Food & Function最新文献

Objectives: The consumption of soft drinks, such as carbonated or non-carbonated beverages, including sugars or artificial sweeteners, flavorings, colorings, acidulants, and preservatives, has recently emerged as a major global public health problem. This review aims to analyse the evidence on the association between soft drink consumption and depressive symptoms among the general population. Methods: Five electronic databases (PubMed, Scopus, Cochrane Library, Epistemonikos, and medRxiv) were searched for relevant articles published up to 31 January 2024. All the studies were evaluated using the Newcastle-Ottawa scale. The pooled odds ratio and 95% confidence intervals (CIs) were estimated using a random-effects model in the presence of heterogeneity. Heterogeneity among the studies was assessed using I² statistics. Egger's test was used to evaluate publication bias. Results: Fifteen studies involving 55 635 cases of depressive symptoms among 521 392 participants were included. The pooled OR of depressive symptoms for the highest versus the lowest consumption of soft drinks was 1.39 (95% CI: 1.26-1.52). The association demonstrated statistical significance in cross-sectional studies (OR = 1.45, 95% CI: 1.24-1.70) and cohort studies (OR = 1.34, 95% CI: 1.19-1.51). In the subgroup analysis, sugar-sweetened beverages (SSBs) and sugar-sweetened carbonated beverages (SSCBs) revealed a rise in the trend of depressive symptoms. The linear dose-response meta-analysis showed no statistically significant association between dose and depressive symptoms. Conclusion: Our findings suggest that more rigorous and targeted policy interventions are warranted to curtail soft drink consumption in order to alleviate the global burden of depression.

Correction for ‘Improvement effect of a next-generation probiotic L. plantarum-pMG36e-GLP-1 on type 2 diabetes mellitus via the gut–pancreas–liver axis’ by Hong Hu et al., Food Funct., 2023, 14, 3179–3195, https://doi.org/10.1039/D3FO00044C.

Acetaminophen (APAP) is a widely used antipyretic and analgesic drug, but excessive or prolonged use can cause liver injury. Sulfated polysaccharides from sea cucumber (SCSP) exhibit diverse bioactivities; however, their protective role against APAP hepatotoxicity remains unclear. Here, SCSP pretreatment significantly alleviated APAP-induced liver injury in mice, as evidenced by reduced hepatic necrosis, serum transaminases, inflammation, and oxidative stress. 16S rRNA sequencing revealed that SCSP preserved gut microbial diversity and enriched beneficial bacterial taxa, partially counteracting APAP-induced dysbiosis. Metabolomics analysis further demonstrated that SCSP remodeled microbiota metabolic outputs and mitigated APAP-induced serum metabolic abnormalities, particularly in amino acid metabolism. Notably, citraconic acid (CA) was identified as a key metabolite restored by SCSP and strongly associated with improved hepatic outcomes, with concordant changes observed between gut and serum. Functional validation confirmed that CA pretreatment protected against APAP-induced liver injury by enhancing antioxidative defenses and reducing inflammatory responses. In vitro, CA reduced oxidative damage and activated the Nrf2 pathway. Collectively, these results support SCSP as a promising preventive prebiotic that enhances hepatic resilience to APAP challenge via modulation of the gut–liver axis, with CA representing an important mechanistic mediator.

Chronic stress primarily induces liver injury through excessive production of reactive oxygen species (ROS), yet the complete underlying mechanisms remain elusive. This study demonstrates that chlorogenic acid (CGA), a natural antioxidant, markedly alleviates chronic restraint stress (CRS)-induced liver injury in rats. Based on histopathological assessment, serum transaminase levels, body weight, and liver coefficient, the optimal CGA dose in this trial was determined to be 100 mg kg⁻¹. CGA treatment significantly reduced liver ROS accumulation, lipid peroxidation, and iron overload, while enhancing glutathione (GSH) levels and regulating iron transport proteins (FPN and TFR1). Mechanistically, CGA may inhibit both ferroptosis and mitochondrial apoptosis via activation of the Nrf2 signaling pathway. These hepatoprotective effects were abolished by the Nrf2 inhibitor brusatol, highlighting the central role of Nrf2 in mediating CGA's antioxidant and cytoprotective actions. This study reveals a novel therapeutic strategy targeting the Nrf2 axis to mitigate oxidative stress and ferroptosis-related liver injury under chronic stress.

Sulforaphane (SFN) is an isothiocyanate derived from cruciferous vegetables. Our previous studies have shown that nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and signal transducer and activator of transcription 3 (STAT3) may play roles in the protective effects of SFN against dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. This study aims to elucidate the underlying mechanisms. GEO database analysis revealed that Nrf2 expression was reduced, while STAT3 expression was elevated in the colonic mucosa of UC patients compared to healthy controls (P < 0.01). In the DSS-induced Caco-2 cell model, Nrf2 siRNA transfection abolished the effects of SFN on enhancing Nrf2 and tight junction protein expression, suppressing inflammatory factors and reducing the phosphorylated-STAT3/STAT3 ratio. In DSS-induced UC mice, SFN alleviated colitic symptoms in wide-type mice, including weight loss, colon edema and shortening, and inflammatory cell infiltration. SFN also reduced the levels of inflammatory cytokines and enhanced tight junction protein expression in wide-type mice with colitis. However, these protective effects were largely abolished in Nrf2 knockout mice. Moreover, in Nrf2 knockout colitis mice, SFN reduced the gut microbial diversity and decreased the relative abundance of Firmicutes at the phylum level, as well as Muribaculaceae and Lachnospiraceae_NK4A136 at the genus level. In conclusion, the protective effects of SFN against UC may involve the regulation of the Nrf2/STAT3 signaling pathway and modulation of the gut microbiota, highlighting Nrf2 as a key mediator of SFN's action.

