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 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.

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.

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.

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.

Children with moderate acute malnutrition (MAM) have an increased risk of iron deficiency, anaemia and death from infectious diseases. The iron-regulating hormone hepcidin is increased in inflammation and may be important in regulating iron metabolism in children with MAM. Asymptomatic malaria has previously been associated with elevated s-hepcidin. We assessed the association between inflammation, iron status, anthropometry and malaria and serum hepcidin (s-hepcidin) and evaluated the effect of food supplementation on s-hepcidin in a secondary analysis in 1019 children with MAM from a randomised intervention trial in Burkina Faso. Children received 12 weeks of supplementation of 500 kcal/d as either corn–soy blend (CSB) or lipid-based nutritional supplements (LNS). S-hepcidin was measured at baseline and after 12 weeks. At baseline, correlates of s-hepcidin were determined using Tobit regression. The effect of supplementation was determined using mixed effects Tobit regression. Children with iron deficiency had 82 % (95 % CI 76, 87) lower s-hepcidin than those without, whereas children with acute infection and inflammation had elevated s-hepcidin. Children with symptomatic malaria had 103 % (95 % CI 32, 210) higher s-hepcidin than afebrile children without detectable malaria, while children with recent or asymptomatic malaria had 51 % (95 % CI 35, 63) lower s-hepcidin. S-hepcidin increased 61 % (95 % CI 38, 87) after 12 weeks of food supplementation with 22 % higher (95 % CI 2, 45) concentration in those who received LNS compared with CSB. Expectedly, morbidity and inflammation were associated with higher, and iron deficiency with lower, s-hepcidin. Further studies are needed to corroborate the finding of decreased s-hepcidin in malnourished children with asymptomatic malaria.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a serious disease and increasingly prevalent in children. MASLD is associated with health consequences such as type 2 diabetes and CVD. While vitamin E is a potent antioxidant that has been proposed to improve liver function and cardiometabolic health including liver markers, lipid profile, glycaemic control and anthropometric measurements. A comprehensive search was conducted up to March 2025. Data on anthropometric measures, liver enzymes (alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transferase (GGT)), glycaemic indices (fasting blood sugar (FBS), insulin, homeostatic model assessment for insulin resistance (HOMA-IR)), lipid profiles (total cholesterol (TC), TAG, LDL-cholesterol, HDL-cholesterol) and serum vitamin E levels were extracted. Statistical analyses were performed using a random-effects model. Eleven randomised controlled trials involving 665 participants were included in this study. Vitamin E significantly reduced ALT (weighted mean difference (WMD) = −5·23 U/L; 95 % CI: −7·72, −2·75; P < 0·001) and AST (WMD = −3·00 U/L; 95 % CI: −4·59, −1·41; P < 0·001), reflecting improved liver function. It also decreased TC (WMD = −5·77 mg/dl; 95 % CI: −11·46, −0·09; P = 0·04) and HOMA-IR (WMD = −0·82; 95 % CI: −1·28, −0·37; P < 0·001), while significantly increasing serum vitamin E levels (WMD = 9·16 mg/l; 95 % CI: 3·29, 15·03; P = 0·002). No significant changes were observed in the BMI, GGT, FBS, insulin, LDL-cholesterol, HDL-cholesterol or TAG levels. Vitamin E supplementation in paediatric MASLD appears to favourably influence key liver enzymes such as ALT, AST and certain metabolic factors including TC, and HOMA-IR levels, supporting its potential role as adjunctive therapy.

Polycystic ovary syndrome is a disorder characterised by insulin resistance, low-grade inflammation and increased adipose tissue. The very low-carbohydrate ketogenic diet has been suggested to reduce obesity risks in polycystic ovary syndrome. This study aimed to update the evidence on the effects of the very low-carbohydrate ketogenic diet in women with polycystic ovary syndrome. Searches were conducted in electronic databases for randomised clinical trials addressing the research question. The values for the meta-analysis were presented as weighted mean difference (WMD). Twelve studies were included in the qualitative analysis and eleven in the quantitative analysis. Significant reductions were observed in anthropometric outcomes: weight (WMD: −9·57 kg; P < 0·0001), waist circumference (WMD: −7·75 cm; P < 0·0009), fat body mass (WMD: −7·44 kg; P = 0·0008), BMI (WMD: −3·45 kg/m2; P < 0·0001) and waist-to-hip ratio (WMD: −0·02; P < 0·0034). Hormonal improvements included free testosterone (WMD: −0·31 ng/dl; P < 0·0001), total testosterone (WMD: −7·21 ng/dl; P < 0·0001), sex hormone-binding globulin (WMD: 15·22 nmol/l; P = 0·0035), luteinising hormone (WMD: −3·97 U/L; P = 0·0008) and luteinising hormone:follicle-stimulating hormone ratio (WMD: −1·04; P = 0·0053), but not for follicle-stimulating hormone levels (WMD: 1·23 mUI/ml; P = 0·12). Significant changes in metabolic markers were seen in blood glucose (WMD: −9·65 mg/dl; P = 0·0031), insulin (WMD: −2·41 mg/dl; P = 0·0387), homeostatic model assessment for insulin resistance (WMD: −2·46; P = 0·0123) and TAG (WMD: −29·95 mg/dl; P = 0·0188). The very low-carbohydrate ketogenic diet shows significant benefits in managing body composition, reducing hyperandrogenism, balancing sex hormones and improving glucose metabolism in polycystic ovary syndrome.

