Obesity has emerged as one of the most prevalent chronic diseases worldwide. Our study was conducted to investigate the anti-obese potential of novel probiotic Bifidobacterium longum subsp. infantis FB3-14 (FB3-14) and the underlying molecular mechanisms in high-fat diet (HFD)-fed mice. The results demonstrated that an 8-week FB3-14 intervention significantly suppressed the HFD-induced body and fat weight gain and abnormal alterations of the serum lipid parameter, restoring the levels of cholesterol (4.29 mmol/L) and low-density lipoprotein cholesterol (3.42 mmol/L). FB3-14 treatment also attenuated adipocyte expansion, hepatic injury, and low-grade systemic inflammation and restored the expressions of lipid-metabolism-related genes, including Hsl, Leptin, and Adiponectin. Furthermore, FB3-14 was observed to reduce the Firmicutes/Bacteroidetes ratio in obese mice; increase the abundance of Akkermansia muciniphila, unclassified_Muribaculaceae, Lachnospiraceae_NK4A136_group, and Bifidobacterim; and upregulate G protein-coupled receptor41 associated with higher levels of butyric acid. These results indicate the protective effectiveness of FB3-14 in HFD-driven obesity and gut microbiota disorders, highlighting the promising potential of FB3-14 as a functional nutrition supplement.

Food allergy (FA) has become a prominent problem in public health. 2′-Fucosyllactose (2′-FL) was reported to alleviate FA symptoms; however, the regulatory mechanism is still unclear. This study evaluated the 2′-FL antiallergic potential in an ovalbumin (OVA)-sensitized mouse model and explored the systemic effects of 2′-FL on gut microecology and the intestinal immune barrier. The results showed that 2′-FL alleviated allergy symptoms, decreased serum allergic indicator levels, enhanced the intestinal barrier, and attenuated low-grade inflammation. The up-regulation of G protein-coupled receptors (GPRs) was associated with higher levels of short-chain fatty acids (SCFAs) in 2′-FL intervention mice. 2′-FL also improved the intestinal microbiota diversity and increased the abundance of Akkermansia, Lachnospiraceae UCG-006, and Ruminococcaceae while suppressing Muribaculaceae, Desulfovibrionaceae, and Erysipelotrichaceae. Additionally, 2′-FL ameliorated the imbalance of Th2/Th1, mainly by decreasing Th2-type immune response and enhanced CD4 + Foxp3 + Treg immunoreaction. These results suggest that 2′-FL restores intestinal barrier defects, gut microbiota disorder, and immune impairment while alleviating ovalbumin-induced allergic symptoms in FA mice.

Cold-brewed jasmine tea (CB-JT) is regarded to possess characteristic flavors and health benefits as a novel resource of functional tea beverages. To investigate the molecular mechanisms underlying CB-JT-mediated protective effects on obesity, we evaluated the serum biochemistry, histological condition, glucose tolerance, gene expression profile and intestinal microbial diversity in high-fat diet (HFD)-fed mice. Our results demonstrate that cold-brewed jasmine tea can significantly attenuate HFD-induced body weight gain, abnormal serum lipid levels, fat deposition, hepatic injury, inflammatory processes as well as metabolic endotoxemia. CB-JT also modified the microbial community composition in HFD-fed mice and altered the balance to one closely resembled that of the control group. The differential abundance of core microbes in obese mice was reversed by CB-JT treatment, including an increment in the abundance of Blautia, Mucispirillum, and Bilophila as well as a decrease in the abundance of Alloprevotella. CB-JT was proved to regulate the mRNA expression levels of lipid metabolism-related genes such as Leptin, Pgc1a Il6, and Il1b in the adipose tissue coupled with Cyp7a1, Lxra, Srebp1c, and Atgl in the liver. These findings indicate that cold-brewed jasmine tea might be served as a potential functional tea beverage to prevent obesity and gut microbiota dysbiosis.

