Carotenoids are tetraterpene compounds acting as precursors to vitamin A, with functions that include protecting eyesight, enhancing immunity, promoting cell growth and differentiation, and providing antioxidative benefits. Lycopene, β-carotene, and astaxanthin are particularly critical for health and have diverse applications in food, health products, and medicine. However, natural carotenoids are encased within cell structures, necessitating mechanical methods to disrupt the cell wall for their extraction and purification—a process often influenced by environmental conditions. Thus, improving the efficiency of carotenoid extraction from natural resources is of great interest. This review delves into the research progress made on the extraction processes, structures, and biological functions of carotenoids, focusing on lycopene, β-carotene, and astaxanthin. Traditional extraction methods primarily involve organic solvent-assisted mechanical crushing. With deeper research and technological advancements, more environmentally friendly solvents, advanced machinery, and suitable methods are being employed to enhance the extraction and purification of carotenoids. These improvements have significantly increased extraction efficiency, reduced preparation time, and lowered production costs, laying the groundwork for new carotenoid product developments.

Hypercholesterolemia is an independent risk factor of cardiovascular disease, which is among the major causes of death worldwide. The aim of this study was to explore whether Bifidobacterium longum strains exerted intra-species differences in cholesterol-lowering effects in hypercholesterolemic rats and to investigate the potential mechanisms. SD rats underwent gavage with each B. longum strain (CCFM 1077, I3, J3 and B3) daily for 28 days. B. longum CCFM 1077 exerted the most potent cholesterol-lowering effect, followed by B. longum I3 and B3, whereas B. longum B3 had no effect in alleviating hypercholesterolemia. Divergent alleviation of different B. longum strains on hypercholesterolemia can be attributed to the differences in bile salt deconjugation ability and cholesterol assimilation ability in vitro. By 16S rRNA metagenomics analysis, the relative abundance of beneficial genus increased in the B. longum CCFM 1077 treatment group. The expression of key genes involved in cholesterol metabolism were also altered after the B. longum CCFM 1077 treatment. In conclusion, B. longum exhibits strain-specific effects in the alleviation of hypercholesterolemia, mainly due to differences in bacterial characteristics, bile salt deconjugation ability, cholesterol assimilation ability, expressions of key genes involved in cholesterol metabolism and alterations of gut microbiota.

Gut microbial colonization is a dynamic balance shaped by host genetics and immunity, microbial ecology, and environmental exposures. This review synthesizes evidence on host barriers and immunity—mucus architecture, antimicrobial peptides, pattern recognition receptors, and secretory IgA—and on genetic loci such as LCT and ABO/FUT2 that modulate nutrient landscapes and strain selection. Microbial adaptability is summarized, including polysaccharide utilization loci and human milk oligosaccharide metabolism, bile salt hydrolase–mediated tolerance, extracellular polysaccharide–driven immune modulation, oxygen—gradient–linked metabolic partitioning, and adhesion mechanisms that secure niche occupancy. Environmental perturbations are evaluated, spanning dietary patterns, protein sources, polyphenols, food additives, pharmaceuticals, and lifestyle factors such as physical activity, circadian alignment, and smoking, which reshape resource competition, barrier integrity, and community resilience. Interaction frameworks that govern stability and dysbiosis are delineated, including competitive inhibition, cross-feeding, quorum sensing, cross-kingdom crosstalk among bacteria, fungi, and phages, and horizontal gene transfer that accelerates adaptation and resistance. Niche elasticity is proposed as a systems metric to quantify stability and recovery after perturbation. Translational strategies combine engineered probiotics, anti-adhesion approaches, and rationally designed phages and lysins with in situ multi-omics to enable mechanism-guided, personalized interventions for food science and microbial engineering.

The potential role of probiotics in mitigating hyperlipidemia has garnered increasing evidence, yet the specific mechanisms warrant further investigation. This study aimed to examine the alterations in short-chain fatty acids (SCFAs), a hypothesized lipid-lowering mechanism of probiotics, in animal models and to evaluate the lipid-lowering effects of probiotics on hyperlipidemic animal models through a meta-analysis of preclinical experiments. Methods: A comprehensive search of PubMed, Web of Science, EMBASE, Cochrane Library and Google Scholar up to June 2024 yielded nine studies that met the inclusion criteria (INPLASY registration number: No. CRD42024559937). The analysis revealed that mice receiving probiotics exhibited a significant increase in SCFA levels compared with control mice (acetic acid: standard mean difference [SMD] = 1.26, 95% confidence interval [CI] 0.80 to 1.72, P < 0.00001, I² = 28%; propionic acid: SMD = 1.99, 95% CI 1.47 to 2.51; butyric acid: SMD = 0.66, 95% CI 0.04 to 1.28, P = 0.04, I² = 22%; acetate: SMD = 4.5, 95% CI 3.57 to 5.42, P < 0.00001, I² = 48%; propionate: SMD = 0.76, 95% CI 0.37 to 1.15, P = 0.0002, I² = 44%; butyrate: SMD = 2.8, 95% CI 2.18 to 3.41, P < 0.00001, I² = 26%). Additionally, probiotic consumption reduced markers of oxidation and inflammation as well as liver damage enzymes. The findings from this meta-analysis suggest that probiotics can enhance SCFA content in the body, decrease lipid levels in animals, improve oxidative stress and inflammation, reduce liver damage, and effectively alleviate hyperlipidemia.

Metabolic-associated fatty liver disease (MAFLD) is a prevalent global health issue closely tied to dietary habits, impacting a significant portion of the adult population. MAFLD is linked to various metabolic disorders, elevating risks of cirrhosis and hepatocellular carcinoma and severely impacting patients’ quality of life. While therapeutic research has progressed, effective food-based interventions remain scarce. Natural products, rich in bioactive compounds and offering health benefits, have gained attention for their potential in managing MAFLD. This study employed network pharmacology and lipidomics to investigate the therapeutic effects of Food and Medicine Homology (FMH) on MAFLD using a high-fat-diet-induced HepG2 cell model. We identified 169 potential bioactive components from Radix Puerariae, Hericium erinaceus, Rhizoma Curcumae longae, Camellia oleifera, and Hoveniae Dulcis Semen, constructing a drug–component–target network that highlighted 34 key targets. The characteristic components of this FMH compound solution (HSD) were identified using UPLC-QTOF-MS/MS. In vitro, HSD significantly reduced intracellular lipid accumulation, decreased inflammatory markers, and mitigated hepatocyte damage. Lipidomics analysis revealed significant alterations in lipid metabolites, suggesting HSD’s potential to modulate sphingolipid and glycerophospholipid metabolism, thus improving MAFLD outcomes. This research underscores the critical role of the FMH complex in modulating lipid metabolism and inflammatory pathways, offering valuable insights for developing FMH-based dietary supplements and functional foods to alleviate MAFLD. By leveraging the synergistic effects of natural compounds, our findings hold significant implications for innovative nutritional strategies in managing this prevalent metabolic disorder.