Exercise is a recognized non-pharmacological treatment for improving glucose homeostasis in type 2 diabetes (T2DM), with resistance exercise (RE) showing promising results. However, the mechanism of RE improving T2DM has not been clarified. This study aims to investigate the effects of RE on glucose and lipid metabolism, insulin signaling, and mitochondrial function in T2DM mice, with a focus on the regulatory role of miR-30d-5p. Our results confirmed that RE significantly improved fasting blood glucose, IPGTT, and ITT in T2DM mice. Enhanced expression of IRS-1, p-PI3K, and p-Akt indicated improved insulin signaling. RE improved glycolipid metabolism, as well as mitochondrial biogenesis and dynamics in skeletal muscle of T2DM mice. We also found that miR-30d-5p was upregulated in T2DM, and was downregulated after RE. Additionally, in vitro, over-expression of miR-30d-5p significantly increased lipid deposition, and reduced glucose uptake and mitochondrial biogenesis. These observations were reversed after transfection with the miR-30d-5p inhibitor. Mechanistically, miR-30d-5p regulates glycolipid metabolism in skeletal muscle by directly targeting SIRT1, which affects the expression of PGC-1α, thereby influencing mitochondrial function and glycolipid metabolism. Taken together, RE effectively improves glucose and lipid metabolism and mitochondrial function in T2DM mice, partly through regulating the miR-30d-5p/SIRT1/PGC-1α axis. miR-30d-5p could serve as a potential therapeutic target for T2DM management.

Fibrosis represents a terminal pathological manifestation encountered in numerous chronic diseases. The process involves the persistent infiltration of inflammatory cells, the transdifferentiation of fibroblasts into myofibroblasts, and the excessive deposition of extracellular matrix (ECM) within damaged tissues, all of which are characteristic features of organ fibrosis. Extensive documentation exists on fibrosis occurrence in vital organs such as the liver, heart, lungs, kidneys, and skeletal muscles, elucidating its underlying pathological mechanisms. Regular exercise is known to confer health benefits through its anti-inflammatory, antioxidant, and anti-aging effects. Notably, exercise exerts anti-fibrotic effects by modulating multiple pathways, including transforming growth factor-β1/small mother decapentaplegic protein (TGF-β1/Samd), Wnt/β-catenin, nuclear factor kappa-B (NF-kB), reactive oxygen species (ROS), microRNAs (miR-126, miR-29a, miR-101a), and exerkine (FGF21, irisin, FSTL1, and CHI3L1). Therefore, this paper aims to review the specific role and molecular mechanisms of exercise as a potential intervention to ameliorate organ fibrosis.

Microplastics (MPs) are pervasive environmental contaminants with significant bioaccumulation potential, posing a growing threat to global health through multi-organ toxicity. This review systematically synthesizes current knowledge on MPs-induced organ-specific damage and its systemic health implications. We detail the accumulation of MPs in major organ systems, including the liver, brain, lungs, kidneys, intestines, heart, and reproductive organs. Furthermore, we emphasize the critical role of inter-organ communication in amplifying toxicity, such as gut-liver axis-mediated hepatotoxicity and gut-brain axis-driven neurotoxicity. Emerging evidence on the transgenerational adverse effects of parental MPs exposure is also discussed. The core cellular and molecular mechanisms across these organs are examined, with a particular focus on oxidative stress, inflammatory activation, mitochondrial dysfunction, and programmed cell death. This review is distinct in its integrative approach, offering a novel perspective by synthesizing organ-specific pathologies with cross-organ communication networks and transgenerational effects, thereby providing a more holistic understanding of MPs’ systemic toxicity. Collectively, this review elucidates the exposure-organ damage correlation, analyzes the underlying pathogenic mechanisms, and aims to provide a scientific foundation for public health risk assessment and informed environmental policy formulation.

