Food & Function最新文献

Obesity and its associated metabolic disorders are major global health concerns, highlighting the need for novel dietary interventions. Xylitol, a polyol widely used as a sugar substitute, has shown metabolic benefits beyond its sweetening properties. However, the potential physiological effects of its enzymatically modified derivatives, particularly β-galactosylated xylitol (XylGal), remain largely unexplored. In this study, we evaluated the impact of XylGal and unmodified xylitol (Xyl) on metabolic health and gut microbiota composition in a murine model of diet-induced obesity. Lean and obese C57BL/6J mice received daily doses of Xyl (50 mg kg^-1) or XylGal (50 and 100 mg kg^-1) for seven weeks. Our findings indicate that both Xyl and XylGal significantly reduced body weight gain, adipose tissue accumulation, and liver weight in obese mice, without affecting food intake. Additionally, Xyl and XylGal modulated glucose homeostasis, with Xyl-treated mice exhibiting improved glucose tolerance. A significant reduction in inflammatory cytokine expression (TNF-α, IL-1β) in abdominal fat was observed, suggesting decreased macrophage infiltration and attenuation of obesity-induced inflammation. High-throughput sequencing of 16S rRNA revealed that both compounds promoted beneficial bacterial genera, including Lachnospiraceae NK4A136 and Eubacterium xylanophilum, while reducing potentially obesity-associated taxa such as Blautia and Colidextribacter. These results suggest that XylGal and Xyl exert prebiotic effects that contribute to their metabolic benefits. Our study provides new insights into the potential of these compounds as functional ingredients for obesity management and metabolic health improvement.

The integration of plant proteins with bioactive compounds offers a promising strategy to enhance their environmental stability. This study investigated the complexation of mung bean protein (MBP) with epigallocatechin gallate (EGCG) and the impact of affinity differences resulting from structural variations of MBP on the performance of the resulting complexes. MBP fractions obtained via ammonium sulfate precipitation displayed distinct protein compositions, especially MBP-60%S, which was mainly 8S vicilin. MBPs and EGCG rely on hydrogen bonding and hydrophobic interactions for spontaneous self-assembly, with hydrogen bonding dominating in highly soluble MBP. EGCG binding induced structural changes in MBPs, including an increase in α-helix content and size, as well as a reduction in β-sheet content and solubility. Notably, MBP-60%S exhibited the strongest affinity for EGCG. These conformational shifts enhanced the thermal stability of EGCG, thereby mitigating the loss of antioxidant capacity due to its thermal degradation. Moreover, the bioaccessibility of EGCG was increased by 1.91-3.22-fold. However, MBP-60%SE showed resistance to gastric digestion, likely due to the altered protein structure and interaction strength. Overall, these findings provide valuable insights into the functionalization of plant proteins, offering a foundation for the development of high-quality functional foods and novel applications of mung bean protein.

Alzheimer's disease (AD) is mainly manifested by cognitive dysfunction, accompanied by excessive β-amyloid (Aβ) deposition and neuroinflammation. The regulation of vagus nerve (VN) signal transmission is crucial for influencing the pathological progression of AD and exploring new therapeutic approaches. Two doses of 2'-fucosyllactose (2'-FL, 500 and 1000 mg kg^-1) were administered orally to AD model mice. 2'-FL rescued spatial and recognition memory deficits in AD mice. Moreover, 2'-FL reduced Aβ deposition and neuroinflammation. 2'-FL enhances c-Fos expression in the solitary tract nucleus (NTS). This suggested that 2'-FL alleviated AD-related cognition by enhancing VN afferent activity. Vagotomy demonstrated that the alleviation of AD-related cognition by 2'-FL depended on the presence of VN. Moreover, 2'-FL enhanced gut barrier function and alleviated gut inflammation. Notably, 2'-FL also reshaped the gut microbiota composition, increasing the relative abundance of Intestinimonas, Muribaculum, and others. Moreover, 2'-FL promoted the production of short-chain fatty acids (SCFAs). Correlation analysis showed that propionate was highly correlated with other related indicators. After vagotomy, although 2'-FL promoted SCFA production, it did not alleviate cognitive impairment. This suggested that the neuroprotective effect of SCFAs could also be partially dependent on the VN. 2'-FL rescued the cognitive deficits in AD mice, which was partly explained by changes in gut microbial composition, production of SCFAs, and the presence of VN.