The gut microbiota plays a crucial role in human health and is key to understanding how various factors modulate its composition in older adults, enabling targeted interventions. This study aims to identify how dietary and lifestyle patterns influence older adults’ gut microbiota profile, considering the plant-based or animal origin of the dietary protein. A cross-sectional observational study was conducted with older adults aged between 60 and 80. Faecal samples were analyzed to determine gut microbiota composition and assess short-chain fatty acid (SCFA) production. Associations between microbiota profiles, dietary patterns, and metabolic markers were conducted through correlation and t tests. The study revealed that a diet rich in plant-based protein was linked to a lower body mass index (BMI) and to a significantly higher relative abundance of Verrucomicrobiota (4.46%) compared to an animal protein diet (1.47%). Firmicutes was the predominant phylum (61.10% relative abundance), while Proteobacteria levels tended to be higher in individuals with high-fat diets and alcohol consumption. Regarding genera, some of them are directly related to gut microbiota diversity and inversely related to BMI, such as Christensenellaceae R-7 group and Akkermansia. Also, Roseburia was significantly associated with valeric acid levels (r = 0.43, p = 1.5 × 10⁻³). High fibre intake was associated with reduced branched-chain SCFA (bc-SCFA) production. Increasing plant-based protein and fibre intake may promote a more favourable gut microbiota composition and enhance resilience against dysbiosis and related age-related conditions. Also, the presence of beneficial genera can increase gut microbiota diversity and decrease BMI, as well as induce healthy gut metabolic profiles. These findings underscore the potential of personalized nutrition and dietary strategies tailored to protein origin and fibre intake to modulate the gut microbiota and improve metabolic health in older adults.

Acute lung injury (ALI) is a syndrome of acute inflammatory lung injury triggered by diverse etiological factors, which can lead to atelectasis, prolonged hypoxemia, severe respiratory distress, and high mortality. There is increasing evidence that the gut microbiota is involved in regulating pulmonary immunity, and the gut–lung axis plays a critical role in pulmonary diseases. The primary objective of this study was to investigate the effect of Lactobacillus fermentum on lipopolysaccharide (LPS)-induced ALI. After the establishment of an LPS-induced ALI model and gavage with L. fermentum, pulmonary edema and inflammatory cell infiltration in mice were significantly reduced. In addition, L. fermentum regulated the gut microecology, restored the gut barrier, remodeled the lung microecology and increased the abundance of Lactobacillaceae through gut–lung cross-talk. Multi-omics results suggested that L. fermentum intervention regulated sphingolipid metabolism and downregulated the PI3K–AKT pathway. Moreover, intervention of lung organoids with the cell-free supernatant (CFS) of L. fermentum significantly reduced LPS-induced autoinflammatory responses and confirmed the down-regulation of the PI3K–AKT signaling pathway. In conclusion, L. fermentum alleviates LPS-induced lung injury by regulating the PI3K–AKT signaling pathway via the gut–lung axis, offering a potential therapeutic approach for ALI.

Cardiovascular diseases remain the leading cause of global mortality, with endothelial dysfunction recognized as a critical initiating event. Hyperlipidemia-induced endothelial lipotoxicity triggers oxidative stress and inflammation, thereby accelerating vascular injury. Given the central role of endothelial cells in maintaining vascular homeostasis, they represent a key therapeutic target for mitigating systemic lipotoxicity. However, specific strategies aimed at countering endothelial lipotoxicity remain limited, highlighting an urgent need for novel pharmacological interventions. 6-Gingerol, a primary bioactive constituent of ginger (Zingiber officinale) and related plants, exhibits potent antioxidant, anti-inflammatory, and anticancer properties. Nevertheless, its potential protective effects against hyperlipidemia-induced endothelial injury and the underlying mechanisms remain incompletely understood. In this study, we investigated the protective effects of 6-gingerol and explored its mechanisms of action using both in vivo and in vitro models of endothelial dysfunction. Our results demonstrated that 6-gingerol effectively ameliorates inflammation and oxidative stress associated with endothelial dysfunction induced by hyperlipidemia. Mechanistically, under Nrf2 knockdown conditions, the antioxidant effects of 6-gingerol were abolished. Similarly, inhibition of Erk with U0126 blocked 6-gingerol-mediated nuclear translocation of Nrf2 and its antioxidant activity, underscoring the critical role of the Erk–Nrf2 axis in mediating these effects. Moreover, transcriptomic analysis and pharmacological interventions using a p38 MAPK inhibitor and an NF-κB inhibitor revealed that 6-gingerol suppresses the release of inflammatory mediators, such as IL-6, via the p38 MAPK–NF-κB signaling pathway. In summary, our study provides evidence that 6-gingerol ameliorates lipotoxicity-induced endothelial injury through coordinated modulation of the Erk–Nrf2 and p38–NF-κB signaling pathways, highlighting its potential as a novel preventive candidate for endothelial dysfunction in cardiovascular diseases.

Correction for ‘Clinical and lipid metabolic responses to diacylglycerol oil administration in Chinese adults with overweight/obesity or central obesity: a randomized, double-blind, placebo-controlled trial’ by Liyuan Qin et al., Food Funct., 2026, https://doi.org/10.1039/D5FO02712H.

Retraction of ‘Stereoisomers of octahydrocurcumin, the hydrogenated metabolites of curcumin, display stereoselective activity on the CYP2E1 enzyme in L-02 cells’ by Dandan Luo et al., Food Funct., 2023, 14, 2822–2835, https://doi.org/10.1039/D2FO03892G.