饮食会影响外周白细胞端粒长度 (LTL)，据报道，多种微量营养素与其相关。锌以其抗氧化特性和免疫调节作用而闻名。然而，关于膳食锌摄入量与LTL之间关系的流行病学调查却很少。本研究分析了膳食锌与 LTL 之间的关联以及炎症和氧化应激在其中的潜在作用。横断面和社区研究。招募了来自中国北京昌平郊区农村社区的 599 名参与者。血清脂质测量了数据、糖化血红蛋白 (HbA1c)、氧化应激标记物和炎症细胞因子水平。通过 24 小时食品召回获得详细的饮食数据。 LTL 使用实时 PCR 检测进行评估。使用 Spearman 分析、限制三次样条 (RCS) 和一般线性回归模型来确定膳食锌摄入量与 LTL 之间的关联。还应用简单的调节模型来分析炎症和氧化应激在其中的作用。最终共有 482 名受试者纳入本次分析。 Spearman分析显示，膳食锌摄入量和能量密度下锌摄入量与LTL呈负相关（r=-0.142和-0.126，均P<0.05），与肿瘤坏死因子-α（TNF-α）呈正相关（r=0.138）和0.202，均P<0.05），而仅膳食锌而不调整能量则与超氧化物歧化酶（SOD）呈正相关。 RCS（非线性 P = 0.933）和多元线性回归（B = -0.084，P = 0.009）表明膳食锌和 LTL 之间存在负线性关联。调整TNF-α而不是SOD可以消除这种关系。中介模型表明，膳食锌对 LTL 的不利影响是由 TNF-α 介导的。高膳食锌可能与端粒磨损相关，而 TNF-α 可以在这种关系中发挥中介作用。未来需要更广泛的队列研究来进一步探讨膳食锌与细胞衰老的关系及具体机制。

Diet can influence peripheral leukocyte telomere length (LTL), and various micronutrients have been reported to correlate with it. Zinc is known for its antioxidant properties and immunomodulatory effects. However, there are few epidemiological investigations on the relationship between dietary zinc intake and LTL. This study analyzed the association between dietary zinc and LTL and the potential role of inflammation and oxidative stress among them.Cross-sectional and community-based study.599 participants from rural communities in the Changping suburb of Beijing, China, were recruited.Serum lipid profile, glycosylated hemoglobin (HbA1c), oxidative stress marker, and inflammatory cytokines levels were measured. Detailed dietary data were obtained using a 24 h food recall. LTL was assessed using a real-time PCR assay. Spearman analysis, restricted cubic splines (RCS), and general linear regression models were used to determine the association between dietary zinc intake and LTL. Simple regulatory models were also applied to analyze the role of inflammation and oxidative stress among them.A total of 482 subjects were ultimately included in this analysis. Spearman analysis showed that dietary zinc intake and zinc intake under energy density were negatively correlated with LTL (r=-0.142 and -0.126, all P <0.05) and positively correlated with tumor necrosis factor-α (TNF-α) (r=0.138 and 0.202, all P <0.05) while only dietary zinc without energy adjustment had a positive correlation with superoxide dismutase (SOD). RCS (P for non-linearity=0.933) and multiple linear regression (B=-0.084, P=0.009) indicated a negative linear association between dietary zinc and LTL. The adjustment of TNF-α rather than SOD could abolish the relationship. The mediation model suggested that the unfavorable effect of dietary zinc on LTL was mediated by TNF-α.High dietary zinc may correlate with telomere attrition, and TNF-α can act as a mediator in this relationship. In the future, more extensive cohort studies are needed to further explore the relationship between dietary zinc and cellular aging and the specific mechanisms.