Anthocyanins, a class of polyphenol flavonoids widely present in various fruits and vegetables, have attracted significant attention due to their potent anti-inflammatory, antioxidant, and anti-aging properties. Recent studies indicate that anthocyanins may play important roles in extending life and preventing or treating age-related diseases. This review systematically summarizes the chemical characteristics of anthocyanins and their potential roles in age-related diseases, including lifespan extension, neurodegenerative diseases, skeletal diseases, cardiovascular diseases, cancer, and metabolic syndrome. Furthermore, we explore the effects of anthocyanins on age-related diseases and their potential mechanisms of action to establish a theoretical foundation for future clinical applications.

Decreased skeletal muscle mass and function are a serious complication of long-term diabetes, often leading to numerous adverse outcomes. The primary pathological features of diabetic sarcopenia include muscle fiber atrophy and interstitial fibrosis. Although resistance exercise (RE) has been reported to mitigate skeletal muscle atrophy in type 2 diabetes mellitus (T2DM), the underlying mechanisms remain unclear. Fibroblast growth factor 21 (FGF21), an exercise-induced cytokine, has been shown to protect against skeletal muscle atrophy at elevated levels. In this study, a T2DM mouse model was established through 12 weeks of high-fat diet feeding and intraperitoneal injection of streptozotocin (STZ) to investigate the effect and mechanism of RE on skeletal muscle atrophy in T2DM mice. Our results demonstrated that 8 weeks of RE significantly decreased body weight, fat mass, triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), fasting blood glucose (FBG), and serum insulin levels in T2DM mice. RE also improved lean mass, glucose tolerance (IPGTT), and insulin tolerance (ITT). Additionally, RE increased skeletal muscle mass cross-sectional area (CSA) while attenuating fibrosis and inflammatory responses in skeletal muscle. Notably, RE upregulated FGF21 expression and activated the PI3K/Akt signaling pathway in diabetic skeletal muscle. RE promoted the phosphorylation of mTOR, 4EBP1, and p70S6K while suppressing the expression of the atrophy-related E3 ubiquitin ligases MuRF1 and MAFbx/Atrogin-1. Furthermore, RE inhibited lipid synthesis and enhanced both lipid oxidation and glucose utilization in skeletal muscle of T2DM mice. RE also improved mitochondrial biogenesis and dynamics in skeletal muscle of T2DM mice. In summary, 8 weeks of RE alleviated skeletal muscle atrophy in T2DM mice via activation of the FGF21/PI3K/Akt signaling pathway, which enhanced protein synthesis, improved glycolipid metabolism and mitochondrial quality control, and attenuated fibrosis and inflammation.

Objectives: This study tested a sequential mediation model examining whether cognitive flexibility and psychological resilience explain the relationship between physical exercise and learning engagement among Chinese college students. Methods: A cross-sectional study was conducted with 670 Chinese college student. Participants completed the Physical Activity Rating Scale, Learning Engagement Scale, Cognitive Flexibility Inventory, and Psychological Resilience Scale. Data were analyzed using SPSS 27.0 and the PROCESS macro (Version 4.2) for serial mediation analysis with 5,000 bootstrap samples. Results: Regression analyses revealed that physical exercise positively predicted cognitive flexibility (β = 0.507, p < 0.001) and psychological resilience (β = 0.381, p < 0.001). Cognitive flexibility further predicted psychological resilience (β = 0.336, p < 0.001) and learning engagement (β = 0.370, p < 0.001). Crucially, the mediation analysis confirmed a significant direct effect of exercise on learning engagement (β = 0.143, 95% CI = [0.068, 0.218]). Three specific indirect effects were significant: through cognitive flexibility (β = 0.188, 95% CI [0.141, 0.234]), through psychological resilience (β = 0.086, 95% CI [0.050, 0.126]), and serially through both (β = 0.038, 95% CI [0.020, 0.059]). Conclusion: This cross-sectional study reveals a significant positive association between physical exercise and learning engagement among Chinese college students. The findings support a model in which cognitive flexibility and psychological resilience act as sequential mediators in this relationship. These results suggest that fostering psychological resources alongside physical activity may be a relevant consideration for promoting student engagement in learning. Future longitudinal and intervention studies are needed to establish causality.