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Sarcopenia, the age-related decline in skeletal muscle mass and function, is a growing health concern in aging populations. Nutritional interventions are increasingly recognized for their therapeutic potential; however, molecular biomarkers that reflect their efficacy are limited. To identify nutrition-responsive genes relevant to sarcopenia, we performed transcriptomic profiling of gastrocnemius muscle from mature and middle-aged mice. Aging-associated differentially expressed genes (DEGs) were filtered based on expression levels and correlation with muscle mass. Functional food interventions, including high- and low-molecular-weight collagen hydrolysates and allulose, were applied, and effect scores were calculated to assess transcriptomic responsiveness. Ajuba, a gene involved in cytoskeletal regulation and tissue remodeling, was significantly downregulated in middle-aged mice, consistent with aging-associated muscle decline. Dietary supplementation restored Ajuba expression across all intervention groups, with the strongest effect observed in the high-molecular-weight collagen group. Ajuba expression also showed strong positive correlations with tibialis anterior mass, hindlimb thickness, and muscle-to-fat ratio. Ajuba was identified as a nutritionally modifiable gene with strong associations to muscle phenotype and dietary response. These findings support Ajuba as a transcriptomic biomarker and potential molecular target for precision nutrition strategies aimed at preventing or mitigating sarcopenia.

Nanomaterials have revolutionized drug delivery by enabling precise control over solubility, stability, circulation time, and targeted release, yet translation from bench to bedside remains challenging due to complex synthesis, unpredictable biological interactions, and regulatory hurdles. Recent advances in artificial intelligence (AI) and big data analytics offer powerful solutions to these bottlenecks by integrating multidimensional datasets—encompassing physicochemical characterization, pharmacokinetics, omics profiles, and preclinical outcomes—to generate predictive models for rational nanocarrier design. Machine learning and deep learning approaches enable the prediction of key parameters such as particle size, drug loading efficiency, and biodistribution, while generative algorithms explore novel chemistries and architectures optimized for specific clinical applications. Nanoinformatics platforms and large-scale data repositories further enhance reproducibility and cross-study comparisons, supporting regulatory science and accelerating clinical translation. This review provides a comprehensive overview of nanomaterial-based drug delivery systems, highlights AI-driven strategies for predictive modeling and optimization, and discusses translational and regulatory perspectives. By bridging nanotechnology, computational modeling, and precision medicine, AI-assisted nanomaterial design has the potential to transform drug delivery into a more efficient, reproducible, and patient-centered discipline.

Aging is closely linked to various health challenges, including cardiovascular disease, metabolic disorders, and neurodegenerative conditions. This study emphasizes the critical role of bioactive compounds derived from marine sources, such as antioxidants, omega-3 fatty acids, vitamins, minerals, and polysaccharides, in addressing oxidative stress, inflammation, and metabolic disorders closely related to aging. Incorporating these materials into functional foods not only provides essential nutrients but also delivers therapeutic effects, thereby promoting healthy aging and mitigating age-related diseases. The growth of the global anti-aging market, particularly in North America, Europe, and Asia, underscores the significance of this study. This review systematically analyzes the current research, identifying key bioactive compounds, their mechanisms of action, and their potential health benefits, thus highlighting the broad applicability of marine-derived bioactive compounds to enhancing healthy aging and improving the quality of life of aging populations.

Regenerative medicine aims to address substantial defects by amplifying the body’s natural regenerative abilities and preserving the health of tissues and organs. To achieve these goals, materials that can provide the spatial and biological support for cell proliferation and differentiation, as well as the micro-environment essential for the intended tissue, are needed. Scaffolds such as polymers and metallic materials provide three-dimensional structures for cells to attach to and grow in defects. These materials have limitations in terms of mechanical properties or biocompatibility. In contrast, biominerals are formed by living organisms through biomineralization, which also includes minerals created by replicating this process. Incorporating biominerals into conventional materials allows for enhanced strength, durability, and biocompatibility. Specifically, biominerals can improve the bond between the implant and tissue by mimicking the micro-environment. This enhances cell differentiation and tissue regeneration. Furthermore, biomineral composites have wound healing and antimicrobial properties, which can aid in wound repair. Additionally, biominerals can be engineered as drug carriers, which can efficiently deliver drugs to their intended targets, minimizing side effects and increasing therapeutic efficacy. This article examines the role of biominerals and their composite materials in regenerative medicine applications and discusses their properties, synthesis methods, and potential uses.

