight, body mass index, fasting blood glucose, caloric efficiency, and plasma leptin levels. EVOO supplementation prevented HFD-induced increase in weight gain and BMI in both sexes. HFD-fed animals had altered satiety. EVOO supplementation decreased immunoreactivity of IBA-1 in the ARC, also attenuates TLR-4 immunoreactivity, interleukin (IL)-6, IL-1β, and tumor necrosis factor-α levels in the ARC of obese animals.

Conclusion: Our results demonstrate that EVOO supplementation seemed promising, improving hypothalamic inflammation in obese animals, therefore might lead to the restoration of adverse metabolic consequences.

Context: Childhood obesity is a pervasive health issue, with sugar consumption implicated not only in its development but also in adverse effects on brain health. While extensive research has explored adult brain processes in response to sweet taste, there is limited understanding of how children's brains activate in similar, contexts.

Method: In this study, 34 children aged 8-12 undent food frequency and sweetness liking assessments before participating in a functional magnetic resonance imaging (fMRI) scan during a gustatory paradigm involving varying sweetness levels. Utilizing independent component analysis (ICA), we examined functional networks engaged during sweet taste perception and after swallowing.

Results: Our study identified distinct brain networks for tasting, swallowing, and a transitional stage linking the two. Children with lower BMI and higher sugar intake showed greater activation in the transition network, suggesting enhanced interoceptive sensitivity.

Conclusion: This novel investigation provides a foundational understanding of how sweetness exposure modulates brain networks in children responding to sucrose solutions, offering valuable insights into the interplay between sugar consumption, childhood obesity, and neural responses.

Objective: The present study investigated the effect of perinatal programming combined with exposure to a western diet on gene expression related to inflammation, neurodegeneration, and synaptic plasticity in the hippocampus of adult rats.

Methods: Male rats from mothers fed either a standard diet or a western diet during gestation and lactation were used. All pups received only the standard chow diet from the 25th postnatal day (PND), and their body weight was analysed. Rats from the two groups fed the maternal diet were then divided on the 195^th PND into four subgroups: two received the standard chow diet, and the others were exposed to the same western diet for two hours over 5 days. Gene expression and biochemical tests were performed on the 200^th PND.

Results: Adult rats submitted to a western diet during pregnancy and lactation showed signs of metabolic programming. In addition, glucose and total protein were found to have increased in the serum. The effect of acute exposure to a western diet is increased cholesterol. The western diet decreased gene expression of inflammatory factors (Il-6, Tnf-α, Nf-κb) and Mapt in the hippocampus. However, the diet stimulation increased Il-6, Tnf-α, Bdnf gene expression and reduced Creb-1 and Trkb expression.

Discussion: Acute exposure to a western diet in adulthood alters pre-translational pathways (Il-6, Tnf-α, Bdnf-Trkb-Creb-1) in the hippocampus of rats previously subjected to early-life western diet, indicating that perinatal programming and later dietary challenges interact to modulate hippocampal plasticity in a time- and diet stimulus-dependent manner.

Objectives: This research was aimed at determining the relationship between compliance with the Mediterranean diet, intuitive eating, and obesity.

Method: This cross-sectional study involved 5240 adults aged 20 to 64 years, from whom data on sociodemographic characteristics, consumption habits, intuitive eating, and anthropometric measurements were collected via an online survey designed using Google Forms. The Intuitive Eating Scale (IES-2) and Mediterranean Diet Adaptation Screener (MEDAS) were also administered to the participants.

Results: Their scores on all the IES-2 and MEDAS subscales were negatively correlated with their body mass indices (BMIs). Of the IES-2 subscales, only reliance on hunger and satiety cues (RHSC) was positively related to the MEDAS scores. The IES-2 subscales RHSC and unconditional permission to eat as well as the MEDAS scores were strong determinants of BMI. The relationship between intuitive eating and BMI was stronger than that between the MEDAS scores and BMI. Intuitive eating and compliance with the Mediterranean diet can positively affect an individual's consumption habits and BMI, ultimately resulting in weight loss, the regulation of body weight, and improved health.

Discussion: These cross-sectional findings suggest a potential mechanism that may partially explain the association between Mediterranean diet adherence, intuitive eating and obesity. However, these results should be interpreted with caution as they do not establish a causal relationship. Randomized clinical trials are needed to confirm this relationship.

Background: Parkinson's disease (PD) is a common neurodegenerative disease, and its pathogenesis may be related to abnormal metabolism of micronutrients.

