Pioglitazone protects HDL2&3 against oxidation in overweight and obese men

Author:

Mceneny Jane1,Mcpherson Peter A1,Mcginty Ann1,Hull Stephen S2,Mccance David R3,Young Ian S1

Affiliation:

1. Centre for Public Health, Queen's University Belfast, Nutrition & Metabolism Group, Grosvenor Road, Belfast BT12 6BJ;

2. Mater Hospital, Belfast Health & Social Care Trust, Belfast BT14 6AB;

3. Regional Centre for Endocrinology & Diabetes, Belfast Health & Social Care Trust, Belfast BT12 6BA, UK

Abstract

Background The worldwide epidemic of obesity is a major public health concern and is persuasively linked to the rising prevalence of diabetes and cardiovascular disease. Obesity is often associated with an abnormal lipoprotein profile, which may be partly negated by pioglitazone intervention, as this can influence the composition and oxidation characteristics of low-density lipoprotein (LDL). However, as pioglitazone's impact on these parameters within high-density lipoprotein (HDL), specifically HDL2&3, is absent from the literature, this study was performed to address this shortcoming. Methods Twenty men were randomized to placebo or pioglitazone (30 mg/day) for 12 weeks. HDL2&3 were isolated by rapidultracentrifugation. HDL2&3-cholesterol and phospholipid content were assessed by enzymatic assays and apolipoprotein AI (apoAI) content by single-radial immunodiffusion. HDL2&3 oxidation characteristics were assessed by monitoring conjugated diene production and paraoxonase-1 activity by spectrophotometric assays. Results Compared with the placebo group, pioglitazone influenced the composition and oxidation potential of HDL2&3. Specifically, total cholesterol (P < 0.05), phospholipid (P < 0.001) and apoAI (P < 0.001) were enriched within HDL2. Furthermore, the resistance of HDL2&3 to oxidation (P < 0.05) and the activity of paroxonase-1 were also increased (P < 0.001). Conclusions Overall, these findings indicate that pioglitazone treatment induced antiatherogenic changes within HDL2& 3 , which may help reduce the incidence of premature cardiovascular disease linked with obesity.

Publisher

SAGE Publications

Subject

Clinical Biochemistry,General Medicine

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