Food frontiers最新文献

Prunes (Prunus domestica L.) are increasingly recognized for their multifaceted health benefits, which are derived from their rich bioactive compounds. This review aims to consolidate current research on the nutritional components and biological activities of prunes, emphasizing their potential in health promotion and disease prevention. We explore the diverse bioactive compounds in prunes, including polyphenols, polysaccharides, and sorbitol, and their implications for antioxidant, anti-inflammatory, and antimicrobial activities. The review also examines prunes' effects on laxation, osteoporosis prevention, immune modulation, and regulation of glycolipid metabolism. Clinical studies and mechanistic insights are discussed to provide a comprehensive understanding of prunes' health benefits. The review concludes that prunes possess significant health benefits, with future research directions focusing on the identification of active compounds, determination of effective doses, mechanistic research, and clinical validation. This scientific basis for prune-based functional foods and pharmaceuticals development contributes to personalized nutrition strategies, offering a comprehensive overview of prunes' potential in healthcare and disease management.

As an important oilseed and food material, the nutritional quality of peanut is influenced by not only the variety but also place of origin. However, research on the geographical impact remains scarce. In this study, nine peanut cultivars were planted at eight sites to determine geographical effects on quality parameters, including fatty acids, sucrose, tocopherols, and phenolic compounds. General linear model analysis showed that the environment of the producing area was a major factor for nutritional indicators except oleic acid in high-oleic acid peanut varieties (η²: genetic 51.20%, environmental 37.46%). Geographic factors accounted for 58.20%, 68.41%, and 37.15% of the variance in total tocopherols, total phenolics, and sucrose, respectively, while the corresponding varietal effects were 57.83%, 71.06%, and 20.13%. Climate–nutrient interaction analysis revealed this was primarily attributed to low-temperature conditions promoting sucrose and phenolic compound biosynthesis (e.g., quercetin). In contrast, elevated temperature and humidity correlated with tocopherol accumulation. Furthermore, we delineated geographical characteristics: Hubei (high oleic acid/tocopherol) and Xinjiang (high sucrose/phenol). This study determined geography's impact, providing strategies for region-specific breeding to advance the industry.

Postbiotics are inanimate microbial cells, cell fragments, or metabolites generated during fermentation and have emerged as a compelling alternative to traditional probiotics and prebiotics. Despite the growing interest in probiotics, comparatively limited attention has been given to the clinical significance and formulation advantages of postbiotics, which offer superior shelf stability under 25°C for ≥12 months and an acceptable safety profile in immunocompromised populations, as evidenced by in vitro and Phase I data. This review bridges this critical gap by systematically exploring the sources, mechanisms of action, health benefits, and food formulation strategies associated with postbiotics. The review provides a critical analysis of recent clinical and preclinical evidence, underscoring the role of postbiotics in immune modulation, metabolic regulation, gut–brain axis signaling, and anti-cancer activity. Additionally, the innovation in formulation technologies was assessed, along with regulatory considerations (European Food Safety Authority/Food and Drug Administration [EFSA/FDA]) and future opportunities involving synthetic biology and personalized nutrition. Drawing on a comprehensive literature review and comparative case analyses, this review presents novel insights that position postbiotics as scientifically validated, in alignment with current regional regulatory frameworks, and technologically feasible agents for next-generation functional foods. Ultimately, the article argues that postbiotics address key limitations of probiotics, namely, safety, viability, and efficacy, while paving the way for advanced microbiome-based interventions in food systems.

