P 6: Markers of systemic inflammation and ApoAI-containing HDL subpopulations in women with and without diabetes

Abstract

Atherosclerosis is a blood vessel inflammatory disease. Besides their role in reverse cholesterol transport (RCT), HDL particles may affect the atherosclerotic process through the modulation of subclinical inflammation. Notably, HDL are a heterogeneous class of particles, differing in size, composition and, probably, in their anti-inflammatory properties. The potential relationships between HDL sub-particles and inflammatory markers have never been explored in diabetic women, who typically shows dysfunctional HDL. In this work, we investigated the relationship between different HDL subclasses and major inflammatory markers in a group of women with and without type 2 diabetes. Eighty type 2 diabetic and 80 control CHD-free women, not taking any hypolipidemic or hormonal drug, and matched for age and menopausal status, participated to the study. Clinical, lifestyle, common laboratory parameters, as well as inflammatory markers and HDL ApoAI-containing subpopulations with two gradient gel electrophoresis technique were measured in all participants. When comparing HDL subpopulations profile in women with and without diabetes, diabetic women showed a decrease of the larger alfa-1(P=0.006), alfa-2 (P=0.005), and pre alfa-1 HDL (P=0.02), and higher levels of the smaller, lipid poor alfa-3 HDL particles (P=0.02). Diabetic women also had higher hsCRP and IL-6 serum levels than non diabetic ones (age- and BMI-adjusted P<0.001, both), whereas no difference in resistin concentration were noted. Overall, inflammatory markers showed significant inverse correlations with the larger ApoAI containing HDL subclasses, and positive correlations with the smaller, less atheroprotective HDL particles. In particular, hsCRP inversely correlated with alfa-1 (P=0.01), pre alfa-1 (P<0.001),and pre alfa-2 (P=0.02); IL-6 inversely correlated with alfa-1 (P<0.001), alfa-2 (P<0.001), pre alfa-1 (P<0.001), pre alfa-2 (P=0.02), and positively with alfa-3 HDL (P=0.03). No correlations between resistin and HDL subpopulations were found. Similar correlations were also noted when considering diabetic and control women, separately, although these correlations were less numerous, especially in controls. These relationships were also confirmed by univariate regression analysis, especially in the diabetic group. Our data show that the larger, more atheroprotective HDL subclasses were associated with lower hsCRP and IL-6 levels, whereas the smaller, lipid poor alfa-3 HDL particles were associated with an increase of these inflammatory markers. These associations were more pronounced in type 2 diabetic women, who typically show dysfunctional HDL. These data suggest that different HDL subclasses may influence CHD risk also through altered anti-inflammatory properties.