Obesity is characterized by abnormal adipose tissue expansion and energy metabolism imbalance. Browning of white adipose tissue (WAT), wherein white adipocytes acquire thermogenic properties similar to brown adipose tissue, represents a key mechanism for increasing energy expenditure. Although ginseng (Panax ginseng C.A. Meyer) is widely recognized as a health-promoting botanical, its role in WAT browning has not been fully elucidated. This review summarizes evidence that ginseng and its bioactive components regulate major thermogenic pathways, including β-adrenergic/cyclic adenosine monophosphate-protein kinase (cAMP-PKA) signaling, AMP-activated protein kinase (AMPK), and the peroxisome proliferator-activated receptor γ (PPARγ)/coactivator 1α (PGC-1α) axis, thereby upregulating key markers such as uncoupling protein 1 (UCP1), PR domain containing 16 (PRDM16) and type II iodothyronine deiodinase (DIO2). These effects promote mitochondrial function and fatty acid oxidation, reduce lipogenesis, alleviate inflammation, and improve insulin sensitivity, collectively fostering a microenvironment conducive to browning. Furthermore, fermentation has been found to enhance the bioactivity and thermogenic efficacy of ginseng. Recent evidence indicates that gut microbiota and their metabolites—such as short-chain fatty acids, unsaturated fatty acids, and bile acids—play a notable role in ginseng-induced thermogenesis via receptors including G-protein-coupled receptor 41/43 (GPR41/43), takeda G-protein-coupled receptor 5 (TGR5), and farnesoid X receptor (FXR). These multi-organ interaction networks involving the gut–fat, gut–liver, and gut–brain axes reflect the role of ginseng in integrating systemic metabolism. In summary, this review discusses the multi-level regulatory network through which ginseng promotes WAT browning, providing a mechanistic basis for its potential application in body weight and metabolic health management.

Background: Oxidative stress, induced by the aging process, has been demonstrated to engender a variety of deleterious effects on the organism. The effectiveness of selenium-enriched Rhodotorula mucilaginosa remains unproven. Methods: In this study, selenium-enriched Rhodotorula mucilaginosa JAASRY1 ( Se-RMSRY ) was comprehensively characterized. Scanning electron microscopy coupled with energy-dispersive X-ray spectroscopy was employed to analyze its morphology and the elemental distribution of selenium. Furthermore, the specific chemical forms of biogenic selenium in Se-RMSRY were identified and quantified using high-performance liquid chromatography-inductively coupled plasma mass spectrometry. The potential of Se-RMSRY to exert antioxidant mechanisms for anti-aging effects was then systematically elucidated. Animal behavioral tests demonstrated behavioral differences induced by Se-RMSRY , thereby evaluating the improvement in aging phenotypes. Histopathological analysis of the hippocampus, liver, and intestine was performed to examine structural integrity and pathological changes. Intracellular reactive oxygen species (ROS) levels were detected using fluorescence-based assays to confirm oxidative stress mitigation. Western blotting was employed to validate the expression of aging-related proteins. Additionally, gut microbiome analysis via 16S rRNA sequencing was carried out to explore the composition and diversity of gut microbiota, thereby uncovering potential links between antioxidant activity and gut health in the anti-aging process. Results: The results showed that selenomethionine (SeMet) was the predominant bioselenium composition of Se-RMSRY , with a concentration of 1213.16 mg/kg. Furthermore, Se-RMSRY significantly enhanced intestinal homeostasis by enriching beneficial Lactobacillus sp. populations and reprogramming microbial metabolism toward carbohydrate utilization while suppressing amino acid metabolism in aging mice ( p < 0.05). Systemic antioxidant capacity was augmented via coordinated activation of the Nrf2/NQO1/HO-1 signaling pathway and glutathione metabolism, with concomitant reductions in hepatic and intestinal oxidative stress markers ( p < 0.05). The intervention attenuated apoptosis through Bcl-2/Bax pathway modulation and improved gut barrier integrity ( p < 0.05), while hippocampal CA1 neuronal preservation correlated with reduced anxiety-like behaviors and enhanced cognitive performance ( p < 0.05). Conclusion: These findings establish Se-RMSRY as a promising dietary intervention against age-related pathologies through gut–microbiota–organ axis regulation, thereby addressing the previously unproven efficacy of Se-RMSRY in counteracting aging-related oxidative stress.

Background: Natto, a well-known fermented soybean product beneficial for bone health, remains unclear in its mechanism. Methods: This study investigated its effect on secondary osteoporosis (OP) in mice. Results: Natto significantly inhibited weight loss, bone quality deterioration, and bone morphological damage, and regulated OPG/RANKL pathway protein expression (p < 0.05) in OP mice. Analysis of 16S rRNA revealed that natto increased gut microbiota α-diversity and the abundance of Sutterella, Roseburia, and Coprococcus, while reducing harmful bacteria such as Streptococcus, Shigella, and Helicobacter. These microbial changes positively correlated with body weight, bone size, and serum osteogenic metabolism in OP mice. Serum metabolomics showed differential metabolites of the natto group enriched in PPAR signaling and primary bile acid biosynthesis. Verification by mRNA and ELISA indicated that the upregulated liver and circulating PPARα by natto may regulate downstream bile acid pathways, linking gut microbiota to multi-organ metabolic functions. Conclusions: In summary, natto may act on gut microbiota to alleviate bone loss via the “gut microbiota–bile acid–OPG/RANKL” network, targeting multiple organs including gut, liver, and bone. This provides a theoretical basis for natto dietary intervention in osteoporosis prevention through the gut–bone axis.