Collagen peptide (CP) and collagen tripeptide (CTP) are supplementary health foods that exhibit several biological effects. However, the effects of collagen on age-associated sarcopenia and its underlying mechanisms are unclear. C57BL/6J mice (n = 24, 12 months old) were divided into three dietary groups and administered AIN93G (aging control, AC; JA BIO, Suwon, Korea), AIN93G plus 0.2% CP, and AING93G plus 0.2% CTP supplement for 12 weeks. The results indicated that the CP and CTP supplements significantly increased the weight of the quadriceps tibialis anterior and gastrocnemius muscles and reduced body fat. A morphological analysis revealed that the spaces within the muscle cells were tight with attenuated fibrosis following CP and CTP supplementation. Immunohistochemistry was applied and a Western blot analysis was performed to determine the underlying mechanisms. The CTP supplement increased the expression of IGF-1, PI3K/AKT, and mTOR, whereas the CP supplement increased the expression of IGF-1 and AMPK in the gastrocnemius of aging mice. CP and CTP ameliorate age-associated sarcopenia through different mechanisms.

d-allulose is an uncommon sugar that provides almost no calories when consumed. Its sweetness is 70% that of sucrose. d-allulose is a metabolic regulator of glucose and lipid metabolism. However, few reports concerning its effect on diabetes and related metabolic disturbances in db/db mice are available. In this study, we evaluated d-allulose’s effect on hyperglycemia, hyperinsulinemia, diabetes and inflammatory responses in C57BL/KsJ-db/db mice. Mice were divided into normal diet, erythritol supplemented (5% w/w), and d-allulose supplemented (5% w/w) groups. Blood glucose and plasma glucagon levels and homeostatic model assessment (HOMA-IR) were significantly lower in the d-allulose group than in the normal diet group, and plasma insulin level was significantly increased. Further, d-allulose supplement significantly increased hepatic glucokinase activity and decreased hepatic phosphoenolpyruvate carboxykinase and glucose-6-phosphatase activity. Expression of glucose transporter 4, insulin receptor substrate 1, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha and AKT serine/threonine kinase 2 were also upregulated by d-allulose supplement in adipocyte and muscle. Finally, d-allulose effectively lowered plasma and hepatic triglyceride and free fatty acid levels, and simultaneously reduced hepatic fatty acid oxidation and carnitine palmitoyl transferase activity. These changes are likely attributable to suppression of hepatic fatty acid synthase and glucose-6-phosphate dehydrogenase activity. Notably, d-allulose also reduced pro-inflammatory adipokine and cytokine levels in plasma. Our results indicate that d-allulose is an effective sugar substitute for improving lipid and glucose metabolism.

Allulose has been reported to serve as an anti-obesity and anti-diabetic food component; however, its molecular mechanism is not yet completely understood. This study aims to elucidate the mechanisms of action for allulose in obesity-induced type 2 diabetes mellitus (T2DM), by analyzing the transcriptional and microbial populations of diet-induced obese mice. Thirty-six C57BL/6J mice were divided into four groups, fed with a normal diet (ND), a high-fat diet (HFD), a HFD supplemented with 5% erythritol, or a HFD supplemented with 5% allulose for 16 weeks, in a pair-fed manner. The allulose supplement reduced obesity and comorbidities, including inflammation and hepatic steatosis, and changed the microbial community in HFD-induced obese mice. Allulose attenuated obesity-mediated inflammation, by downregulating mRNA levels of inflammatory response components in the liver, leads to decreased plasma pro-inflammatory marker levels. Allulose suppressed glucose and lipid metabolism-regulating enzyme activities, ameliorating hepatic steatosis and improving dyslipidemia. Allulose improved fasting blood glucose (FBG), plasma glucose, homeostatic model assessment of insulin resistance (HOMA-IR), and the area under the curve (AUC) for the intraperitoneal glucose tolerance test (IPGTT), as well as hepatic lipid levels. Our findings suggested that allulose reduced HFD-induced obesity and improved T2DM by altering mRNA expression and the microbiome community.