Lactic acid bacteria (LAB) are frequently used as health supplements. They enhance digestion, regulate immunity, improve gut microbiota, and prevent and manage diseases. Autophagy has a crucial role in the prevention and treatment of tumors, cardiovascular diseases, and pathogenic infections. Research has indicated that autophagy is a significant pathway by which LAB improve health. In this review, we provide a comprehensive review on cellular and animal studies (a total of 45 studies) and summarize the LAB roles and possible mechanisms for regulating autophagy and enhancing health. Moreover, it identified challenges and opportunities of LAB in regulating autophagy to improve health. LAB provided numerous advantages and had great potential for regulating autophagy to improve health due to its ability to inhibit the proliferation of intracellular pathogens, remove harmful bacteria, alleviate pathogen-induced inflammation, reduce oxidative stress, improve the intestinal barrier, downregulate apoptotic protein, promote cancer cell apoptosis, inhibit cancer cell proliferation, and suppress drug and toxin responses. Moreover, it identified challenges from the aspects of strain selection, dose–response studies, targeted strain delivery, mechanistic analyses, and clinical studies, then predicted the opportunities for future research. This will have an important enlightening and guiding effect on the basic and clinical research of LAB to improve human health and the development of LAB dietary supplements.

Heat stress (HS) induces intestinal inflammation and dysbiosis, and Bifidobacterium exhibits anti-HS roles in the intestinal tract. l-theanine (LTA) increases intestinal Bifidobacterium abundance in HS-exposed mice and may modulate Hsf1 to alleviate HS-mediated intestinal immune injury; however, the underlying mechanism remains unclear. This study found that LTA alleviated HS-induced MODE-K cell inflammatory injury by modulating Hsf1, and this effect was absent when Hsf1 expression was inhibited. In heat-stressed Hsf1 knockout (KO) mice, LTA failed to regulate colon immunity and the expression of Hsf1 and its target proteins Hsp70 and Hsph1. Bifidobacterium longum (BL) ameliorated HS-induced intestinal injury in pseudo-germ-free mice and inhibited the expression of Hsf1 and its target proteins, indicating its potential against HS; LTA in combination with BL was more effective than BL or LTA alone in modulating the above indices. Compared to the BL group, 200 µM LTA intervention using an in vitro co-culture system increased BL abundance. Moreover, the co-culture supernatant increased MODE-K cell viability and IL-10 and sIgA secretion under HS conditions, and this effect was not conspicuous following the targeted inhibition of Hsf1. These findings suggest that LTA mediates Hsf1 modulation of intestinal immunity by increasing the abundance of B.longum to alleviate HS. These findings provide scientific evidence for the development of anti-HS functional foods and the extensive application of LTA.

This study investigated the structural characteristics and anti-inflammatory potential of Tremella fuciformis stem byproduct-derived polysaccharide TFP-1. Structural analysis revealed that TFP-1 is an acetylated heteropolysaccharide composed of mannose, xylose, fucose, and glucuronic acid in a molar ratio of 6.18:1.09:2.13:1. It likely has a 3-α-d-Manp backbone, branched by T-α-l-Fucp, 2-β-d-Xylp, and T-β-d-GlcAp at the O-2 position, with partial acetylation at C6-OH of mannoses. The anti-inflammatory activity of TFP-1 was also assessed. It was shown to inhibit the production of inflammatory factors in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages by regulating the NF-κB pathway. These findings suggest TFP-1 may serve as a potential anti-inflammatory supplement.

Lonicera caerulea berry polyphenols (LCBP) exhibit multiple physiological effects. In this study, we investigated the role of LCBP in reducing cholesterol accumulation in rats with type 2 diabetes mellitus (T2DM) and its underlying mechanism. LCBP reduced the content of neutral lipids in the aorta and decreased the plaque area by 47.3% (p < 0.01) compared with that in the model group. LCBP also reduced the expression of CD11b and F4/80 in peritoneal macrophages. The cholesterol efflux rate in the LCBP group increased significantly by 61.2% (p < 0.01). Western blotting and immunohistochemical experiments revealed that LCBP promoted cholesterol efflux via a dual mechanism of activating silent information regulator 1 (SIRT1) in macrophages in a high-glucose environment and the miR-33/SREBP2-ABCA1 pathway. SIRT1 activation enhanced the effects of LCBP on cholesterol regulation. Molecular dynamics simulation experiments revealed that the three main monomer components of LCBP—cyanidin-3-glucoside, catechin, and chlorogenic acid—could stably bind to the active site of SIRT1 and serve as key components in the regulation of cholesterol by this protein. This study provides new insights into the use of LCBP as a functional food additive for T2DM-related atherosclerosis.