A significant association between tomato consumption and a lower risk of developing hypertension has been reported. In this study, we aimed to investigate the relationship between tomato intake and prehypertension risk among Korean adults. Hypertension was defined according to the criteria established by the Korean Society of Hypertension. The study participants were selected from the Health Examinees cohort study. Tomato consumption was measured using an FFQ and categorised into quintiles based on the amount consumed. Higher tomato consumption was associated with a lower risk of prehypertension in men (hazard ratio (HR) 0·86, 95 % CI 0·80, 0·92, Pfor trend 0·0005). Women in the highest quintile also showed a similar trend (HR 0·94, 95 % CI 0·90, 0·99, Pfor trend 0·0091). Stratified analyses revealed a reduced risk of prehypertension across all subgroups, except underweight individuals and those with a history of alcohol consumption (all Pfor interaction < 0·05). These findings indicate that higher tomato intake may offer potential advantages for managing blood pressure levels.

Acute effects of a daily dose of red wine may cause deterioration of visual function; however, there is limited information on healthy individuals. This study aims to investigate acute effects of daily red wine consumption on visual function and retinal microvasculature in healthy young adults through a randomised self-controlled design and to explore the molecular mechanisms using an animal model. In healthy young adults’ study, twenty-seven adults with follow-up at baseline, 0·5 h and 2 h after consuming 300 ml of either red wine or water underwent blood biochemistry, visual function, morphology and blood flow of retinal and choroidal vasculatures, and cerebral blood flow (CBF) evaluation. Acute red wine consumption caused abnormal changes in retinal function (multifocal visual electrophysiology) that preceded changes in vision. Macular vessel diameter index (VDI) increased significantly at 0·5 h but decreased significantly at 2 h, despite increased regional CBF following red wine consumption, which was consistent with increased choroidal thickness and decreased retinal thickness. Animal experiments conducted on Brown Norway rats demonstrated a significant decrease in retinal VDI and vessel area density (VAD) associated with increased reactive oxygen species production following red wine administration, as well as decreased endothelial nitric oxide synthase (eNOS) and increased endothelin-1 (ET-1) levels in the retina. Consequently, red wine consumption caused abnormal changes in retinal function and microvascular constriction in healthy young adults, and an animal model suggested that the underlying mechanism may involve the regulation of eNOS and ET-1 levels in the retina. These findings imply the potential detrimental effects of drinking habits on individuals with retinal ischaemic diseases.

The dietary antioxidant quality score (DAQS) is a valid and reliable tool for assessing the overall antioxidant potency of a diet by considering the synergetic effects of dietary antioxidants. Non-alcoholic fatty liver disease (NAFLD) is linked to the imbalance of the body’s oxidant and antioxidant defense system. The objective of the present research was to investigate the possible associations between DAQS and odds of NAFLD in a large population of the Azar cohort study. The present propensity score–matched case–control study was applied to a population of 14 655 individuals. Demographic, anthropometric and dietary data were gathered, and biochemical markers were measured. The DAQS was evaluated based on the daily dietary intake of vitamin E, vitamin A, vitamin C, Se and Zn, compared with the daily recommended intake. The multivariable logistic regression analysis was employed to determine the association between DAQS with NAFLD-related outcomes. After propensity score matching based on age, gender and body mass index (BMI), participants were allocated into NAFLD (n 660) and non-NAFLD (n 1234) groups. Findings indicated significant differences in age, weight, BMI, waist:hip ratio, TAG, HDL-cholesterol and LDL-cholesterol and dietary intake between percentiles of DAQS in NAFLD patients. Nonetheless, no significant associations were observed between DAQS and NAFLD before and after propensity score matching. Comparing the results to prior research underlines the need for a comprehensive approach for exploring the association between dietary antioxidants, serum antioxidant level and biochemical indices in NAFLD, which is essential for the efficient clarification of the underlying mechanisms.

The association between salt and salted food consumption and oral, pharyngeal and oesophageal cancers remains inconclusive. To address this, we conducted a large-scale nationwide cohort study in Japan, a region globally recognised for its high-salt consumption. In a baseline survey conducted from 1988 to 1990, salt consumption was evaluated using a self-administered FFQ in a sample of 42 535 participants aged 40–79 years. Over a median 14·4-year follow-up period, 145 incident cases of oral (n 43), pharyngeal (n 17) and oesophageal (n 85) cancers were observed. A Cox proportional hazards model was used to estimate the hazard ratio (HR) and 95 % CI after adjusting for age, sex, smoking status, alcohol consumption and fruit and vegetable consumption. High-salt consumption was associated with a higher risk of oral, pharyngeal and oesophageal cancers combined; the multivariable HR for the highest v. lowest tertiles of salt consumption was 1·67 (95 % CI: 1·08, 2·61, P-trend = 0·01). An excess risk was primarily observed for oral and oesophageal cancers. Among the salt sources, miso soup consumption was positively associated with the combined risk of oral, pharyngeal and oesophageal cancers; however, the consumption of other high-salt foods was not. In conclusion, high-salt consumption was associated with a higher combined risk of oral, pharyngeal and oesophageal cancers.

