Food & Function最新文献

Tackling metabolic syndrome (MetS) using functional fermented food has recently attracted much attention. A vegetable-fermented maize - and fruit-based probiotic functional food (maize 5% and fruits 30%) was previously designed, which was enriched in papaya/melon carotenoids and dispersible phytosterols to obtain a cholesterol-lowering effect. The aim of this work was to investigate the effect of this new functional food on an HFD (high-fat diet)-induced MetS rat model focusing on lipid and glucose metabolic disorders and considering vitamin A status. Male Sprague-Dawley rats (n = 36) were randomly divided into 4 groups (n = 9): a control group (C); an HFD group; and two HFD groups receiving 1.44 g per rat per day of the functional fermented food during the three months of the experiment following a preventive (HFD-P) or a curative (HFD-C) mode. The intake of the functional food decreased the adipose tissue amount by 1.5 times in preventive and curative mode groups and restored their LDL cholesterol and triglyceride levels to C level. The area of hepatic lipid droplets was reduced in both HFD-P and HFD-C groups compared with HFD group, which was associated with a reduction in inflammation and lipid oxidation. Both the HFD-P and HFD-C groups alleviated HFD-induced insulin resistance, as evidenced by the return of fasting insulin levels and the HOMA-IR index to control levels. However, only the HFD-C group improved the glucose tolerance test and skeletal muscle insulin sensitivity. Notably, alteration in vitamin A status in HFD rats was restored with HFD-C and HFD-P. Altogether, these results support the potential of this nutritional strategy to prevent MetS.

The incidence of depression is on the rise, and currently available antidepressants often exhibit limited efficacy in many patients. Additionally, the underlying mechanisms of depression remain poorly understood. Research has shown that neuroinflammation, driven by M1 microglial phenotypic polarization, contributes to neuronal abnormalities implicated in the development of depression. Eicosapentaenoic acid (EPA) has emerged as a promising therapeutic agent for depression. However, the specific target of EPA's anti-stress effects is yet to be identified. This study aimed to explore the pathogenesis of depression and elucidate the central regulatory mechanisms underlying EPA's antidepressant efficacy. In this study, mice were orally administered EPA for five consecutive weeks. During this period, they were subjected to daily chronic unpredictable mild stress (CUMS) and treated with lipopolysaccharide (LPS, 0.5 mg kg⁻¹, intraperitoneally) every other week. The results demonstrated that EPA significantly alleviated neuronal degeneration in the medial prefrontal cortex. Furthermore, EPA improved synaptic plasticity impairments induced by CUMS combined with LPSs, as indicated by the increased protein levels of Nlgn1, PSD95, GAP43, and Syn. EPA also reduced neuroinflammation by inhibiting M1 microglial polarization and NLRP3 inflammasome activation. Notably, EPA exerted antidepressant-like effects by modulating GPR120. These findings suggest that EPA intake can mitigate abnormal mood and behavior induced by elevated immune-inflammatory signals. These findings suggest that EPA intake can attenuate abnormal moods and behaviors induced by elevated immune-inflammatory signals. Therefore, EPA may be a promising strategy for the clinical treatment of inflammatory depression.

Malus hupehensis leaves (MHL), consumed as a daily beverage in Chinese folk tradition and recently recognized as a new food material, are abundant in polyphenols and bioactive compounds that demonstrate hypoglycemic, lipid-lowering, and anti-inflammatory effects. However, the antidiabetic mechanisms have not been fully elucidated. This study aimed to investigate the protective mechanisms of Malus hupehensis leaves’ extract (MHLE) against type 2 diabetes mellitus (T2DM). The results showed that MHLE effectively ameliorated glucose and lipid metabolic abnormalities in db/db mice, and attenuated hepatic macrophage activation. Transcriptomic analysis of the liver revealed that MHLE primarily affects genes involved in inflammatory responses and inhibited the TLR4/MAPK pathway to reduce hepatic inflammation. Metagenomic sequencing identified changes in gut microbiota composition and showed that MHLE restored the abundance of Lachnospiraceae bacterium, Oscillospiraceae bacterium, and Clostridia bacterium while reducing the abundance of Escherichia coli, thereby ameliorating gut dysbiosis. The integrated regulation of metabolism, immune response, and the microbial environment by MHLE significantly alleviated symptoms of T2DM. This study offers strong scientific evidence for the potential use of MHL as a functional food.

