饮食晚期糖基化终产物(dAGEs)的摄入及其与肌肉减少症和虚弱的关系——鹿特丹研究。

Bone Pub Date : 2022-09-01 DOI:10.2139/ssrn.4088382
Komal Waqas, Jinluan Chen, Tianqi Lu, Bram van der Eerden, F. Rivadeneira, A. Uitterlinden, T. Voortman, M. Zillikens
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引用次数: 2

摘要

对小鼠的研究表明,饮食摄入晚期糖基化终产物(dAGEs)与肌肉骨骼健康恶化之间存在关系,但缺乏人体研究。我们调查了饮食摄入羧甲基赖氨酸(dCML) (AGE原型)与基线和5 年随访后肌肉减少症风险之间的关系,并对基于人群的鹿特丹研究的参与者进行了身体虚弱的单一评估。采用insight双能x线吸收仪获得阑尾瘦质量(ALM),采用液压手测力仪获得手握力(HGS)。低ALM和弱HGS的受试者被归类为肌肉减少症。虚弱(是/否)的定义是存在≥3个因素,而前虚弱的定义是存在1或2个因素,即疲惫、虚弱、行动迟缓、体重减轻或体力活动不足。dCML采用食物频率问卷和page数据库计算。采用Logistic回归分析来评估基线和随访时身体虚弱和普遍肌肉减少症的几率以及发生肌肉减少症的几率。2782名参与者年龄66.4 ± 9.9 岁,dCML摄入量3.3 ± 1.3 mg/天,在两个时间点都有肌肉减少症的数据。其中84人在基线时患有肌肉减少症,73人在随访时出现肌肉减少症。我们观察到dCML摄入量增加一个SD与基线时普遍的肌少症相关[比值比,OR = 1.27(1.01-1.59)],而在5年随访中dCML与肌少症发生率无关联[OR = 1.12(0.86-1.44)]。对于虚弱,我们分析了3577名参与者,其中1972人处于虚弱前期,158人处于虚弱状态。当以非虚弱受试者作为参考时,我们发现dCML与虚弱前[OR = 0.99(0.91-1.07)]或虚弱[OR = 1.01(0.83-1.22)]均无关联。我们的研究结果显示,横切面上的损伤与肌肉减少症有关,但纵向上没有,在纵向上观察到不确定的结果,可能是由于肌肉减少症的发生率非常低。在横断面上与虚弱没有关联。
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Dietary advanced glycation end-products (dAGEs) intake and its relation to sarcopenia and frailty - The Rotterdam Study.
Studies on mice have shown a relationship between dietary intake of advanced glycation end-products (dAGEs) and deterioration of musculoskeletal health, but human studies are absent. We investigated the relationship between dietary intake of carboxymethyllysine (dCML) - an AGE prototype - and risk of sarcopenia at baseline and after 5 years of follow-up and a single evaluation of physical frailty in participants from the population-based Rotterdam Study. Appendicular lean mass (ALM) was obtained using insight dual-energy X-ray absorptiometry and hand grip strength (HGS) using a hydraulic hand dynamometer. Subjects with both low ALM and weak HGS were classified as having sarcopenia. Frailty (yes/no) was defined by presence of ≥3 and pre-frailty by presence of 1 or 2 components namely, exhaustion, weakness, slowness, weight loss or low physical activity. dCML was calculated using a food frequency questionnaire and dAGE databases. Logistic regression analysis was used to evaluate the odds of physical frailty and prevalent sarcopenia at baseline and follow-up and incident sarcopenia. 2782 participants with an age 66.4 ± 9.9 years and dCML intake 3.3 ± 1.3 mg/day, had data on sarcopenia at both time points. Of whom 84 had sarcopenia at baseline and 73 developed sarcopenia at follow-up. We observed an association of one SD increase in dCML intake with prevalent sarcopenia at baseline [odds ratio, OR = 1.27 (1.01-1.59)] and no association of dCML with incident sarcopenia at 5-year follow-up [OR = 1.12 (0.86-1.44)]. For frailty we analyzed 3577 participants, of whom 1972 were pre-frail and 158 were frail. We observed no association of dCML with either pre-frailty [OR = 0.99 (0.91-1.07)] or frailty [OR = 1.01 (0.83-1.22)] when non-frail subjects were used as reference. Our results show an association of dAGEs with sarcopenia cross-sectionally but not longitudinally where inconclusive findings are observed possibly due to a very low incidence of sarcopenia. There was no association with frailty cross-sectionally.
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