Chronic stress can lead to serious health problems, including elevated blood glucose, intestinal dysbiosis, villous shortening, decreased enzyme activity and hepatic steatosis. Here, we investigate the protective effects of the magnesium-L-theanine (Mg-T) combination on chronic variable stress (CVS)-induced liver and intestinal damage. Fifty-six rats were divided into two groups: normal and stressed, and supplemented with different doses of Mg-T (0, 100, 200 and 400 mg/kg). The results showed that CVS-treated rats had reduced body weight, serum insulin levels, magnesium levels, intestinal barrier proteins and nutrient transporters. However, Mg-T supplementation improved these parameters in a dose-dependent manner. Mg-T treatment reduced CVS-induced glucose, corticosterone and triglyceride levels while alleviating liver and intestinal damage. Histological analysis revealed that Mg-T alleviated CVS-induced intestinal damage, characterised by villus shortening, reduced crypt depth and inflammation. CVS-induced increases in hepatic triglycerides and lipogenic markers (SREBF1, FASN) were attenuated by Mg-T supplementation, while metabolic regulators such as PPARγ and SIRT-1 were upregulated. Moreover, Mg-T restored the expression of intestinal barrier proteins (Claudin-1, Occludin, ZO-1) and mucosal protein (MUC-2). CVS treatment reduced the expression of nutrient transporters (SGLT1, GLUT2) and amino acid carriers; however, Mg-T supplementation increased the protein levels of these markers. Our data demonstrate that Mg-T has significant protective effects against CVS-induced metabolic, hepatic and intestinal disturbances, highlighting its potential as a therapeutic intervention for managing chronic stress-related health problems.

This study has investigated the relationship between the gut microbiota composition and the growth performance in pigs from birth to the finishing stage, focusing on nutrient metabolism. Of fifty-nine crossbred pigs [(Landrace × Large Yorkshire) × Duroc] from seven sows, individuals with high and low daily gain (DG) were assigned to high DG (HDG, n 11) and low DG (LDG, n 8) groups. Faecal samples collected at weaning (21 d), growing (95–106 d) and finishing (136–152 d) stages were analysed for amino acids, SCFA and microbial composition using 16S rRNA sequencing. Although birth and weaning weights were similar in both groups, the HDG group had significantly higher weights in the growing and finishing stages (P < 0·01). The microbial composition of the LDG group revealed a higher abundance of f_Lachnospiraceae;__ at weaning (P < 0·05), whereas the HDG group contained a higher abundance of g_Streptococcus and g_Prevotella 7 at the finishing stage (P < 0·05). Functional analysis revealed increased amino acid metabolism in the HDG group at the finishing stage (P < 0·05). During the growing stage, total free faecal amino acid content was low in the HDG group (P < 0·05); at weaning, levels of isobutyric and isovaleric acids, key amino acid fermentation products (P < 0·05, P < 0·01), were higher. These findings indicate growth stage-specific differences in the gut microbiota and metabolic profiles between groups with different growth performance, suggesting that microbial and metabolic characteristics may influence growth performance.

This study aimed to investigate the effects of caffeic acid (CA) on the inflammatory response induced by hydrogen peroxide (H2O2) in porcine small intestinal epithelial cells (IPEC-J2 cells) and to elucidate the potential molecular mechanisms involved. Firstly, we treated IPEC-J2 cells with different concentrations of H2O2 to establish the inflammation model caused by oxidative stress. Subsequently, we treated IPEC-J2 cells with CA and/or H2O2 to investigate the effect of CA on the inflammatory response of IPEC-J2 cells induced by H2O2. In addition, IPEC-J2 cells were treated with a nuclear factor kappa-B (NF-κB) inhibitor and a Nucleotide-binding Oligomerization Domain (NOD)-like receptor thermal protein domain associated protein 3 (NLRP3) inhibitor, so as to investigate the molecular mechanism by which CA alleviates H2O2-induced damage in porcine intestinal epithelial cells. The changes in cell morphology, intestinal epithelial cell damage and the expression of genes related to the NF-κB/NLRP3 signalling axis were examined. The results showed that CA attenuated H2O2-induced intestinal epithelial cell injury, and the mechanism may be related to the inhibition of NF-κB-mediated NLRP3 inflammasome activation. These findings were expected to provide a theoretical basis for more reasonable and effective application of CA, and provide new ideas for nutritional regulation measures to alleviate intestinal inflammation in piglets.

