Della Corte Karen A, Penczynski Katharina, Kuhnle Gunter, Perrar Ines, Herder Christian, Roden Michael, Wudy Stefan A, Remer Thomas, Alexy Ute, Buyken Anette E
Public Health Nutrition, Paderborn University, Paderborn, Germany.
Department of Food Safety, German Federal Institute for Risk Assessment (BfR), Berlin, Germany.
Front Nutr. 2021 Jan 18;7:615684. doi: 10.3389/fnut.2020.615684. eCollection 2020.
To examine the prospective relevance of dietary sugar intake (based on dietary data as well as urinary excretion data) in adolescent years for insulin sensitivity and biomarkers of inflammation in young adulthood. Overall 254 participants of the DONALD study who had at least two 3-day weighed dietary records for calculating intakes of fructose, glucose, sucrose, total, free, added sugars, total sugars from sugar-sweetened beverages (SSB), juice, and sweets/sugar or at least two complete 24 h urine samples ( = 221) for calculating sugar excretion (urinary fructose and urinary fructose + sucrose) in adolescence (females: 9-15 years, males: 10-16 years) and a fasting blood sample in adulthood (18-36 years), were included in multivariable linear regression analyses assessing their prospective associations with adult homeostasis model assessment insulin sensitivity (HOMA2-%S) and a pro-inflammatory score (based on CRP, IL-6, IL-18, leptin, chemerin, adiponectin). On the dietary intake level, no prospective associations were observed between adolescent fructose, sucrose, glucose, added, free, total sugar, or total sugar from SSB, juice or sweets/sugar intake and adult HOMA2-%S ( > 0.01). On the urinary level, however, higher excreted fructose levels were associated with improved adult HOMA2-%S ( = 0.008) among females only. No associations were observed between dietary or urinary sugars and the adult pro-inflammatory score ( > 0.01). The present study did not provide support that dietary sugar consumed in adolescence is associated with adult insulin sensitivity. The one potential exception was the moderate dietary consumption of fructose, which showed a beneficial association with adult fasting insulin and insulin sensitivity.
为研究青少年时期膳食糖摄入量（基于膳食数据以及尿排泄数据）与青年期胰岛素敏感性及炎症生物标志物之间的前瞻性关联。DONALD研究中共有254名参与者，他们在青少年期（女性：9 - 15岁，男性：10 - 16岁）至少有两份为期3天的称重膳食记录，用于计算果糖、葡萄糖、蔗糖、总糖、游离糖、添加糖、来自含糖饮料（SSB）、果汁和糖果/糖的总糖摄入量，或者至少有两份完整的24小时尿样（n = 221），用于计算青少年期的糖排泄量（尿果糖和尿果糖 + 蔗糖），并在成年期（18 - 36岁）采集了空腹血样。这些参与者被纳入多变量线性回归分析，以评估他们与成人稳态模型评估胰岛素敏感性（HOMA2-%S）和促炎评分（基于CRP、IL - 6、IL - 18、瘦素、chemerin、脂联素）之间的前瞻性关联。在膳食摄入水平上，未观察到青少年期的果糖、蔗糖、葡萄糖、添加糖、游离糖、总糖或来自SSB、果汁或糖果/糖的总糖摄入量与成人HOMA2-%S之间存在前瞻性关联（P > 0.01）。然而，在尿水平上，仅在女性中，较高的尿果糖排泄水平与改善的成人HOMA2-%S相关（P = 0.008）。未观察到膳食糖或尿糖与成人促炎评分之间存在关联（P > 0.01）。本研究未提供证据支持青少年期摄入的膳食糖与成人胰岛素敏感性相关。一个可能的例外是适度的膳食果糖消费，它与成人空腹胰岛素和胰岛素敏感性呈有益关联。