Method: This study included 316 PD patients who visited the Second Affiliated Hospital of Xinjiang Medical University from January 2021 to December 2023. Patients were divided into two groups: those with both PD and diabetes mellitus(PD-DM group), and those with PD without DM(PD-NDM group). Inductively coupled plasma-mass spectrometry was employed to determine the levels of micronutrients, including calcium (Ca), magnesium (Mg), and iron (Fe), in serum samples. Next, demographic characteristics, clinical parameters, and micronutrient differences were compared between the two groups. Furthermore, the correlation between micronutrients and the progression of PD, as well as motor and non-motor symptoms, was analyzed. Finally, logistic regression was used to investigate the factors influencing PD with DM.

Result: The PD-DM group had higher serum Ca(2.27 ± 0.14 vs 2.22 ± 0.12) and lower Mg (0.83 ± 0.08 vs 0.89 ± 0.06) and Fe (14.28 ± 5.13 vs 16.45 ± 6.81) than the PD-NDM group (P < 0.05). Ca levels were negatively correlated with age of onset, UPDRS-I, and non-motor symptoms. Mg levels correlated with UPDRS score and substantia nigra echo area(P < 0.05). Logistic regression identified high Ca, low Mg, and low Fe as independent predictors of PD with DM (P < 0.05).

Conclusion: Patients with PD and DM exhibit distinct micronutrient metabolic abnormalities, notably higher Ca and lower Mg and Fe levels.

Objectives: Accumulative evidence links MIND diet with a reduced risk of Alzheimer's disease, but the connecting mechanisms remain unclear. We explored whether this dietary patterns and its components was associated with Amyloid beta (Aβ) deposition in dementia-free middle-life individuals.

Methods: 250 participants [65 (58, 73) years, 63.2% women] underwent neurological cognitive assessments and dietary assessment (through four 24-hour dietary recalls). Aβ concentrations were measured in cerebrospinal fluid samples. MIND diet adherence was examined both as a continuous variable and as a distribution-based categorical variable using quartiles (Q1-Q4), with higher quartiles reflecting higher adherence. Multivariate logistic regression analyses were conducted using MIND diet adherence (continuous or quartile-based) as the independent variable and Aβ deposition as the dependent variable.

Results: Compared to lower MIND adherence (Q1), higher adherence (Q4) was associated with less pathological Aβ concentrations (OR = 0.431, 95% CI: 0.195-0.950, p = 0.037). Each 1-SD increase in adherence was associated with a 26% reduction in the odds of having pathological Aβ concentrations (OR = 0.736, 95% CI: 0.563-0.962, p = 0.025). Among MIND diet components, only leafy vegetables intake showed a significant association with Aβ burden (OR = 0.519, 95% CI: 0.277-0.972, p = 0.040, q = 0.485).

Discussion: These cross-sectional findings suggest a potential mechanism that may partially explain the association between MIND diet adherence and cognitive function. Ηowever, they should be interpreted with caution, as the study sample may not be representative of community-based populations. Randomized clinical trials are needed to confirm this relationship.

Introduction: Limited research has examined the combined effects of dietary sodium intake on depressive symptoms. The objective of this study was to evaluate the association between frequently adding salt to food and depressive symptoms, as well as the underlying mechanisms.

Methods: A total of 15,471 adults from the 2007 to 2018 National Health and Nutrition Examination Survey (NHANES) were included in the study. Depressive symptoms were defined as a total score of ≥10 on the Patient's Health Questionnaire (PHQ-9). Participants self-reported the frequency of adding salt to their foods, categorized as never or rarely, sometimes, usually, or always. Multivariable logistic regression analyses were conducted to evaluate the association between frequently adding salt to food and risk of depression. Bidirectional Mendelian randomization (MR) analysis was employed to investigate the potential causal relationship.

Results: In the multivariate model, a significant positive association was observed between frequently adding salt to food and the risk of depression. After adjusting for covariates, a higher self-reported frequency of adding salt to food was significantly associated with an elevated risk of depression (OR: 1.26; 95% CI: 1.16-1.38; P < 0.001). Furthermore, MR analysis indicated that higher salt intake was causally linked to an 11% increased risk of depressive symptoms and 28% increased risk of major depressive disorder.

Conclusions: Frequently adding salt to food is positively associated with depression. These findings suggest that reducing the frequency of adding salt to foods at the table may be an effective strategy to lower risk of depression in the general population.