There is a lack of knowledge available on how cats adjust their macronutrient partitioning due to the consumption of single-macronutrient meals. The objective of this study was to evaluate consumption of a single meal of ingredients that contained foods of strictly carbohydrates (CHO), fat (FAT) or protein (PRO), on energy expenditure (EE) and macronutrient metabolism in cats. Ten domestic shorthair adult cats (1·9 years; 4·12 kg) were fed 22–24 g of chicken fat (FAT), 56–62 g of whey protein solution (PRO) or 54–56 g of cornstarch solution (CHO) for a single day in a randomised complete block design. Indirect calorimetry was conducted for 24 h post-feeding. Mean average EE over 24 h was highest in cats fed PRO (44 kcal/kg BW) and FAT (43 kcal/kg BW) compared with that in cats fed CHO (42 kcal/kg BW; P < 0·01). During 0 to 4 h, cats fed FAT had greater EE (49 kcal/kg BW), suggesting that cats respond to oxidising more dietary fat over protein in the early postprandial stage. Mean 24 h respiratory quotient (RQ) was greatest for cats fed CHO (0·76) followed by PRO (0·75) and FAT (0·74; P < 0·05). During 4 to 8 h, the RQ of cats fed PRO was the greatest (0·77), suggesting that cats initially increase gluconeogenesis from amino acids for subsequent glucose oxidation. In comparison to omnivores and herbivores, obligate carnivores have unique responses to single macronutrient intake, where they apparently generate energy from carbohydrate metabolism and rely more on gluconeogenic precursors.

This study examined the efficacy of a probiotic in reducing depressive symptom severity in people with subthreshold depression. In a double-blind, randomised, placebo-controlled trial, a probiotic (1 × 10^9 live cells per strain: Limosilactobacillus fermentum LF16 (DSM26956), Lacticaseibacillus rhamnosus LR06 (DSM21981), Lactiplantibacillus plantarum LP01 (LMG P-21021) and Bifidobacterium longum 04 (DSM23233)) or placebo was taken daily for 12 weeks. Data were collected at baseline, 6 and 12 weeks including psychological symptom severity (Beck Depression Inventory, BDI; Patient Health Questionnaire, PHQ; Hospital Anxiety Depression Scale, HADS; and Depression Anxiety and Stress Scale, DASS). Biomarkers of glycaemia, inflammation (high-sensitivity C-reactive protein, hs-CRP), antioxidant status (total glutathione (GSH)) and stress (cortisol awakening response, CAR) were also measured. Thirty-nine participants (nineteen probiotic; twenty placebo) were enrolled. There were no significant between-group differences in the examined psychological symptom severity scores, despite certain significant within-group changes observed in both groups from baseline to 6 and/or 12 weeks of follow-up. Regarding biomarkers, the probiotic group showed reduced hs-CRP (–1520; 95 % CI –273·7, −2766·2 ng/dl) and CAR (–0·28; 95 % CI −0·05, −0·51 μg/dl) at 12 weeks, but increased total GSH (3·9; 95 % CI 0·1, 7·5 ng/dl) at 6 weeks, compared with the placebo. The current study reported favourable decreases in depressive symptoms in both groups. Although the within-group changes observed in the probiotic group were supported by favourable inflammatory, antioxidant status and stress biomarker changes compared with the placebo, further research is required to shed more light on the role of gut microbiota modulation on emotional regulation.