In type 2 diabetes mellitus (DM), there is a combination of impaired insulin secretion and resistance in the target tissues. In the case of the liver, these events lead to decreased insulin effectiveness and increased glucagon levels, resulting in an imbalance that promotes excessive hepatic gluconeogenesis and glycogenolysis, contributing to hyperglycemia. Effective management of hyperglycemia and insulin resistance is crucial, underscoring the need for innovative liver-specific interventions. Polyphenols, renowned for their diverse biological activities, have emerged as promising candidates to treat type 2 DM. Based on a literature review spanning the last decade, this comprehensive systematic review thoroughly evaluates the effectiveness of polyphenols in targeting hepatic pathways for managing type 2 DM. The focus will be on assessing how polyphenols affect key targets, including protein tyrosine phosphatase 1B (PTP1B), the glucagon receptor, glucokinase, glycogen phosphorylase, and fructose 1,6-bisphosphatase. While there has been considerable attention on polyphenols as PTP1B inhibitors, studies on their impact on other targets have been comparatively limited. Notably, there is a lack of studies exploring polyphenols as glucagon receptor antagonists. Among polyphenols, flavonoids exhibit significant potential across diverse pathways, with hydroxy groups playing a pivotal role in their biological activities. However, further research, especially in cellular and animal models, is warranted to thoroughly validate their efficacy.

Collagen peptides have shown potential in improving skin conditions. Based on this, we hypothesized that the protease-resistant portion of these peptides might act as a prebiotic to enhance collagen synthesis by modulating the gut microbiota and activating the TGF-β pathway. In vivo rat models and everted gut sac experiments demonstrated that hydroxyproline-containing tripeptide-rich collagen peptides (CTP) exhibited superior absorption compared to high molecular weight collagen peptides. In a skin collagen-deficient mouse model, CTP supplementation significantly increased skin collagen content by 119.95% compared to the control group. Transcriptomic analysis showed that CTP enhanced skin collagen synthesis and inhibited inflammation-related collagen degradation through the TGF-β pathway, involving anti-inflammatory cells such as plasma cells. Gut microbiota analysis showed that CTP increased the gut microbiota α diversity (Shannon index) and altered the microbial community structure (UniFrac distances), characterized by increased abundance of short-chain fatty acid (SCFA)-producing bacteria, Lachnoclostridium and Roseburia, and enhanced SCFA production. These effects were linked to the delivery of Pro-Hyp to the hindgut according to metabolome analysis, promoting TGF-β-producing cells in the gut and contributing to activation of the TGF-β pathway in the skin. Overall, our study provides novel insights into the mechanism by which CTP promotes skin collagen synthesis through gut microbiota remodeling and TGF-β pathway activation, highlighting the potential of CTP to exhibit prebiotic-like properties for skin health improvement.

Procyanidin B1 (PB1) is a natural polyphenol abundant in whole-grain highland barley as well as in many fruits, vegetables, and medicinal plants. The current study investigated the hepatoprotective effect and potential mechanism of PB1 against hepatic fibrosis. C57BL/6 mice with hepatic fibrosis were induced with thioacetamide (TAA), followed by the administration of PB1 or a positive control, silymarin, or followed by gene silencing of the thyroid hormone-responsive protein (THRSP). Hepatic stellate cells (HSCs) were stimulated with transforming growth factor β (TGF-β) or an isolated mouse peritoneal macrophage (MPM)-primed conditioned medium and cultured with PB1, silymarin or the THRSP agonist. MPMs were cultured in the presence of LPS/ATP and/or PB1. It was found that PB1 decreased the release of inflammatory factors, such as caspase-1 and IL-1β. Moreover, PB1 could activate THRSP and decrease P2X7r-modulated NLRP3 inflammasome activation in the TAA-induced mice. Additionally, PB1 inhibited the expressions of α-SMA, collagen I, the TIMP-1/MMP13 ratio, inflammatory factors, P2X7r, and NLRP3 and increased THRSP expression in activated HSCs and macrophages. THRSP deficiency attenuated the regulatory effect of PB1 on the reverse inflammation of activated HSCs, promoting hepatic fibrosis in vivo and in vitro. PB1 reversed the activation of HSCs by increasing the THRSP-mediated P2X7r/NLRP3 axis, similar in function to THRSP overexpression. PB1 could reverse the activation of HSCs and mitigate hepatic inflammation and fibrogenesis in TAA-induced hepatic fibrosis. Targeting THRSP-mediated P2X7r/NLRP3 is crucial for PB1's action against hepatic fibrosis, underscoring a promising approach and the utility of PB1 for the treatment of hepatic fibrosis.