Objective: Targeting the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway represents a promising therapeutic strategy for multiple sclerosis (MS). However, approved drugs like dimethyl fumarate (DMF) often induce severe side effects. This study investigated the natural flavonoid luteolin (LUT) as a potential dietary supplement alternative to DMF in a cuprizone (CPZ)-induced demyelination mouse model of MS.Methods: Mice were randomly assigned to five groups: control, CPZ model, CPZ+DMF (15 mg/kg), CPZ+LUT (25 mg/kg), and CPZ+LUT (50 mg/kg). Motor coordination and spatial memory were assessed via rotarod and Morris water maze tests. Myelin integrity was evaluated by Luxol fast blue staining and myelin basic protein (MBP) immunofluorescence/Western blot. Oxidative stress was measured by assessing superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) levels. Nrf2 pathway activation was analyzed by nuclear translocation of Nrf2 and expression of downstream proteins (HO-1, NQO1) via Western blot. Molecular docking simulated interactions between compounds and the Keap1 protein.Results: LUT treatment significantly restored motor coordination and spatial memory, with efficacy comparable to DMF. It promoted MBP expression, attenuated oxidative damage by modulating SOD, CAT, GSH-Px, and MDA levels, and preserved myelin integrity. Furthermore, LUT markedly facilitated Nrf2 nuclear translocation and upregulated HO-1 and NQO1 expression. Molecular docking indicated that LUT possessed stronger binding affinity to the target protein Keap1 and a lower potential for off-target toxicity compared to the primary active metabolite of DMF.Conclusion: Luteolin exerts significant neuroprotective effects, primarily via Nrf2 pathway activation, with efficacy parallel to DMF but a superior safety profile. These findings identify LUT as a promising natural compound, bridging functional foods and MS therapy, and provide a foundation for developing LUT-enriched dietary regimens as an adjunct treatment strategy for MS.

Objectives: This study, using the Youth Risk Behavior Surveillance Survey 2021 (YRBS 2021) focused on exploring the sex differences in the associations between sugar-sweetened beverages (SSB) (soda and sports drinks) and cognitive difficulties (memory, concentration, and decision-making); as well as the mediation effect of sleep on the associations.

Methods: 8,229 from the YRBS 2021 data were included in the study. SSB consumption was treated as a continuous variable with various levels of frequencies, as well as coded as a categorical variable with three levels (non-drinker, non-daily drinker, and daily drinker). Cognitive difficulty was a binary variable. Sleep was treated as a continuous variable with durations of hours. Regression models and bootstrapping methods were used in this study.

Results: Compared to non-drinkers, increased odds of cognitive difficulties were observed in girls (OR: 1.49; 95% CI: 1.18-1.87) and boys soda daily-drinkers (OR: 1.53; 95% CI: 1.24-1.87); and girls sports-drink daily-drinkers (OR: 1.39; 95% CI: 1.08-1.80). Sleep, as a mediator, affected the associations of overall SSB consumption (βs = .01; p < .001) and soda consumption (βs = .02; p < .001) with cognitive difficulties among boys and girls; as well as the path between sports drink consumption and cognitive difficulties in boys (β = .01; p < .001).

Discussion: SSB consumption is associated with both shorter sleep duration and greater cognitive difficulties among adolescents, with sleep acting as a meaningful pathway linking consumption to cognitive functioning. Reducing SSB intake and promoting healthier behaviors may improve both sleep and cognitive health in youth.

Objective: Epilepsy treatments often lead to vitamin D (VitD) deficiency. Although vitamin D₃ (VitD₃) has been shown to reduce epileptic symptoms by 43%, its preventive effects remain unclear. This study investigated the potential of VitD pretreatment in two common acute epilepsy mouse models and explored its effects on seizure severity, latency, and molecular mechanisms involving calcium-sensing receptor (CaSR), phosphatase and tensin homolog (PTEN), and autophagy.

Methods: Mice were randomly divided into nine groups (n = 15). VitD or vehicle was administered 40 min before pentylenetetrazole (PTZ) or kainic acid (KA) given intraperitoneal injection (i.p). Seizure behavior and electroencephalograms (EEGs) were recorded for 60 min. After 24 h, hippocampal tissues were analyzed histologically and assessed for expression of autophagy-related proteins, CaSR, and PTEN.

Results: Both PTZ and KA induced acute seizures (Racine Grade IV+), with corresponding high-amplitude EEG spikes, neuronal damage, and mossy fiber sprouting. CaSR and autophagy markers were upregulated, while PTEN was downregulated, especially in the KA group. VitD pretreatment reduced seizure frequency, prolonged latency, alleviated hippocampal damage, downregulated CaSR and autophagy markers, and upregulated PTEN. These effects were milder than those of valproate. Combined VitD and Oroxin B treatment further improved outcomes.

Conclusions: (1) PTZ-induced seizures increased CaSR and decreased PTEN, triggering autophagy and worsening symptoms. (2) KA-induced epilepsy caused more severe damage with stronger autophagy activation. (3) VitD pretreatment mitigated seizures by modulating CaSR, PTEN, and autophagy, showing greater efficacy in the PTZ model.