Polycystic ovary syndrome (PCOS) is a common hormonal disorder in women of reproductive age, associated with increased risks of metabolic disorders, depression and reduced quality of life. This study examined the impact of the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet on mental health, PCOS-related quality of life (PCOSQ), anthropometric indices, hirsutism, and metabolic/hormonal parameters in women with PCOS. Total of 52 women with PCOS, aged between 18 and 45 years, were randomly assigned to either the low calorie MIND diet group or the control group. Anthropometric data, depression and anxiety scores, serum levels of gonadotropins (luteinizing hormone [LH], follicle-stimulating hormone [FSH]), PCOSQ, and Ferriman-Gallwey score were evaluated before and after the intervention. Outcomes were assessed at baseline and at the end of the 8-week follow-up period. After 8 weeks, the MIND diet significantly reduced depression (β –3·03; 95 % CI: [–5·36, –0·70]; P = 0·011) and anxiety (β –3·54; 95 % CI: [–6·60, –0·49]; P = 0·024) scores compared with the control group. The MIND diet group exhibited significant increases in the emotion (β 0·63; 95 % CI: [0·18, 1·08]; P = 0·007) and body hair (β 0·65; 95 % CI: [0·03, 1·28]; P = 0·04) domains of the PCOSQ compared to the control group. The changes in other parameters did not show significant differences between the two groups. Both the MIND diet and control groups showed improvements in weight and BMI, with a slight advantage for the MIND diet group. These findings suggest that the MIND diet may be beneficial for improving mental health and some aspects of PCOSQ in women with PCOS.

Obesity and depression are highly prevalent diseases that are strongly correlated. At the same time, there is a growing gap in care, and treatment options should be improved and extended. Positive effects of a Mediterranean diet on mental health have already been shown in various studies. In addition to the physiological effects of nutrients, the way food is eaten, such as mindful eating, seems to play a role. The present study investigates the effect of a Mediterranean diet and mindful eating on depression severity in people with clinically diagnosed major depressive disorder and obesity. Participants will be randomised to one of the four intervention groups (Mediterranean diet, mindful eating, their combination and a befriending control group). The factorial design allows investigating individual effects as well as potential synergistic effects of the interventions. The study consists of a 12-week intervention period, where five individual appointments will take place, followed by a 12-week follow-up. The primary outcome is depression severity. Secondary outcomes are remission of depression, assessor-rated depression severity, quality of life, self-efficacy, BMI, waist:hip ratio and body composition; adherence to the Mediterranean diet and mindful eating will also be assessed. Alongside mediator and moderator analysis, a microbiome analysis, a qualitative evaluation and an economic analysis will be conducted. The study investigates an important health issue in a vulnerable target group. It allows to draw valuable conclusions regarding the effectiveness of different interventions and therefore contributes to improving available care options for people suffering from depression and obesity.

Dieting is a global emerging trend in recent years as more people strive to adhere to food restriction plans for weight management in obese people and to achieve desired slim body. This strategy may have unforeseen repercussions in females that may affect reproductive potential. Therefore, we aimed to investigate the impact of dietary stress on reproductive hormone levels, histoarchitecture of the ovary, autophagy and apoptosis markers in the rat ovary. Data suggest that dietary stress caused due to food deprivation decreased body weight and ovary weight, luteinising hormone, follicular-stimulating hormone and estradiol-17β levels. The dietary stress reduced the number of primary follicles, altered the histoarchitecture of the ovary, increased number of fragmented and irregularly shaped oocytes. Dietary stress induced autophagy signalling by inhibiting mammalian target of rapamycin and increasing Lamp-1, LC-3 and Beclin-1 in the ovarian follicles. In addition, dietary stress induced proapoptotic signalling pathway by decreasing Bcl-2 and increasing Bax as well as cytochrome-c expressions in the ovary. Taken together, these findings suggest that dietary stress caused due to food deprivation reduced reproductive hormones levels, induced autophagy and apoptotic signalling pathways that affected histoarchitecture of the ovary, ovarian function, oocyte quality and thereby reproductive potential.

