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随机对照婴儿期饮食干预对白细胞端粒长度的影响——特殊图尔库冠心病危险因素干预项目(STRIP)。

Effects of Randomized Controlled Infancy-Onset Dietary Intervention on Leukocyte Telomere Length-The Special Turku Coronary Risk Factor Intervention Project (STRIP).

机构信息

Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, 20520 Turku, Finland.

Centre for Population Health Research, University of Turku and Turku University Hospital, 20520 Turku, Finland.

出版信息

Nutrients. 2021 Jan 22;13(2):318. doi: 10.3390/nu13020318.

Abstract

Reduced telomere length (TL) is a biological marker of aging. A high inter-individual variation in TL exists already in childhood, which is partly explained by genetics, but also by lifestyle factors. We examined the influence of a 20-year dietary/lifestyle intervention on TL attrition from childhood to early adulthood. The study comprised participants of the longitudinal randomized Special Turku Coronary Risk Factor Intervention Project (STRIP) conducted between 1990 and 2011. Healthy 7-month-old children were randomized to the intervention group ( = 540) receiving dietary counseling mainly focused on dietary fat quality and to the control group ( = 522). Leukocyte TL was measured using the Southern blot method from whole blood samples collected twice: at a mean age of 7.5 and 19.8 years ( = 232; intervention = 108, control = 124). Yearly TL attrition rate was calculated. The participants of the intervention group had slower yearly TL attrition rate compared to the controls (intervention: mean = -7.5 bp/year, SD = 24.4 vs. control: mean = -15.0 bp/year, SD = 30.3; age, sex and baseline TL adjusted β = 0.007, SE = 0.004, = 0.040). The result became stronger after additional adjustments for dietary fat quality and fiber intake, serum lipid and insulin concentrations, systolic blood pressure, physical activity and smoking (β = 0.013, SE = 0.005, = 0.009). A long-term intervention focused mainly on dietary fat quality may affect the yearly TL attrition rate in healthy children/adolescents.

摘要

端粒长度缩短是衰老的生物标志物。端粒长度在儿童期已经存在个体间的高度差异,这部分可由遗传解释,但也可由生活方式因素解释。我们研究了 20 年饮食/生活方式干预对从儿童期到成年早期端粒损耗的影响。该研究包括纵向随机特库大学冠状动脉危险因素干预项目(STRIP)的参与者,该项目于 1990 年至 2011 年进行。健康的 7 个月大的儿童被随机分为干预组(=540),接受主要侧重于饮食脂肪质量的饮食咨询,以及对照组(=522)。使用 Southern blot 法从全血样本中测量白细胞端粒,这些样本在两次采集:平均年龄为 7.5 岁和 19.8 岁(=232;干预=108,对照=124)。计算每年端粒损耗率。与对照组相比,干预组的每年端粒损耗率较慢(干预:平均=-7.5bp/年,SD=24.4 岁;对照:平均=-15.0bp/年,SD=30.3;年龄、性别和基线 TL 调整后 β=0.007,SE=0.004,=0.040)。在进一步调整饮食脂肪质量和纤维摄入量、血清脂质和胰岛素浓度、收缩压、体力活动和吸烟情况后,结果更强(β=0.013,SE=0.005,=0.009)。主要关注饮食脂肪质量的长期干预可能会影响健康儿童/青少年的每年端粒损耗率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc06/7911579/3cf225b81865/nutrients-13-00318-g001.jpg

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