8395 Exploring the Relationship of Dietary Advanced Glycation End-products (AGEs) with Glycemic Control among Adults with Type 1 Diabetes (T1D)

Abstract

Abstract Disclosure: C.E. Nevarez: None. A.B. Murthy: None. G. Jung: None. B. Gray: None. E. Cagliero: None. V. Aroda: None. E.W. Yu: None. Introduction: Accumulation of advanced glycation end products (AGEs) are thought to play a crucial role in the pathophysiology of diabetic complications, yet the contributions of dietary AGE (dAGE) intake to systemic AGE levels and glycemic control have not been established. Utilizing a newly developed methodology for evaluating dAGEs, our objective was to test whether dAGE impact systemic AGEs and glycemic outcomes in adults with longstanding Type 1 Diabetes (T1D). Methods: We examined adults aged 50+ years participating in the T1D BEACON cohort (n=97 T1D, n=53 non-diabetic controls). We developed a novel algorithm to quantify dietary AGE intake by associating items from the 2014 Block Food Frequency Questionnaire with their AGE content (as determined by ELISA from a previously published dataset; Urribarri et al., 2010). Daily dAGE intake was normalized using the nutrient density method (Willett et al., 1997). Additional measurements included autofluorescent skin AGEs (AGE Reader, DiagnOptics Technologies), diabetic history, hemoglobin A1C and 14-day continuous glucose monitoring to assess percentage time in glucose target range (70-180 mg/dL). We compared dAGEs between T1D and controls and evaluated associations of dAGEs with outcomes using independent t-tests, Pearson’s correlations, and multivariate linear regression with adjustments for age, sex, and body mass index (BMI). Results: Mean age and sex distribution was similar in the T1D and control groups (63.54 ± 6.7 yrs, 50.7% female). BMI was higher in the T1D group (27.9 ± 5.0 vs. 26.0 ± 4.9 kg/m^2, p = 0.031). The mean ± SD duration of diabetes in the T1D cohort was 46.1 ± 9.8 yrs, with A1c of 7.1 ± 1.0%. Utilizing our novel algorithm, the mean daily normalized dAGE intake was higher in the T1D than control groups (8.8 ± 2.3 kU/kcal vs. 7.9 ± 2.5 kU/kcal, p = 0.046) although this did not remain significant after multivariate adjustment (adj p = 0.123). Skin AGEs were higher in the T1D group (3.0 vs 2.5 AU, adj p<0.001). Within the full cohort, dAGE intake was significantly correlated with skin AGEs (r = 0.32, adj. p = 0.003), which was driven primarily by association within the T1D group (r = 0.32, adj p = 0.002). Additionally, dAGE intake was associated with higher A1C values within the full cohort (r = 0.27, adj. p = 0.019), and there was a trend that higher dAGE correlated with decreased time in target glucose range (r = -0.22, adj p = 0.062). Conclusion: Our analyses have revealed novel associations between dAGE intake, skin AGEs, and glycemic outcomes among adults with type 1 diabetes, underscoring the contribution of dietary patterns to systemic AGEs and physiological outcomes within diabetic populations. Future investigations will be needed to validate this novel dAGE assessment in external cohorts and to evaluate the potential impact of dietary AGE intake upon diabetic complications. Presentation: 6/1/2024