Medina-Bravo P, Medina-Urrutia A, Juarez-Rojas JG, Cardoso-Saldaña G, ˜Jorge-Galarza E, Posadas-Sanchez R, Coyote-Estrada N, Nishimura-Meguro E, Posadas-Romero C. Glycemic control and high-density lipoprotein characteristics in adolescents with type 1 diabetes.
Pediatric Diabetes 2013: 14: 399–406.
Background
Recent evidence suggests that high-density lipoprotein (HDL)physicochemical characteristics and functional capacity may be more important that HDL-C levels in predicting coronary heart disease. There is little data regarding HDL subclasses distribution in youth with type 1 diabetes.
Objective
To assess the relationships between glycemic control and HDL subclasses distribution, composition, and function in adolescents with type 1 diabetes.
Methods
This cross-sectional study included 52 adolescents with type 1 diabetes aged 12–16 years and 43 age-matched non-diabetic controls. Patients were divided into two groups: one in fair control [hemoglobin A1c (HbA1c) < 9.6%] and the second group with poor glycemic control (HbA1c ≥ 9.6%). In all participants, we determined HDL subclasses distribution, composition, and the ability of plasma and of isolated HDL to promote cellular cholesterol efflux. Levels of soluble adhesion molecules were also measured.
Results
Although both groups of patients and the control group had similar HDL-C levels, linear regression analyses showed that compared with non-diabetic subjects, the poor control group had a lower proportion of HDL2b subclass (p = 0.029), triglyceride enriched (p = 0.045), and cholesteryl ester depleted (p = 0.028) HDL particles. Despite these HDL changes, cholesterol efflux was comparable among the three groups. The poor control group also had significantly higher intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 plasma concentrations.
Conclusions
In adolescents with type 1 diabetes, poor glycemic control is associated with abnormalities in HDL subclasses distribution and HDL lipid composition, however, in spite of these HDL changes, the ability of HDL to promote cholesterol efflux remains comparable to that of healthy subjects.
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