(1) Objective: This study aimed to examine the prevalence of metabolic syndrome (MetS) in children aged 6–14 years in Beijing, and to determine whether sedentary behavior is a risk factor. (2) Methods: Using a multistage stratified cluster random sampling method, 3460 students were selected for the Nutrition and Health Surveillance in Schoolchildren of Beijing (NHSSB). Data on children’s sedentary behavior time and MetS indicators were collected using the questionnaires, physical measurements, and laboratory tests. MetS was defined according to the CHN2012 criteria, and logistic regression analysis was used to compare the effects of different sedentary time on MetS and its components. (3) Results: The overall prevalence of MetS among children aged 6–14 in Beijing was 2.4%, and boys, suburban children, and older age were associated with a higher prevalence (χ² values were 3.947, 9.982, and 27.463, respectively; p < 0.05). In boys, the prevalence rates of abdominal obesity, hyperglycemia, high triglycerides (TG), and low high-density lipoprotein cholesterol (HDL-C) were higher in the high-level sedentary behavior group than those in the low-level sedentary behavior group (p < 0.05); and in girls, the prevalence rates of high TG, low HDL-C, and MetS were higher in the high-level sedentary behavior group than those in the low-level sedentary behavior group (p < 0.05). After adjusting for confounding factors, the multivariate logistic regression results showed that compared with children with low-level sedentary behavior, the risks of abdominal obesity and low HDL-C were higher in boys with high-level sedentary behavior (odds ratio (OR) 1.51, 95% confidence interval (CI) 1.10–2.07, p = 0.011; OR 2.25, 95% CI 1.06–4.76, p = 0.034, respectively); while the risk of abdominal obesity was higher in girls with medium and high-level sedentary behavior (OR 1.52, 95% CI 1.01–2.27, p = 0.043; OR 1.59, 95% CI 1.04–2.43, p = 0.032, respectively). (4) Conclusions: Higher sedentary behavior time was related to the higher risk of MetS components among children aged 6–14 in Beijing. Reducing sedentary behavior may be an important method for preventing metabolic diseases.

Background/Objectives: Dihydromyricetin (DHM), a flavonoid with abundant natural sources, potent bioactivity, and high safety, holds promise for translational applications, particularly in mitigating skin aging. However, its role and underlying mechanisms in counteracting skin aging induced by advanced glycation end products (AGEs) remain unclear. Methods: Eight-week-old male Sprague-Dawley (SD) rats were subcutaneously injected with 500 mg/kg D-galactose and administered DHM via gavage for 11 weeks. Additionally, senescent human skin fibroblasts (HFF-1) induced by AGEs were used for further investigation. Results: DHM treatment significantly alleviated D-galactose-induced skin aging in rats, with the most pronounced effects observed in the moderate-dose group (100 mg/kg). Compared to the aging group, DHM enhanced skin elasticity and preserved collagen levels. Moreover, DHM promoted cell proliferation in the skin. Further studies on AGE-induced senescent fibroblasts revealed that DHM markedly reduced multiple senescence-associated markers and stimulated cell proliferation by approximately a 1.5-fold increase. Transcriptomic analysis indicated that DHM upregulated genes related to the cell cycle and DNA repair while suppressing AGE-RAGE signaling and its downstream pathways. Notably, DHM downregulated AGER, the gene encoding the receptor for AGEs (RAGE). Molecular docking analysis demonstrated that DHM shares a binding site with other known RAGE inhibitors. Surface plasmon resonance (SPR) analysis further confirmed the high binding affinity of DHM to RAGE (K_D = 28.7 μM), which was stronger and more stable than that of FPS-ZM1 (K_D = 40.7 μM). Conclusions: DHM may attenuate glycation-induced skin aging in rats by functioning as a RAGE inhibitor, thereby suppressing AGE-RAGE signaling, delaying cellular senescence, and promoting cell proliferation.

With the increasing frequency of ultraviolet (UV) exposure in daily life and the exploration of anti-photoaging strategies, natural plant-derived compounds with anti-skin-aging properties have garnered significant attention. This study aimed to evaluate the efficacy of zein-chitosan-based nanocarriers in enhancing the bioavailability of epigallocatechin gallate (EGCG) and to elucidate its mechanisms in ameliorating skin photoaging. Utilizing a Balb/c mouse model of photoaging, we monitored skin conditions, analyzed skin barrier function parameters, and observed changes in skin tissue structure and collagen fibers through hematoxylin–eosin (H&E) and Masson staining. Immunohistochemical staining was employed to assess COL1A1 levels in the skin, while enzyme-linked immunosorbent assay (ELISA) was used to measure antioxidant enzymes, inflammatory cytokines, matrix metalloproteinases (MMPs), and NF-kB levels. The effects of orally administered EGCG nanoparticles on UV-induced skin aging were investigated. UV exposure significantly increased skin roughness, impaired skin barrier function, thickened the epidermis, reduced collagen content, decreased antioxidant enzyme activity, and elevated levels of inflammatory cytokines, MMPs, and NF-kB in the model group compared to the normal control group. EGCG nanoparticles markedly ameliorated these photoaging manifestations, with some indicators showing superior improvement compared to free EGCG. These findings suggest that EGCG nanoparticles exhibit enhanced anti-photoaging effects over free EGCG, highlighting the potential of nanocarriers as a promising strategy to improve the bioavailability of EGCG.