This study investigates how the consumption of interesterified palm oil (IPO) affects the metabolic and morphological features of brown adipose tissue (BAT) in C57BL/6 mice fed a high-fat diet. Mice were divided into four groups: control, high-fat diet (lard), high-fat diet with palm oil (PO; HFP) and high-fat diet with IPO (HFI). The HFP and HFI groups exhibited significant body weight gain, increased fat mass and impaired glucose metabolism. Histological analyses revealed lipid infiltration in BAT, leading to structural remodelling from multilocular to unilocular adipocytes, which are hallmark features of the whitening process. This morphological shift was accompanied by reduced nuclear density and impaired vascularisation. Gene expression analysis indicated downregulation of key thermogenic markers, including Ucp1, Pparγ and Prdm16, especially in the HFI group. Increased expression of endoplasmic reticulum stress markers such as Chop and Atf4 and inflammatory cytokines (TNF-α and IL-6) highlighted the pro-inflammatory and pro-apoptotic microenvironment induced by PO and IPO. These changes culminated in a loss of BAT thermogenic capacity, as evidenced by decreased uncoupling protein 1 levels and impaired adaptive thermogenesis. Our findings underscore the detrimental effects of PO, mainly IPO, on BAT functionality, exacerbating obesity-related metabolic dysfunctions such as insulin resistance and glucose intolerance. The results emphasise the need for caution in the dietary use of these fats, particularly in ultra-processed food formulations, given their potential role in promoting adipose tissue remodelling and metabolic imbalances.

Around 55 million people worldwide live with dementia, and more are expected due to population ageing. We aimed to investigate associations between healthy diet and mild cognitive impairment and dementia in 1753 older adults aged 60–64 from the PATH (Personality and Total Health Through Life Cohort) study. Healthy diet was defined by the Mediterranean-DASH diet Intervention for Neurological Delay (MIND) and two dietary guideline quality scores (Dietary Guideline Index (DGI) and Index Diet Quality (IDQ)), which were calculated from baseline FFQ. Higher dietary scores indicated higher diet quality. Incidence of Alzheimer’s disease/vascular dementia (National Institute of Neurological Disorders criteria) and mild cognitive impairment (Winbald criteria) was assessed after 12 years of follow-up using validated questionnaires with nominated proxies. Logistic regression explored associations between dietary scores and cognitive function, adjusting for demographics, lifestyle factors and medical preconditions. Adjusted logistic regression comparing the per unit linear increase in diet scores showed MIND (OR = 0·82, 95 % CI = 0·68, 0·99), but not DGI (0·99 (0·97, 1·00)) or IDQ (1·12 (0·95, 1·32)), was significantly associated with lower odds of developing cognitive impairment. In conclusion, a healthier neuroprotective dietary pattern is associated with better cognitive function over time, whereas dietary patterns generated from general dietary guidelines did not show a significant association. Further research and well-designed clinical studies are needed to determine the effects of the MIND diet on cognitive impairment in older adults without a family history of dementia.

This study evaluated the effect of different medium-chain to long-chain fatty acid (MCFA:LCFA, M:L) ratios on growth performance, intestinal function, antioxidant capacity and gut microbiota in piglets. A total of 250 piglets were randomly assigned to five groups with five replicates, each containing ten pigs. The diets, containing varying amounts of MCFA-rich coconut oil and LCFA-rich soyabean oil, resulted in M:L ratios of 0, 2·1, 4·2, 8·8 and 33·8 %. Results showed that both final body weight and average daily weight gain increased as the M:L ratio increased (P < 0·05), while the 8·8 % M:L ratio diet exhibited the lowest feed:gain ratio (P < 0·05). As the M:L ratio increased, the contents of superoxide dismutase and glutathione peroxidase were increased, and MDA was decreased in serum (P < 0·05). The 8·8 and 33·8 % M:L diets improved ileal and jejunal morphology (P < 0·05), as indicated by greater villus height and villus height:crypt depth ratios. Furthermore, increasing M:L ratios from 0 to 33·8 % increased expression of tight junction proteins occludin and ZO-1 in the jejunum (P < 0·05). The 33·8 % M:L ratio reduced microbial α-diversity (P < 0·05), while 8·8 % M:L diet significantly increased the abundance of beneficial bacteria (e.g. Lactobacilli, Prevotella) and decreased harmful bacteria (e.g. Escherichia-Shigella, Enterococcus) in the cecum (P < 0·05). In summary, our study found that 8·8 % of dietary M:L ratios significantly improved growth performance, likely through modulating intestinal function, antioxidant activity and gut microbial composition.

