Abstract：
BACKGROUND: Selenoprotein P (SELENOP) transports selenium to extrahepatic tissues and is a biomarker of selenium status. Low soil selenium leads to low dietary selenium intake. A consequence is an increased risk of cardiovascular disease.
OBJECTIVE: To investigate clinical aspects associated with SELENOP deficiency, including biomarkers of inflammation, quality of life, and mortality within 12 years, and the effect of dietary selenium and coenzyme Q10 supplementation on SELENOP.
METHODS: SELENOP was determined at inclusion and after four years of supplementation in 403 elderly community-living participants low in selenium receiving selenium yeast (200 μg/day) and coenzyme Q10 (200 mg/day), or placebo. Pre-intervention, the average serum selenium level was 67 μg/L. T-tests, repeated measures of variance, Cox proportional regressions analyses, Kaplan-Meier graphs and ANCOVA analyses were applied. Associations with biomarkers of inflammation, telomere length, quality of life and mortality were investigated. Benchmark modelling was used to determine the serum selenium concentration at which the saturation levels of SELENOP and GPx3 was achieved. Comparison with GPx3 and serum selenium to identify increased mortality risk was performed, and the effect of supplementation on SELENOP levels were evaluated.
RESULTS: Inverse associations were observed between the level of SELENOP at inclusion and biomarkers for inflammation. At follow-up, shorter telomere lengths were seen in those with low levels of SELENOP at inclusion, whereas high levels of SELENOP were associated with better quality of life and decreased mortality. SELENOP had increased prognostic power compared to GPx3 and selenium. Saturation of SELENOP was achieved at a serum selenium level of 146 μg/L, and for GPx3 at 99 μg/L. Supplementation induced higher levels of SELENOP.
CONCLUSIONS: Significant associations between SELENOP and inflammation, length of telomeres, quality of life, and mortality were observed. Thus, selenium supplementation improved SELENOP expression, thereby facilitating systemic selenium bioavailability and resulting in the observed positive health effects.
OBJECTIVE: To investigate clinical aspects associated with SELENOP deficiency, including biomarkers of inflammation, quality of life, and mortality within 12 years, and the effect of dietary selenium and coenzyme Q10 supplementation on SELENOP.
METHODS: SELENOP was determined at inclusion and after four years of supplementation in 403 elderly community-living participants low in selenium receiving selenium yeast (200 μg/day) and coenzyme Q10 (200 mg/day), or placebo. Pre-intervention, the average serum selenium level was 67 μg/L. T-tests, repeated measures of variance, Cox proportional regressions analyses, Kaplan-Meier graphs and ANCOVA analyses were applied. Associations with biomarkers of inflammation, telomere length, quality of life and mortality were investigated. Benchmark modelling was used to determine the serum selenium concentration at which the saturation levels of SELENOP and GPx3 was achieved. Comparison with GPx3 and serum selenium to identify increased mortality risk was performed, and the effect of supplementation on SELENOP levels were evaluated.
RESULTS: Inverse associations were observed between the level of SELENOP at inclusion and biomarkers for inflammation. At follow-up, shorter telomere lengths were seen in those with low levels of SELENOP at inclusion, whereas high levels of SELENOP were associated with better quality of life and decreased mortality. SELENOP had increased prognostic power compared to GPx3 and selenium. Saturation of SELENOP was achieved at a serum selenium level of 146 μg/L, and for GPx3 at 99 μg/L. Supplementation induced higher levels of SELENOP.
CONCLUSIONS: Significant associations between SELENOP and inflammation, length of telomeres, quality of life, and mortality were observed. Thus, selenium supplementation improved SELENOP expression, thereby facilitating systemic selenium bioavailability and resulting in the observed positive health effects.
摘要：
背景：硒蛋白P（SELENOP）将硒转运至肝外组织，是硒状态的生物标志物。低土壤硒导致低膳食硒摄入量。结果是心血管疾病的风险增加。
目的：研究与SELENOP缺乏相关的临床方面，包括炎症的生物标志物，生活质量,和12年内的死亡率，以及日粮硒和辅酶Q10对SELENOP的影响。
方法：在接受硒酵母（200μg/天）和辅酶Q10（200mg/天）的403名硒含量低的老年社区生活参与者中，在纳入和补充四年后确定了SELENOP，或安慰剂。干预前,平均血清硒水平为67μg/L。T-tests,重复测量方差，Cox比例回归分析，应用Kaplan-Meier图和ANCOVA分析。与炎症的生物标志物有关，端粒长度,对生活质量和死亡率进行了调查.基准模型用于确定达到SELENOP和GPx3饱和水平的血清硒浓度。与GPx3和血清硒进行比较，以确定死亡风险增加，并评估了补充对SELENOP水平的影响。
结果：观察到包含时SELENOP水平与炎症生物标志物之间的反向关联。在后续行动中,在纳入时SELENOP水平较低的端粒长度较短，而高水平的SELENOP与更好的生活质量和降低的死亡率相关.与GPx3和硒相比，SELENOP的预后能力增加。在146μg/L的血清硒水平下达到SELENOP的饱和度，GPx3为99μg/L补充诱导更高水平的SELENOP。
结论：SELENOP与炎症之间存在显著关联，端粒的长度，生活质量,并观察到死亡率。因此，补硒改善SELENOP表达，从而促进全身硒的生物利用度，并导致观察到的积极健康影响。
目的：研究与SELENOP缺乏相关的临床方面，包括炎症的生物标志物，生活质量,和12年内的死亡率，以及日粮硒和辅酶Q10对SELENOP的影响。
方法：在接受硒酵母（200μg/天）和辅酶Q10（200mg/天）的403名硒含量低的老年社区生活参与者中，在纳入和补充四年后确定了SELENOP，或安慰剂。干预前,平均血清硒水平为67μg/L。T-tests,重复测量方差，Cox比例回归分析，应用Kaplan-Meier图和ANCOVA分析。与炎症的生物标志物有关，端粒长度,对生活质量和死亡率进行了调查.基准模型用于确定达到SELENOP和GPx3饱和水平的血清硒浓度。与GPx3和血清硒进行比较，以确定死亡风险增加，并评估了补充对SELENOP水平的影响。
结果：观察到包含时SELENOP水平与炎症生物标志物之间的反向关联。在后续行动中,在纳入时SELENOP水平较低的端粒长度较短，而高水平的SELENOP与更好的生活质量和降低的死亡率相关.与GPx3和硒相比，SELENOP的预后能力增加。在146μg/L的血清硒水平下达到SELENOP的饱和度，GPx3为99μg/L补充诱导更高水平的SELENOP。
结论：SELENOP与炎症之间存在显著关联，端粒的长度，生活质量,并观察到死亡率。因此，补硒改善SELENOP表达，从而促进全身硒的生物利用度，并导致观察到的积极健康影响。
