Abstract

Purpose: 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.Methods: 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 (n = 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).Results: 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 (p > 0.01). On the urinary level, however, higher excreted fructose levels were associated with improved adult HOMA2-%S (p = 0.008) among females only. No associations were observed between dietary or urinary sugars and the adult pro-inflammatory score (p > 0.01).Conclusion: 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.

Highlights

  • It has been proposed that dietary sugar intake plays a causal role in the development of type 2 diabetes (T2D) [1,2,3,4], yet data on this topic are conflicting [5, 6]

  • Dietary fructose that occurs naturally in whole fruits and vegetables provides only modest amounts of fructose combined with phytochemicals and fiber [9, 10], amounts as well as types/sources of ingested fructose are of importance when considering its relation to risk factors of T2D [11]

  • Sucrose, glucose, total sugar, free sugar and added sugar intakes as well as the urinary sugars are shown in Tables 3– 5

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Summary

Introduction

It has been proposed that dietary sugar intake plays a causal role in the development of type 2 diabetes (T2D) [1,2,3,4], yet data on this topic are conflicting [5, 6]. High intake levels of fructose administered in such intervention and acute studies do not represent common intake patterns consumed habitually over time. Dietary fructose elicits lower insulin secretion as compared to dietary glucose [12,13,14], and there is some evidence indicating that fructose intake/substitution can beneficially affect blood glucose levels [15, 16]. Clarifications from prospective studies concerning the role of dietary fructose and other sugar types in the development of insulin sensitivity are needed

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