Arterial Elasticity in adolescents with insulin resistance and type 1 diabetes — ASN Events
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  2. Poster Session 2
  3. Arterial Elasticity in adolescents with insulin resistance and type 1 diabetes

Arterial Elasticity in adolescents with insulin resistance and type 1 diabetes (#204)

Mandy Ho 1 2 , Paul Benitez-Aguirre 1 2 , Kim Donaghue 1 2 , Paul Mitchell 3 , Louise Baur 1 2 , Alicia Jenkins 4 5 , Maria Craig 1 2 6 , Chris Cowell 1 2 , Sarah Garnett 1 2
  1. University of Sydney, Sydney, NSW, Australia
  2. The Children’s Hospital at Westmead, Sydney, NSW, Australia
  3. Centre for Vision Research, Westmead Millennium Institute, Sydney, NSW, Australia
  4. St Vincents Hospital, Melbourne, Victoria, Australia
  5. Faculty of Medicine, Melbourne University, Melbourne, Victoria, Australia
  6. School of Women and Children’s Health, University of New South Wales, Sydney, NSW, Australia

Introduction
Reduced small arterial elasticity (SAE) in adults is associated with increased risk of cardiovascular events. The data relating to the association between arterial elasticity, obesity and glycaemic status in adolescents is limited and conflicting. This study aimed to determine if SAE differed between obese adolescents with clinical insulin resistance (IR), adolescents with type 1 diabetes (T1D) and healthy non-obese controls.

Methods
The IR group (n=68) were participants of a RCT, RESIST.1 The T1D group were recruited through the Diabetes Complications Assessment Centre at The Children’s Hospital at Westmead (n=91). The 63 age- and sex-matched healthy controls were a convenience sample of school children. All participants were aged 10-18 years. Arterial elasticity was measured using radial tonometry pulse wave analysis. Stepwise multiple regression analyses were performed to understand the determinants of SAE.

Results
The BMI z-scores of the IR and T1D groups and controls were 2.31±0.32, 0.59±0.65 and -0.07±0.95, (P<0.001), respectively. SAE values were higher in the IR group (11.6±4.8ml/mmHgx100) compared with the other groups (T1D: 8.3±2.3ml/mmHgx100, Controls: 8.2±2.3ml/mmHgx100). Weight was the strongest predictor of SAE, explaining 19%, 32% and 33% of variance in the IR, T1D groups and controls, respectively. Age predicted the SAE in the IR and T1D groups but not controls. After adjustment for weight and diastolic blood pressure, for every one year increase in age, the SAE decreased by 0.67 and 0.34 units in the IR and T1D groups, respectively. There was no significant association with fasting insulin (IR group) or HbA1c (TID group). Overall, the best predictive model for SAE, explaining 48% of variance, included weight (β=0.136, P<0.001), diastolic blood pressure (β=-0.152, P<0.001) and age (β=-0.292, P=0.007).

Conclusion
Obese adolescents with clinical IR and T1D may have an earlier loss of SAE compared with non-obese controls, which may reflect an increased risk of premature cardiovascular disease.