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Hemoglobin A1c (HbA1c) monitoring over time is thought to facilitate care and support diabetes management goals, but only half of youth and young adults with diabetes report ≥3 HbA1c tests/year despite poor glycemic control. We explored disparities in HbA1c testing over time and association with HbA1c levels and microvascular complications (retinopathy, neuropathy, or nephropathy) in the SEARCH for Diabetes in Youth study. Individuals diagnosed with diabetes at In conclusion, we report that mainly healthcare-related factors are associated with disparities in HbA1c testing frequency over time in youth-onset type 1 and type 2 diabetes, and these disparities are associated with HbA1c levels in type 1 diabetes. Disclosure K. A. Sauder: None. R. Dagostino: Consultant; Self; AstraZeneca, Biogen, Daiichi Sankyo. D. Dabelea: None. J. M. Stafford: None. S. R. Ehrlich: None. A. D. Liese: None. S. M. Marcovina: None. A. K. Mottl: Advisory Panel; Self; Bayer U. S. C. Pihoker: None. S. Saydah: None. A. S. Shah: None. Funding National Institutes of Health; Centers for Disease Control and Prevention

Poor cognition has been observed in children and adolescents with type 1 (T1D) and type 2 (T2D) diabetes. Differences in cognition between young adults with youth-onset T1D and T2D, however, have not been explored, nor is the effect of shared etiologic processes, e.g., poor glycemic control, on cognition fully understood. Using data from SEARCH for Diabetes in Youth, a multicenter, observational cohort study, we compared cognition between young adults with youth-onset T1D and T2D, testing whether glycemic control modified the relationship between diabetes type and cognition. Cognition was assessed via the NIH Toolbox Cognition Battery and age-corrected composite Fluid Cognition scores used. Glycemic control was estimated from repeated measures of HbA1c. Linear regression modeling was used to test the interaction effect of diabetes type and glycemic control on Fluid Cognition score while controlling for sex, race/ethnicity, waist-height ratio, duration of diabetes, depression, alcohol and drug use, any hypoglycemic episode in the past year, parental highest level of education, household income, and clinic site. The T2D group (n = 254) had significantly lower Fluid Cognition scores, compared to the T1D group (n = 953) (mean [SD] 84.7 [17.3] vs. 95.4 [16.8], p Disclosure A. Shapiro: None. D. Dabelea: None. J.M. Stafford: None. R. Dagostino: Consultant; Self; Amgen, AstraZeneca, Celgene, Daiichi Sankyo. C. Pihoker: None. A.D. Liese: None. A.S. Shah: None. A. Bellatorre: None. J.M. Lawrence: None. L. Henkin: None. G. Wilkening: None. Funding National Institute of Diabetes and Digestive and Kidney Diseases (1UC4DK108173-01)

Individuals with diabetes are at high risk for heart failure with preserved ejection fraction due to diabetic cardiomyopathy (DCM), defined as abnormal myocardial structure and function in the absence of overt coronary artery disease. DCM leads to myocardial fibrosis and remodeling with one of the first signs being left ventricular (LV) diastolic dysfunction. The objective was to compare the prevalence of diastolic dysfunction among young adults with type 1 diabetes (T1D) vs. type 2 diabetes (T2D) with diabetes diagnosed in childhood. Participants had T1D or T2D and were enrolled in the SEARCH for Diabetes in Youth Study. Cardiovascular risk factors and diastolic function via echocardiography were measured at an in-person visit, after an average disease duration of 10.9 years (both groups). Unadjusted means were compared between those with T1D and T2D, p Disclosure A.S. Shah: None. D. Dabelea: None. L.M. Dolan: None. S. Isom: None. R. Dagostino: Consultant; Self; Amgen, AstraZeneca, Celgene, Daiichi Sankyo. L.E. Wagenknecht: None. G. Imperatore: None. S. Saydah: None. A.D. Liese: None. J.M. Lawrence: None. C. Pihoker: None. E.M. Urbina: None. Funding Centers for Disease Control and Prevention (1U18DP006131, U18DP006133, U18DP006134, U18DP006136, U18DP006138, U18DP006139); National Institutes of Health (1UC4DK108173)

Limited information exists regarding the evolution of dyslipidemia in youth with type 2 diabetes (T2D). Understanding dyslipidemia risk factors may influence treatment. We studied 212 youth with T2D not on lipid lowering therapy (68% female, 43% non-Hispanic black, mean age 14.9±2.7y at baseline, mean follow-up 7.0±2.0y). Dyslipidemia was defined as HDL-C100mg/dL, or triglycerides (TG)>150mg/dL. Progression was defined as normal lipids at baseline, dyslipidemia at follow-up; regression as dyslipidemia at baseline, normal at follow-up; stable abnormal as dyslipidemia at both; stable normal as normal at both. Associations of A1c and abdominal adiposity (waist to height ratio, WHtR) over time (area under the curve, AUC) with progression and stable abnormal were examined and relative risks estimated. HDL-C progressed, regressed, was stable normal and stable abnormal in 12%, 11%, 62%, and 14%, respectively. Corresponding LDL-C values were 16%, 13%, 43% and 29%; TG were 17%, 11%, 56% and 16%. Each 1% increase in A1c AUC was associated with 13% higher risk of TG>150mg/dL and 22% higher risk of LDL-C>100mg/dL, after adjusting for WHtR (Table). There were no significant associations with WHtR. In youth with T2D, 33% and 45% had progression or stable dyslipidemia of TG and LDL-C, respectively. Higher A1c over time is associated with worse TG and LDL-C, highlighting the importance of glycemic control. Disclosure R.P. Brady: None. A.S. Shah: None. E.T. Jensen: None. J.M. Stafford: None. R. Dagostino: Consultant; Self; Amgen, AstraZeneca, Celgene, Daiichi Sankyo. L.M. Dolan: None. L.M. Knight: None. G. Imperatore: None. C.B. Turley: None. A.D. Liese: None. E.M. Urbina: None. J.M. Lawrence: None. C. Pihoker: None. S.M. Marcovina: None. D. Dabelea: None. Funding Centers for Disease Control and Prevention (1U18DP006131, U18DP006133, U18DP006134, U18DP006136, U18DP006138, U18DP006139); National Institutes of Health (1UC4DK108173)