Over the past two decades, the occurrence of hyperuricemia and its influence on health have drawn lots of concern all over the world. Despite significant advances in understanding the pathogenesis of hyperuricemia in various studies, effective medications without side effects are not available. Nutraceutical supplements have attracted much attention due to their beneficial and non-toxic side effects compared to chemical compounds. In the present study, mice with hyperuricemia induced by potassium oxalate and hypoxanthine were given hydrolysate of goat milk casein (HGMC) to investigate its beneficial effects on hyperuricemia. HGMC significantly alleviated body weight loss and abnormal water consumption in hyperuricemic mice. Further study showed that HGMC effectively eliminated renal histological damage in mice with hyperuricemia. Real-time PCR and western blot results revealed that HGMC alleviated protein levels of inflammation-associated proteins and cellular pyroptosis-associated proteins, including NLRP3, TNF-α, Caspase1 and TGF-β. Intestinal microbial sequencing showed that supplementation of HGMC increased the abundance of beneficial bacteria and decreased pathogenic flora. In conclusion, our results suggest that the beneficial effects of HGMC on hyperuricemia are associated with regulating inflammation and modulating intestinal bacteria in mice.

Benzoic acid is a naturally occurring compound found in fruits and is also commercially synthesized as an additive in the food, feed, and pharmaceutical industries. This study investigated the effects of benzoic acid as a dietary supplement on inflammation and intestinal injury in acute Escherichia coli (ETEC)-infected or healthy mice. Thirty-six BALB/c mice were divided into three groups, with 12 mice in each group for a 16-day feeding trial. In group 1, mice were fed a basal diet, six mice were sacrificed, and six mice were intraperitoneally injected with phosphate-buffered saline on day 15. Groups 2 and 3 were fed a basal diet and a diet containing 0.6% benzoic acid, respectively. Half of the mice in each group were sacrificed, while the others were intraperitoneally injected with ETEC on day 15. The results indicated that benzoic acid had no adverse effects on healthy mice regarding growth, organ indices, inflammation, intestinal injury parameters, and cecal short-chain fatty acid levels. Importantly, benzoic acid reduced inflammation in ETEC-infected mice, as evidenced by decreased serum IL-1β, TNF-α, and INF-γ levels, along with increased jejunal TLR-2 and MyD88 mRNA expression. Besides, benzoic acid mitigated intestinal injury in ETEC-infected mice by increasing the jejunal villus height (VH) and the ratio of VH to crypt depth, elevating jejunal Occludin mRNA levels, decreasing serum D-lactate and diamine oxidase levels, and increasing the cecal acetic acid level. 16s rRNA sequencing revealed that benzoic acid altered the β-diversity of ETEC-infected mice and increased the abundances of Erysipelotrichaceae, Faecalibaculum, and Turicibacter in their gut microbiota. Spearman correlation analysis further indicated that the protective effects of benzoic acid against ETEC infection were closely linked to specific gut microbiota, namely Erysipelotrichaceae, Faecalibaculum, Bifidobacterium, and Limosilactobacillus. Collectively, these findings suggest that benzoic acid could serve as a safe dietary supplement for healthy mice and may alleviate inflammation and intestinal injury in mice with acute ETEC infection.

A high-salt diet (HSD) can result in numerous health issues, including exacerbation of intestinal inflammation. Therefore, there is an immediate necessity of developing dietary supplements that can mitigate colitis exacerbated by a HSD. This study examined the impact of Lactobacillus plantarum HGD228 on colitis exacerbated by a HSD and the mechanisms underlying its alleviation. HGD228 treatment significantly enhanced colonic goblet cells and MUC2, upregulated ZO-1 and occludin, inhibited epithelial cell apoptosis, and mitigated colitis exacerbated by a HSD. Moreover, HGD228 significantly regulated oxidative stress-related enzymes, including SOD, GSH-PX, and CAT. HGD228 treatment significantly suppressed the NF-κB pathway induced by a HSD and regulated the levels of cytokines, including TNF-α, IL-10, and IL-1β. Furthermore, HGD228 reestablished the gut microbiota altered by HSDDSS, increasing Bifidobacterium while decreasing Escherichia–Shigella and Clostridium sensu stricto 1. HGD228 treatment also enhanced the production of butyric acid and acetic acid, suppressed pro-inflammatory cytokines, and strengthened the intestinal mucosal barrier. Therefore, HGD228 enhanced the production of beneficial metabolites by regulating inflammatory cytokines and oxidative stress, preserving the mucosal barrier, and enhancing gut microbiota, and mitigated colitis aggravated by a HSD. These results will aid in clinical trials of probiotics and the development of dietary supplements for colitis, with promising application value.