The gut microbiota is crucial in Alzheimer's disease (AD) progression. This study investigated the effects of milk fat globule membrane (MFGM) on AD-related cognitive deficits and mechanisms involving the gut microbiota–brain axis using APP/PS1 mice. Behavior, physiological indicators, neuroinflammation, and microRNAs (miRNAs) in the hippocampus were examined. Then, serum differential metabolites were explored and used to evaluate anti-neuroinflammatory and neuroprotective effects in vitro. To further clarify the reasons for alterations in serum metabolites, the role of MFGM on gut microbiota was explored. Then, APP/PS1 mice (AD^COH) were co-housed with MFGM-fed APP/PS1 mice (AD+MFGM^COH) to allow microbiota transfer via coprophagy. MFGM mitigated learning and memory deficits, neuronal damage, synaptic dysfunction, and blood–brain barrier leakage, associated with suppression of β-amyloid (Aβ) accumulation and Tau phosphorylation (p-Tau^Ser396). It alleviated neuroinflammation via suppressing expression of inflammatory factors, microglial activation marker ionized calcium-binding adaptor molecule 1 (IBA-1) and NLRP3 pathway, which might be correlated with the modulation of miRNA profile in the hippocampus. Moreover, metabolomic analysis identified resolvin D1 (RVD1) and anandamide (AEA) were enriched due to MFGM supplementation. These metabolites regulated miRNAs, suppress neuroinflammation via inhibiting inflammatory factors, IBA-1 expression, and NLRP3 pathway in BV2 cells, and attenuate p-Tau^Ser396 in SH-SY5Y cells. Furthermore, MFGM modulated gut microbiota and effects of MFGM on cognitive impairment were proved to be associated with increased serum RVD1 and AEA mediated by gut microbiota. In summary, MFGM attenuated AD-related cognitive impairment through suppressing neuroinflammation, correlated with the modulation of gut microbiota-serum RVD1/AEA–brain axis, indicating it could delay AD progression.

The cover image is based on the Research Article Gut Microbiota-Bile Acid Metabolism Axis Drive Anti-Diabetic Effects of Polygonatum cyrtonema Polysaccharide on Glycolipid Metabolism and Intestinal Inflammation by Qiang Yu et al., https://doi.org/10.1002/fft2.70105.

Medulla Tetrapanacis (MT) is traditionally consumed as herbal soup to manage mastitis. Although scientific evidence supports its anti-inflammatory effect, no study has investigated its effect on ulcerative colitis (UC). This study aimed to investigate the effect of MT water extract and its underlying mechanisms both in vitro and in vivo. Dextran sulfate sodium (DSS) was used to induce UC in zebrafish for assessing the effect of MT water extract on oxidative stress, inflammation, and migration of neutrophils. A DSS-induced UC mouse model was further employed to examine the effect of MT on oxidative stress, inflammation, macrophage phenotype, histopathology, and intestinal barrier integrity. Moreover, bone-marrow-derived macrophages (BMDMs) were used to elucidate the actions of MT on regulating polarization and energy metabolism. In vitro results showed that MT water extract significantly suppressed lipopolysaccharide and interferon-gamma-induced M1 polarization in BMDMs by reprogramming energy metabolism via suppressing hypoxia-inducible factor-1α (HIF-1α)/glycolysis. In zebrafish, MT water extract remarkably reduced neutrophil intestinal infiltration, reactive oxygen species generation, and expressions of pro-inflammatory genes (inducible nitric oxide synthase [iNOS], cyclooxygenase-2 [COX-2], interleukin [IL]-6, and IL-1β) in DSS-induced UC. Furthermore, MT treatment alleviated symptoms and histopathological damage in DSS-induced UC in mice, restored the balance of M1/M2 macrophages in the colon, attenuated inflammation and oxidative stress, and preserved intestinal barrier integrity. In conclusion, MT water extract ameliorated DSS-induced UC by regulating macrophage polarization through reprogramming of energy metabolism via suppressing HIF-1α/glycolysis, suppressing oxidative stress, and maintaining intestinal barrier integrity. These findings support the application of MT for managing UC.