Osteoporosis is a systemic skeletal disease characterized by low bone mass and micro-architectural deterioration of bone tissue, with a consequent increase in bone fragility and fracture susceptibility. In an aged society with increased life expectancy, the incidence rate of osteoporosis is also rapidly increasing. Inadequate nutrition may negatively influence bone metabolism. Recently, many studies have investigated the functionality of milk-derived exosomes, which play important roles in cell-to-cell communication. However, there are few reports of how milk-derived exosomes influence osteoblast proliferation and differentiation. Here, we determined whether bovine colostrum-derived exosomes promote anti-osteoporosis in vitro and in vivo. Tartrate-resistant acid phosphatase-stained cells were significantly inhibited in Raw264.7 cells treated with exosomes, indicating reduced osteoclast differentiation. We induced osteoporosis in mice using glucocorticoid pellets after orally administering exosomes for 2 mo. Interestingly, the bone mineral density of exosome-fed mouse groups was significantly improved compared with the glucocorticoid-induced osteoporosis group without exosome treatment. In addition, Lactobacillus were decreased in the gut microbiota community of osteoporosis-induced mice, but the gut microbiota community composition was effectively restored by exosome intake. Taken together, we propose that exosomes isolated from bovine colostrum could be a potential candidate for osteoporosis prevention, bone remodeling improvement, and inhibition of bone resorption. To our knowledge, this is the first time that a protective effect of milk exosomes against osteoporosis has been demonstrated in vivo. Our results strongly suggest that bovine colostrum exosomes might be used as a prophylaxis to prevent the onset of osteoporosis. Indeed, our results offer promising alternative strategies in the nutritional management of age-related bone complications.

Although the prevalence of metabolic disorders has progressively increased over the past few decades, metabolic disorders can only be effectively treated with calorie restriction and improved physical activity. Recent research has focused on altering the gut microbiome using prebiotics, probiotics, and postbiotics because various metabolic syndromes are caused by gut microbial dysbiosis. Postbiotics, substances produced or released by microorganism metabolic activities, play an important role in maintaining and restoring host health. Because postbiotics have a small amount of literature on their consumption, there is a need for more experiments on short- and long-term intake. This review discusses current postbiotic research, categories of postbiotics, positive roles in metabolic syndromes, and potential therapeutic applications. It covers postbiotic pleiotropic benefits, such as anti-obesity, anti-diabetic, and anti-hypertensive qualities, that could aid in the management of metabolic disorders. Postbiotics are promising tools for developing health benefits and therapeutic goals owing to their clinical, technical, and economic properties. Postbiotic use is attractive for altering the microbiota; however, further studies are needed to determine efficacy and safety.

Background/Objectives: Dietary patterns, including high-fat and high-carbohydrate diets (HFDs and HCDs), as well as non-dietary factors such as food additives and antibiotics, are strongly linked to metabolic endotoxemia, a critical driver of low-grade chronic inflammation. This review explores the mechanisms through which these factors impair intestinal permeability, disrupt gut microbial balance, and facilitate lipopolysaccharide (LPS) translocation into the bloodstream, contributing to metabolic disorders such as obesity, type 2 diabetes mellitus, and inflammatory bowel disease. Methods: The analysis integrates findings from recent studies on the effects of dietary components and gut microbiota interactions on intestinal barrier function and systemic inflammation. Focus is given to experimental designs assessing gut permeability using biochemical and histological methods, alongside microbiota profiling in both human and animal models. Results: HFDs and HCDs were shown to increase intestinal permeability and systemic LPS levels, inducing gut dysbiosis and compromising barrier integrity. The resulting endotoxemia promoted a state of chronic inflammation, disrupting metabolic regulation and contributing to the pathogenesis of various metabolic diseases. Food additives and antibiotics further exacerbated these effects by altering microbial composition and increasing gut permeability. Conclusions: Diet-induced alterations in gut microbiota and barrier dysfunction emerge as key mediators of metabolic endotoxemia and related disorders. Addressing dietary patterns and their impact on gut health is crucial for developing targeted interventions. Further research is warranted to standardize methodologies and elucidate mechanisms for translating these findings into clinical applications.

Resistant starch serves as a prebiotic in the large intestine, aiding in the maintenance of a healthy intestinal environment and mitigating associated chronic illnesses. This study aimed to investigate the impact of resistant starch-enriched brown rice (RBR) on intestinal health and functionality. We assessed changes in resistant starch concentration, structural alterations, and branch chain length distribution throughout the digestion process using an in vitro model. The efficacy of RBR in the intestinal environment was evaluated through analyses of its prebiotic potential, effects on intestinal microbiota, and intestinal function-related proteins in obese animals fed a high-fat diet. RBR exhibited a higher yield of insoluble fraction in both the small and large intestines compared to white and brown rice. The total digestible starch content decreased, while the resistant starch content significantly increased during in vitro digestion. Furthermore, RBR notably enhanced the growth of four probiotic strains compared to white and brown rice, displaying higher proliferation activity than the positive control, FOS. Notably, consumption of RBR by high-fat diet-induced obese mice suppressed colon shortening, increased Bifidobacteria growth, and improved intestinal permeability. These findings underscore the potential prebiotic and gut health-promoting attributes of RBR, offering insights for the development of functional foods aimed at preventing gastrointestinal diseases.

Radish (Raphanus sativus L.) is a rich source of nutrients and its greens have reported functionalities. This study aimed to investigate the effects of a water-soluble extract from radish greens (WERG) on adipogenesis in 3T3-L1 adipocytes and high-fat diet-induced obesity in model mice. We also quantified the phytochemical composition of WERG such as glucoraphenin and ferulic acid. These findings show that treatment with 100 μg mL⁻¹ WERG reduced lipid accumulation in 3T3-L1 adipocytes, whereas in mice, the administration of 100 mg kg⁻¹ WERG reduced weight gain and hepatic lipid accumulation and improved the levels of serum lipid biomarkers. Furthermore, WERG treatment improved intestinal permeability and suppressed the activities of harmful intestinal enzymes in feces, thus improving gut health. It also inhibited metabolic endotoxemia and inflammatory marker levels in serum. Moreover, WERG reduced the expression of lipid-metabolism-related proteins in the liver and white adipose tissue. Collectively, these results indicate that WERG may potentiate the anti-obesity effect by improving gut health and regulating lipid metabolism.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading global liver disorder. Parsnip (Pastinaca sativa), rich in dietary fiber and medicinal properties, has shown health benefits, but its effects on MASLD are largely unexplored. This study evaluated the prebiotic and anti-MASLD effects of parsnip root water-soluble extract (PRE) in a mouse model. Mice fed a high-fat diet with 50 or 100 mg/kg PRE for eight weeks showed reduced fat accumulation, improved serum metabolic profiles, and decreased liver injury markers. PRE also lowered hepatic lipogenic protein levels induced by the high-fat diet. Additionally, PRE enhanced gut health by reducing endotoxins, improving intestinal permeability, and upregulating tight junction proteins. These results indicate that PRE can improve gut health, prevent MASLD, and support its potential as a dietary supplement to enhance metabolic health.