Background: Based on our extensive cohort study, the Maternal Nutrition and Infant Investigation (MUAI), this research investigated the associations between human milk oligosaccharide (HMO) intake during the postnatal period and allergic disease development and gut microbiome composition in early childhood through long-term follow-up. Methods: Human breast milk (HBM) samples at five lactation stages and fecal samples of infants and young children were collected. Children aged 5 years included in this study were categorized into allergic and non-allergic groups via standardized allergen testing. Results: The findings indicated that higher HMO intake levels across five distinct lactation periods may be linked to a reduced incidence of allergies in children. The consumption of six major structurally representative HMOs was significantly associated with alterations in the gut microbiota profiles of young children. Moreover, there were notable differences in gut microbiota composition between allergic and non-allergic children. Specifically, beneficial bacteria such as Bifidobacterium, Akkermansia, and Ruminococcus were significantly enriched, in addition to the levels of metabolite propionic acid, a beneficial short-chain fatty acid, which were notably higher in the non-allergic group. To further validate the relationship between Bifidobacterium abundance and early HMO intake, the analysis revealed that a differential strain biomarker, Bifidobacterium adolescentis (B. adolescentis), exhibited significant correlations with specific HMOs at different lactation stages, particularly showing a strong positive correlation with 2′-fucosyllactose (2′-FL) content. Conclusions: These findings suggest that early-life HMO intake is associated with long-term differences in allergic outcomes, potentially through modulation of gut microbiota composition, particularly the enrichment of B. adolescentis.

2′-Fucosyllactose (2′-FL) represents a significant constituent within human milk oligosaccharides, and its benefits for intestinal health and neurodevelopment in infants and young children have been widely recognized. However, the mechanism by which 2′-FL influences early-life behavioral development through the gut–brain axis remains incompletely understood. In this study, we investigated the effects of neonatal 2′-FL supplementation on behavioral development in Sprague-Dawley (SD) rats and explored its potential microbiota-metabolite regulatory mechanisms. After 4 consecutive weeks of oral gavage beginning on postnatal day 2, rats receiving 2′-FL showed significantly increased average movement speed and central-area exploration time in the open field test. From a systemic perspective, 2′-FL lowered blood diamine oxidase (DAO) and D-lactic acid (D-LA) concentrations while elevating colonic mRNA levels of tight junction protein-related genes, consequently enhancing intestinal barrier stability. In addition, 16S rRNA sequencing showed that 2′-FL reshaped the gut microbiota structure and significantly enriched Lactobacillus, Bacteroides, and short-chain fatty acid (SCFA)-associated taxa represented by Lachnospiraceae_NK4A136_group. Untargeted metabolomics revealed that 2′-FL induced systemic metabolic remodeling, characterized by upregulation of the bioactive metabolites dehydroepiandrosterone sulfate (DHEA-S) and deoxycholic acid (DCA), and downregulation of the glucocorticoid-related corticosterone. Western blot validation further showed higher hippocampal protein expression of postsynaptic density protein 95 (PSD95), brain-derived neurotrophic factor (BDNF), and synaptophysin in the 2′-FL group, supporting enhanced synaptic plasticity-related signaling. In summary, neonatal 2′-FL intervention enhanced exploratory behavior and was accompanied by increased hippocampal synaptic plasticity-related protein expression in rats, potentially through coordinated regulation of gut microbiota composition and systemic metabolism.

Background: Joint inflammation is significantly connected with progressive joint deterioration, potentially increasing the incidence of persistent major clinical challenges and global disability. Nutrient-based preventive strategies have been explored to investigate the interventive efficacy of the proposed prescribed formula for joint inflammation. However, the synergistic ameliorative effects of the nutritional formula should be evaluated to investigate its impact on joint inflammation. Methods: A prescribed formula including turmeric (T), N-acetylglucosamine (G), enzymatically hydrolyzed bone powder (E), and undenatured type II collagen (U) was comprehensively evaluated for its synergistic effects on joint inflammation and the underlying mechanisms. A rat model established using the Hulth method was used to evaluate the interventive effects in vivo. Moreover, in vitro analysis using the murine chondrogenic cell line ATDC5 was performed to validate the intervention and its mechanism of action. Results: The prescribed formula was shown to synergistically reduce levels of inflammation-related cytokines, reduce oxidative stress, and enhance bone metabolism to promote joint regeneration. Micro-Computed Tomography (Micro-CT) analysis revealed restoration of joint architecture and ameliorated physiological status upon formula intervention. In vitro analysis further validated the synergistic alleviation of inflammation and oxidation, as well as reductions in MMP13 and CTX-1 levels, which implies that modulating bone metabolism alleviates the deterioration and inflammation of joint architecture. Conclusions: The synergistic formula in this study achieves synchronous modulation of several core pathological pathways, yielding synergistic modulation of joint inflammation. Nutrient-based interventions or preventive strategies show promising effects against joint inflammation and progressive mechanistic deterioration.