Alcohol abuse, a global health problem, is closely associated with many pathological processes, such as dyslipidemia and cardiovascular disease. In particular, excessive alcohol consumption promotes dyslipidemia and liver damage, such as hepatic steatosis, fibrosis, and cirrhosis. Beeswax alcohol (BWA) is a natural product used for its antioxidant properties that has not been evaluated for its efficacy in alcohol-induced liver injury. In the present study, zebrafish were exposed to 1% ethanol with supplementation of 10% fermented black rice bran (BRB-F), 10% BWA, or 10% mixtures of BWA+BRB-F (MIX). The BRB-F, BWA, and MIX supplementation increased the survival rate dramatically without affecting the body weight changes. In histology of hepatic tissue, alcoholic foamy degeneration was ameliorated by the BWA or MIX supplements. Moreover, dihydroethidium (DHE) and immunohistochemistry staining suggested that the MIX supplement decreased the hepatic ROS production and interleukin-6 expression significantly owing to the enhanced antioxidant properties, such as paraoxonase. Furthermore, the MIX supplement improved alcohol-induced dyslipidemia and oxidative stress. The BWA and MIX groups showed lower blood total cholesterol (TC) and triglyceride (TG) levels with higher high-density lipoprotein-cholesterol (HDL-C) than the alcohol-alone group. The MIX group showed the highest HDL-C/TC ratio and HDL-C/TG ratio with the lowest low-density lipoprotein (LDL)-C/HDL-C ratio. In conclusion, BWA and BRB-F showed efficacy to treat alcohol-related metabolic disorders, but the MIX supplement was more effective in ameliorating the liver damage and dyslipidemia, which agrees with an enhanced antioxidant and anti-inflammatory activity exhibited by BWA/BRB-F in a synergistic manner.

Recently, there has been a global shift in diet towards an increased intake of energy-dense foods that are high in sugars. D-allulose has received attention as a sugar substitute and has been reported as one of the anti-obesity food components; however, its correlation with the intestinal microbial community is not yet completely understood. Thirty-six C57BL/6J mice were divided in to four dietary groups and fed a normal diet (ND), a high-fat diet (HFD, 20% fat, 1% cholesterol, w/w), and a HFD with 5% erythritol (ERY) and D-allulose (ALL) supplement for 16 weeks. A pair-feeding approach was used so that all groups receiving the high-fat diet would have the same calorie intake. As a result, body weight and body fat mass in the ALL group were significantly decreased toward the level of the normal group with a simultaneous decrease in plasma leptin and resistin. Fecal short-chain fatty acid (SCFA) production analysis revealed that ALL induced elevated total SCFA production compared to the other groups. Also, ALL supplement induced the change in the microbial community that could be responsible for improving the obesity based on 16S rRNA gene sequence analysis, and ALL significantly increased the energy expenditure in Day(6a.m to 6pm). Taken together, our findings suggest that 5% dietary ALL led to an improvement in HFD-induced obesity by altering the microbiome community.

D-allulose, a rare sugar, has been proposed to have potential benefits in addressing metabolic disorders such as obesity and type 2 diabetes (T2D). However, the precise mechanisms underlying these effects remain poorly understood. We aimed to elucidate the mechanisms by which D-allulose influences obesity-induced insulin resistance. We conducted gene set enrichment analysis on the liver and white adipose tissue of mice exposed to a high-fat diet (HFD) along with the white adipose tissue of individuals with obesity. Our study revealed that D-allulose effectively suppressed IFN-γ, restored chemokine signaling, and enhanced macrophage function in the livers of HFD-fed mice. This implies that D-allulose curtails liver inflammation, alleviating insulin resistance and subsequently impacting adipose tissue. Furthermore, D-allulose supplementation improved mitochondrial NADH homeostasis and translation in both the liver and white adipose tissue of HFD-fed mice. Notably, we observed decreased NADH homeostasis and mitochondrial translation in the omental tissue of insulin-resistant obese subjects compared to their insulin-sensitive counterparts. Taken together, these results suggest that supplementation with allulose improves obesity-induced insulin resistance by mitigating the disruptions in macrophage and mitochondrial function. Furthermore, our data reinforce the crucial role that mitochondrial energy expenditure plays in the development of insulin resistance triggered by obesity.