Wang Ruijian, Shen Jin, Han Chunqing, Shi Xiaodong, Gong Yan, Hu Xiping, Jia Zhongtang, Wang Miaomiao, Wu Yu
MOE Medical Basic Research Innovation Center for Gut Microbiota and Chronic Diseases, Wuxi School of Medicine, Jiangnan University, Wuxi 214126, China.
Laboratory of Modern Environmental Toxicology, Wuxi School of Medicine, Jiangnan University, Wuxi 214126, China.
Nutrients. 2025 Apr 29;17(9):1513. doi: 10.3390/nu17091513.
Lead (Pb), a pervasive environmental toxicant with specific toxicity to bone, has been recognized as a significant etiological factor in the pathogenesis of osteoporosis. While dietary fiber (DF) demonstrates anti-osteoporotic potential, its protective role against Pb-induced bone loss remains unexplored. This study analyzed the association between dietary fiber, blood lead, and osteoporosis based on the NHANES database, and validated it by constructing a lead exposed mouse model. Micro CT was used to evaluate bone microstructure, ELISA was used to detect bone markers, q-PCR/Western blot was used to measure intestinal tight junction protein, flow cytometry was used to analyze Treg cells in colon/bone tissue, GC-MS was used to detect short chain fatty acids, and 16S rRNA sequencing was used to analyze changes in gut microbiota. The regulatory mechanism of dietary fiber on bone metabolism and intestinal barrier in lead exposed mice was systematically evaluated. Based on NHANES data analysis, it was found that dietary fiber can reduce the risk of osteoporosis in lead exposed populations. Animal experiments have shown that dietary fiber intervention significantly increases bone density, improves bone microstructure and metabolic indicators, repairs intestinal barrier damage caused by lead exposure, and regulates immune balance in lead exposed mice. At the same time, it promotes the generation of short chain fatty acids and the proliferation of beneficial gut microbiota. These findings indicate that DF mitigates Pb-induced osteoporosis through gut barrier restoration, SCFA-mediated immunomodulation, and microbiota-driven Treg cell expansion along the gut-bone axis.
铅（Pb）是一种普遍存在的环境毒物，对骨骼具有特殊毒性，已被公认为是骨质疏松症发病机制中的一个重要病因。虽然膳食纤维（DF）具有抗骨质疏松的潜力，但其对铅诱导的骨质流失的保护作用仍未得到探索。本研究基于美国国家健康与营养检查调查（NHANES）数据库分析了膳食纤维、血铅与骨质疏松症之间的关联，并通过构建铅暴露小鼠模型进行了验证。使用显微CT评估骨微结构，酶联免疫吸附测定（ELISA）检测骨标志物，定量聚合酶链反应/蛋白质免疫印迹法（q-PCR/Western blot）测量肠道紧密连接蛋白，流式细胞术分析结肠/骨组织中的调节性T细胞（Treg），气相色谱-质谱联用仪（GC-MS）检测短链脂肪酸，16S核糖体RNA测序分析肠道微生物群的变化。系统评估了膳食纤维对铅暴露小鼠骨代谢和肠道屏障的调节机制。基于NHANES数据分析发现，膳食纤维可以降低铅暴露人群患骨质疏松症的风险。动物实验表明，膳食纤维干预可显著增加骨密度，改善骨微结构和代谢指标，修复铅暴露引起的肠道屏障损伤，并调节铅暴露小鼠的免疫平衡。同时，它促进短链脂肪酸的生成和有益肠道微生物群的增殖。这些发现表明，膳食纤维通过恢复肠道屏障、短链脂肪酸介导的免疫调节以及沿着肠-骨轴由微生物群驱动的Treg细胞扩增来减轻铅诱导的骨质疏松症。
