Lynae J Hanks1, James Heath Pelham2, Shalini Vaid2, Krista Casazza3, Ambika P Ashraf4. 1. Department of Pediatrics/Division of Pediatric Endocrinology and Metabolism, Children's of Alabama, University of Alabama at Birmingham (UAB), CPPII M30, 1601 4th Ave S., Birmingham, AL 35233, United States. 2. UAB School of Medicine, University of Alabama at Birmingham, 1720 2nd Ave South, Birmingham, AL 35294-0113, United States. 3. Department of Pediatrics/Division of General Pediatrics and Adolescent Medicine, CPP1 310, 1601 4th Ave S., Birmingham, AL 35233-1711, United States. 4. Department of Pediatrics/Division of Pediatric Endocrinology and Metabolism, Children's of Alabama, University of Alabama at Birmingham (UAB), CPPII M30, 1601 4th Ave S., Birmingham, AL 35233, United States. Electronic address: AAshraf@peds.uab.edu.
Abstract
AIM: Diabetes-associated glucoregulatory derangements may precipitate atherogenesis in childhood and CVD risk, particularly with obesity. We aimed to delineate lipoprotein profile differences between children with type 1 and 2 diabetes who are overweight/obese. METHODS: Data were obtained from electronic medical records of patients ≥85th BMI percentile with type 1 (n=159) and type 2 (n=77) diabetes, ages 12-19y. Group differences were evaluated by correlations and general linear modeling analysis, adjusting for BMI, HbA1c, and diabetes duration. RESULTS: There were no group differences in TC, LDL, or non-HDL. Fewer subjects with type 1 diabetes had low HDL (17 vs. 30%; P<0.05). While no difference in HbA1c level was observed between groups, HbA1c was positively correlated with TC (P≤0.0001), LDL (P≤0.0001), non-HDL (P≤0.0001), ApoB100 (P≤0.0001), and LDL pattern B (P≤0.0001). In adjusted models, apoB100 (85.4 vs. 91.3mg/dl; P<0.05) and incidence of LDL pattern B (21 vs. 42%; P<0.01) were lower in subjects with type 1 diabetes. BMI was inversely correlated with HDL, HDL-2 and HDL-3 (all P≤0.0001). The correlation of BMI with HDL-2 and HDL-3 were attenuated when evaluating subjects by diabetes type. CONCLUSIONS: Despite having no difference in absolute LDL levels, children with type 2 diabetes were more likely to have small, dense LDL particle pattern, higher apo B100 and lower total HDL, HDL-2, and HDL-3 fractions. Furthermore, poor glycemic control was associated with abnormal lipoprotein profiles in patients with both type 1 and 2 diabetes.
AIM: Diabetes-associated glucoregulatory derangements may precipitate atherogenesis in childhood and CVD risk, particularly with obesity. We aimed to delineate lipoprotein profile differences between children with type 1 and 2 diabetes who are overweight/obese. METHODS: Data were obtained from electronic medical records of patients ≥85th BMI percentile with type 1 (n=159) and type 2 (n=77) diabetes, ages 12-19y. Group differences were evaluated by correlations and general linear modeling analysis, adjusting for BMI, HbA1c, and diabetes duration. RESULTS: There were no group differences in TC, LDL, or non-HDL. Fewer subjects with type 1 diabetes had low HDL (17 vs. 30%; P<0.05). While no difference in HbA1c level was observed between groups, HbA1c was positively correlated with TC (P≤0.0001), LDL (P≤0.0001), non-HDL (P≤0.0001), ApoB100 (P≤0.0001), and LDL pattern B (P≤0.0001). In adjusted models, apoB100 (85.4 vs. 91.3mg/dl; P<0.05) and incidence of LDL pattern B (21 vs. 42%; P<0.01) were lower in subjects with type 1 diabetes. BMI was inversely correlated with HDL, HDL-2 and HDL-3 (all P≤0.0001). The correlation of BMI with HDL-2 and HDL-3 were attenuated when evaluating subjects by diabetes type. CONCLUSIONS: Despite having no difference in absolute LDL levels, children with type 2 diabetes were more likely to have small, dense LDL particle pattern, higher apo B100 and lower total HDL, HDL-2, and HDL-3 fractions. Furthermore, poor glycemic control was associated with abnormal lipoprotein profiles in patients with both type 1 and 2 diabetes.
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