Postprandial metabolic disturbances are exacerbated in type 2 diabetes (T2D). Cocoa and carob, despite showing promising effects on these alterations in preclinical studies, have not yet been jointly tested in a clinical trial. Therefore, this acute, randomised, controlled, crossover nutritional trial evaluated the postprandial effects of a cocoa–carob blend (CCB) in participants with T2D (n = 20) and overweight/obesity. The subjects followed three treatments: hypercaloric breakfast (high-sugar and high-saturated fat, 900 kcal) as the control (treatment C); the same breakfast together with 10 g of the CCB, with 5.6 g of dietary fibre and 1.6 g of total polyphenols (treatment A); and the same breakfast after consuming the CCB (10 g) the night before (treatment B). Various analyses were performed, including the determination of the clinical markers of T2D (fasting and postprandial glucose and insulin, GLP-1, and glycaemic profile), satiety evaluation, analysis of exosomal miRNA expression and ex vivo determination of inflammation modulation. No effect on glucose homeostasis (glucose, insulin, and GLP-1) was found in the study population. However, eight exosomal miRNAs were found to be significantly modified owing to CCB supplementation compared with treatment C, with three of them (miR-20A-5p, miR-23A-3p, and miR-17-5p) associated with an improvement in insulin sensitivity. Furthermore, the CCB caused a decrease in hunger feelings (0–120 min), as assessed by the visual analogue scale (VAS). Finally, treatment A caused a significant decrease in the glucose increment within 0–30 min of treatment in subjects with overweight. No significant modifications were found in the other assessed parameters. The acute intake of the CCB by subjects with T2D showed modest although significant results, which need to be validated in a long-term randomised controlled trial.

Punicic acid (PA) is a chief component of pomegranate seed oil with several health benefits. In this study, the in vitro immunomodulatory activity of PA was assessed using RAW264.7 cells, revealing that PA activated the macrophages, facilitated the concentration of immune-related cytokines and enzymes, and regulated the immune-related NF-κB and MAPK signaling pathways. Further, the in vivo immune-enhancing effect of PA was evaluated with the cyclophosphamide (CTX)-induced immune-compromised mouse model with 16S rDNA amplicon sequencing and relative quantification of lipidome. Results indicated that high doses of PA (200 mg kg⁻¹) remarkably restored CTX-induced immune injury by enhancing the innate and adaptive immunity to stimulate the secretion of immune-related factors. In addition, PA improved gut microbiota dysbiosis and ameliorated lipid metabolism disorders. Our research provides a theoretical basis for the exploitation of PA as a functional component with immune-enhancing effects and adds to the potential health uses of pomegranate seed oil.

The interactions between food components and digestive tract enzymes can affect nutrient absorption and impact an individual's health. Certain components, particularly polyphenols, are reported to inhibit digestive enzymes and are commonly referred to as anti-nutritional factors. Reports on this subject often contradict each other, highlighting the need for consistent methodologies to assess the potential impact of bioactive compounds. This study evaluated the “in vitro” activity of pepsin, trypsin, and chymotrypsin using ovalbumin, gluten, and haemoglobin as substrates in the presence or absence of twenty-five bioactive natural compounds belonging to different chemical classes at gastro-intestinal physiological concentrations (0.1 mM). The results indicate that bioactives may have opposite effects on proteolytic activity depending on the substrate/enzyme combination and bioactives structure. With ovalbumin as substrate, piceid and resveratrol were described as strong chymotrypsin activators (+1.46- and 1.17-fold change, respectively), phloridzin dihydrate as a weaker activator (+0.41-fold change), while phloretin was a strong inhibitor (−0.65-fold change). A computational approach based on molecular docking and dynamics simulations was used to investigate the interactions between selected bioactives, chymotrypsin and ovalbumin. The “in silico” study included piceid and phloridzin dihydrate, as well as their respective aglycones (resveratrol and phloretin). The results obtained through computational modelling indicate that all four bioactives can interact with chymotrypsin. However, only those bioactives that enhance in vitro proteolytic activity induce a partial unfolding of ovalbumin's structure. This suggests that the effect of bioactive compounds on protein digestion may be substrate-dependent, and may vary depending on the specific protein being digested.

In this study, pancreatic lipase (PL) inhibitory peptides were identified from a lotus seed protein (LSP) hydrolysate and the potential mechanism was investigated. The LSP hydrolysate was isolated and purified, and six PL inhibitory peptides were screened; in particular, Phe-Leu-Leu (FLL) and Glu-Phe-Phe (EFF) exhibited the strongest inhibitory activity. Molecular docking results indicated that FLL and EFF interacted with residues around the PL active site through hydrogen bonding and hydrophobic interactions. The Lineweaver–Burk curve revealed that FLL acted as a mixed-type inhibitor, while EFF exhibited non-competitive inhibition of PL. Additionally, fluorescence spectroscopy, circular dichroism (CD), and ultraviolet-visible (UV-Vis) spectrometry analyses confirmed that FLL and EFF altered the microenvironment and secondary structure of PL by increasing the β-sheet content and reducing the α-helix content, thereby decreasing the catalytic activity of PL. Molecular dynamics simulation further confirmed that PL–peptide complexes exhibited a more stable state and compact structure. In summary, FLL and EFF could be used in the development of food supplements for obesity prevention.