This study investigated the association between dietary flavonoid intake and hearing impairment in older adults aged ≥ 70 years, using cross-sectional data from the National Health and Nutrition Examination Survey 2009–2010 and 2017–2018. Flavonoid intake was estimated from two 24-h dietary recalls and categorised as low or high based on the median intake (85·4 mg/d). Hearing impairment was defined using a pure-tone average > 25 dB in one or both ears. Among the 1492 participants, 55·7 % had bilateral hearing impairment, 15·6 % had unilateral hearing impairment and 28·7 % had normal hearing. These categories were mutually exclusive, based on the presence of hearing impairment in one or both ears. After adjusting for sociodemographic, behavioural and dietary covariates, low flavonoid intake was associated with a 45 % greater odds of bilateral hearing impairment (adjusted OR = 1·45; 95 % CI 1·03, 2·04; P = 0·034), but not associated with unilateral impairment. Marginal associations were also observed for specific flavonoid subclasses, including flavan-3-ols and catechins. A significant interaction with age was observed, whereas no significant interactions were detected with race or sex. These findings suggest that low flavonoid intake may be a modifiable dietary factor associated with age-related bilateral hearing loss. Increasing dietary flavonoid consumption may be associated with benefits for sensory health and could play a modest role in reducing the risk of hearing impairment in older adults, though further research is needed to confirm these findings.

Family meals are positively associated with healthier diets among children and parents. We aimed to deepen the understanding of these relationships by exploring the associations between shared meals and dietary quality among children, fathers and mothers. A subset of parent-child dyads (296 children aged 3–6 years, 103 fathers, 293 mothers) from the DAGIS Intervention baseline assessment was included in this cross-sectional study. The parents reported how often they shared meals with the child and filled in a food frequency questionnaire assessing their child’s and their own food consumption. A Healthy Food Intake Index (HFII) describing dietary quality was calculated for all family members. We used linear regression to investigate the associations between shared meals and the HFII of the children, fathers and mothers. Models were adjusted for child’s age and gender, parent’s age and educational level and number of children in the household. Children whose fathers reported less frequently sharing a weekend lunch with the child had a lower HFII (B estimate –1·58, 95 % CI –2·66, –0·50). The association remained close to statistical significance with adjustments (B estimate –0·99, 95 % CI –2·17, 0·19). A less frequently shared weekend lunch was also borderline significantly associated with lower HFII among the fathers (adjusted model, B estimate –1·13, 95 % CI –2·30, 0·04). Fathers should be encouraged to share meals with their family, since it might have a role in the dietary quality of both children and fathers. Future studies should recognise fathers as important contributors to a healthy home food environment.

This study examined factors associated with stunting in children aged < 2 years in eastern Indonesia. Data were derived from three national cross-sectional surveys of Indonesia. The outcome variable was stunting (low length-for-age) in children aged < 2 years. Nineteen potential predictors from community- to individual-level characteristics were identified. Multilevel analyses were performed, adjusting for cluster sampling with random effects for cluster and strata. We used data from the 2010, 2013 and 2018 Indonesian Basic Health Research. Information from 6076 children aged < 2 years from Nusa Tenggara Barat, Nusa Tenggara Timur, Sulawesi, Maluku and Papua regions were used. We found that the proportion of stunted children aged < 2 years in eastern Indonesia decreased between 2010 and 2018. Significant predictors of stunting included living in West Nusa Tenggara (adjusted OR (aOR) = 1·09; 95 % CI 1·02, 1·16) and East Nusa Tenggara region (aOR = 1·36; 95 % CI 1·28, 1·45), belonging to a household with three or more children aged under 5 years (aOR = 1·32; 95 % CI 1·11, 1·56), being from a poor household (aOR = 1·17; 95 % CI 1·06, 1·30) and born to less educated mother (aOR = 1·26; 95 % CI 1·02, 1·56). Furthermore, stunting were more likely among males (aOR = 1·29, 95 % CI 1·19, 1·40), those aged 12–23 months (aOR = 2·01; 95 % CI 1·65, 2·45), with low birth weight (aOR = 1·91; 95 % CI 1·40, 2·60) and with gestational age < 37 weeks at birth (aOR = 1·14; 95 % CI 1·05, 1·24). Multiple factors contribute to stunting in eastern Indonesia, highlighting the need for comprehensive and targeted initiatives. Poverty reduction, healthcare system improvement, family planning and continued health promotion strategies are necessary to reduce stunting prevalence.