While the effects of multidisciplinary weight loss (WL) on resting energy expenditure remain unclear in adolescents with obesity, the potential presence of adaptive thermogenesis (AT) has never been explored, which was the objective of the present work. Twenty-six adolescents (14·1 (sd 1·5) years) with severe obesity completed a 9-month inpatient multidisciplinary intervention followed by a 4-month follow-up. Anthropometric measurements, body composition (dual X-ray absorptiometry) and resting energy expenditure (REE, indirect calorimetry) were assessed before (T0) and after 9 months of WL intervention (T1) and after a 4-month follow-up (T2). AT, at the level of REE, was defined as a significantly lower measured v. predicted (using regression models with baseline data) REE. Two pre-cited REE equations were used, using both fat mass and fat-free mass (FFM) (predicted REE using equation 1) or FFM only (predicted REE using equation 2). Measured and predicted REE significantly decreased between T0 and T1 (P < 0·001) and remained lower at T2 compared with T0 (measured REE: P = 0·017; predicted REE: P < 0·001). Predicted REE using equation 2 was significantly higher than measured REE at T1 (P = 0·012), suggesting the presence of AT. FFM at T0 was negatively correlated with ATp1T1 (Rho = –0·428; P = 0·033) and ATp2T1 (Rho = –0·485; P = 0·014). The variation of FFM between T0 and T1 was negatively correlated with AT at T1 and T2. These preliminary results suggest the existence of AT in response to WL in adolescents with obesity, independently of the degree of WL. AT was associated with subsequent body weight and fat regain, suggesting AT may represent a damper to WL attempts while increasing the adolescents’ risks for subsequent weight and adiposity rebounds.

Evidence regarding the association between dietary choline intake and mortality in individuals with diabetes remains limited. This study aimed to evaluate the relationship between dietary choline intake and all-cause, CVD and cancer-related mortality among adults with diabetes. A total of 4712 participants with diabetes were included from the National Health and Nutrition Examination Survey 2007–2018 cycles. Dietary choline intake was estimated using two 24-h dietary recalls, and mortality outcomes were ascertained via linkage to National Death Index records through 31 December 2019. Cox proportional hazards models and Kaplan-Meier analyses were employed to assess the associations between choline intake and mortality. Restricted cubic spline models were used to examine potential non-linear relationships, and threshold analyses were conducted to identify inflection points. Over a median follow-up of 6·42 years, 805 deaths were documented, including 267 from CVD and 126 from cancer. A U-shaped association was observed between dietary choline intake and all-cause mortality (Pfor non-linearity < 0·0001). Compared with the lowest quartile, multivariable-adjusted hazard ratios for all-cause mortality were 0·64 (95 % CI 0·47, 0·88) for the second quartile, 0·59 (0·43, 0·82) for the third and 0·69 (0·43, 1·09) for the highest quartile. No significant associations were found between choline intake and either CVD or cancer mortality. These findings indicate a U-shaped relationship between dietary choline intake and all-cause mortality in individuals with diabetes, with intakes between 286·77 and 538·86 mg/d associated with the lowest risk – providing potential implications for dietary guidance in diabetes management.

Growing evidence indicates a link between diet and depression risk. We aimed to examine the association between an inflammatory diet index and depression utilising extensive data from UK biobank cohort. The energy-adjusted dietary inflammation index (E-DII) was calculated to quantify the potential of daily diet, with twenty-seven food parameters utilised. The E-DII scores were classified into two categories (low v. high) based on median value. To mitigate bias and ensure comparability of participant characteristics, propensity score matching was employed. To ascertain the robustness of these associations, sensitivity analyses were conducted. Subgroup analyses were performed to evaluate the consistency of these associations within different subpopulations. Totally, 152 853 participants entered the primary analyses with a mean age of 56·11 (sd 7·98) years. Employing both univariate and multivariate logistic regression models, adjustments were made for varying degrees of confounding factors (socio-demographics, lifestyle factors, common chronic medical conditions including type 2 diabetes and hypertension). Results consistently revealed a noteworthy positive correlation between E-DII and depression. In the context of propensity score matching, participants displaying higher E-DII scores exhibited an increased likelihood of experiencing incident depression (OR = 1·12, 95 % CI: 1·05, 1·19; P = 0·000316). Subgroup analysis results demonstrated variations in these associations across diverse subpopulations. The E-value for the point-estimate OR calculated from the propensity score matching dataset was 1·48. Excluding individuals diagnosed with type 2 diabetes or hypertension, the findings consistently aligned with the positive association in the primary analysis. These findings suggested that consumption of a diet with higher pro-inflammatory potential might associated with an increase of future depression risk.