Oleosomes, native lipid droplets abundant in the plant kingdom, especially in oilseeds, can be extracted in simple steps and have been suggested as lipid carriers or natural substitutes for oil droplets in emulsion-like products for foods, cosmetics and pharmaceuticals. Oleosomes are good candidates as lipid carriers via the oral route due to their limited hydrolysis during gastric digestion and slow hydrolysis in the small intestinal phase. The factors that affect oleosomes' ability to resist in vitro digestion, particularly the influence of their membrane molecular composition and density, remain unknown. Therefore, oleosome lipid hydrolysis was investigated in a model of small intestinal digestion and compared with oil droplets stabilized by whey proteins and/or phospholipids and with oleosomes having lower membrane density. To showcase that the lipid hydrolysis rate can also affect cargo release, oleosomes were loaded with cannabidiol (CBD) and the CBD release was tracked. Oleosomes exhibited significantly slower lipid digestion than the droplets stabilised by whey proteins and/or phospholipids, which were rapidly digested. The low lipid hydrolysis of oleosomes during intestinal digestion has been attributed to the unique structure of the oleosome membrane proteins, oleosins, which have a long amphipathic helix pinned into the oleosome oil core and out of reach for bile salts and enzymes. Oleosomes with lower membrane density exhibited faster lipid hydrolysis, probably because the digestive enzymes could better adsorb on the interface to access the core lipids. The results elucidate the factors that affect the lipid digestion of oleosomes and demonstrate the dynamic nature of oleosomes for the controlled release of lipophilic cargos, such as CBD, in the intestinal tract.

Correction for 'Effects of the DailyColors™ polyphenol supplement on serum proteome, cognitive function, and health in older adults at risk of cognitive and functional decline' by Mary O'Leary et al., Food Funct., 2025, 16, 4505-4520, https://doi.org/10.1039/d4fo06259k.

Ferulic (FA) and vanillic (VA) acids are phenolic compounds with antioxidant activity and health benefits. Our previous research indicated that the utilization of maize dietary fiber by the human gut microbiota might be negatively impacted by phenolic compounds. This study investigated the effects of FA and VA at different concentrations (0, 0.3, 3, 30 mg g^-1) on soluble and insoluble maize bran fibers during in vitro fecal fermentation. High VA (30 mg g^-1) reduced insoluble fiber utilization (p = 0.016), increased branched-chain fatty acid production (p = 0.024), and was associated with increased Veillonellaceae and Bacteroidaceae abundances. Low FA (0.3 mg g^-1) improved soluble fiber utilization (p = 0.017) and enhanced propionate production (p = 0.013). High FA (30 mg g^-1) elevated propionate (p = 0.015) and butyrate (p = 0.004) production. FA and VA reduced Streptococcaceae and Peptostreptococcaceae abundances. These findings highlight the complex interplay between phenolic compounds and dietary fiber utilization with implications for dietary strategies promoting gut health.

Acrylamide (ACR) present in starchy and cereal-based heat-processed foods raises a global health concern. While amino acids (AAs) have been suggested as effective scavengers of acrylamide, there is a dearth of information about the cellular response to amino acid-acrylamide (AA-ACR) adducts. In this work, we conducted a detailed comparison of the effects of ACR versus AA-ACR adducts on two human gastrointestinal cell lines, namely, Caco-2 and HCT-15. Adducts of lysine, glycine, cysteine, and methionine with ACR were prepared under optimised reaction conditions and characterized by a combination of ESI-MS and MS/MS. Exposure of Caco-2 and HCT-15 to these adducts resulted in significant reduction in the formation of reactive oxygen species (ROS) and the prevention of abnormal accumulation of the cells in the G1 phase. The analysis of apoptosis and necrosis in the cell lines treated with AA-ACR clearly indicated the ability of AAs to sequester ACR and block oxidative stress induction that would otherwise be observed, completely precluding apoptosis and necrosis. Sequestration of ACR with each of the four AAs prevented the loss of mitochondrial membrane potential and the induction of autophagy that would otherwise occur upon exposure to ACR. The hitherto untested behaviour of human gastrointestinal cells towards AA-ACR presented in this work supports the application of AAs for the mitigation of ACR in foods.