Previous studies have reported co-morbidities of autoimmune thyroid disorders (AITD), including Hashimoto’s disease and Graves’ disease and celiac disease (CeD), as well as the possible beneficial effects of a gluten-free diet (GFD) on AITD. Nonetheless, it remains uncertain whether there is a genetic causal relationship between AITD and CeD, while the beneficial effects of a GFD are controversial. This study aims to explore the causal relationship between CeD and AITD, particularly with Hashimoto’s disease, and to determine whether a GFD is beneficial for AITD. We performed a two-sample Mendelian randomisation analysis on data from the largest meta-analysis summary statistics of AITD, CeD and GFD. Genetic instrumental variables were established by pinpointing SNP that relate to corresponding factors. In assessing sensitivity and heterogeneity, we conducted examinations of MR Egger, weighted median, simple mode, weighted mode and MR Egger intercept tests. Hashimoto’s disease was found to play a pathogenic role in increasing the risk of CeD (ORIVW = 1·544 (95 % CI 1·153, 2·068), P = 0·00355), and our Mendelian randomisation study does not support genetic liability related to CeD with Graves’ disease and GFD with AITD. This study supports the positive correlation between Hashimoto’s disease risk and CeD risk, while GFD has no protective effect on AITD and may exert its effect through other mechanisms. These findings provide valuable insights into potential targets for disease intervention and treatment at the genetic level.

This study systematically evaluates the effects of probiotic interventions on gut microbiota and clinical outcomes in diabetic patients to determine the optimal target population and conditions for effective use, with an emphasis on precision treatment. A comprehensive search was performed across PubMed, Web of Science, Cochrane Library, Embase, China National Knowledge Internet (CNKI), and Wanfang databases until April 2024. Randomized controlled trials (RCTs) assessing probiotics as adjunctive therapy for diabetes were included. The control group received standard care, and the intervention group received probiotics alongside standard care. Data were managed with Endnote and Excel, and analyses were conducted using Revman 5.3 and Stata 16. Twelve RCTs involving 1113 participants were included. Probiotics significantly increased fecal Lactobacillus (standardized mean difference (SMD) 1.42, P < 0.0001, I2 = 95 %) and Bifidobacterium levels (SMD 1.27, P < 0.0001, I2; = 90 %) and reduced fasting plasma glucose (SMD −0.35, P = 0.004). Subgroup analysis showed that shorter intervention durations (≤ 3 months) improved FPG, HbA1c, and Bifidobacterium levels, while younger patients (≤ 60 years) experienced the most significant improvements in Bifidobacterium levels. In conclusion, probiotics improve gut microbiota and clinical outcomes in diabetic patients, with intervention duration and patient age as key factors influencing treatment effectiveness.

Diet can affect health directly or by altering the gut microbiota; thus, there are strong interrelationships between the gut immune system, gut microbiota and diet. This study examined the effects of ingesting AIN-93M purified diet (PD) on gut immune function and gut microbiota in DO11·10 mice, in which T cell–dependent and T cell–independent (TI) IgA can be analysed separately. Ingestion of the PD for 2 weeks reduced both T cell–dependent and TI secretory IgA in the faeces compared with non-PD, whereas the diet did not affect T cell–dependent and TI serum IgA. Ingestion of the PD had no effect on systemic immune system splenocyte responses. Ingestion of the PD reduced intestinal tissue expression levels of B-cell activating factor and A proliferation–inducing ligand, cytokines involved in TI-IgA production and polymeric Ig receptor, which transports IgA into the intestinal lumen. Co-abundance group (CAG) analysis of the intestinal microbiota was conducted based on correlations between changes in the abundance of bacterial genera, and the correlations between CAG and IgA were determined. The Allobaculum-dominated CAG expanded following ingestion of the PD, accompanied by an inverse correlation with the decrease in faecal IgA, whereas the Lactobacillus-dominated CAG shrank relative to the Allobaculum-dominated CAG. These results suggest that TI-IgA suppresses the expansion of some intestinal bacteria and that ingestion of the PD induces dysbiosis via impaired IgA secretion into the intestinal lumen.