Aim: ApoA-I and HDL promote cellular cholesterol efflux in the early stages of the reverse cholesterol transport (RCT) pathway. A low plasma HDL-C level is characteristic of atherogenic dyslipidemia in patients with type 2 diabetes. We evaluated plasma lipid levels and the expression of factors related to RCT in type 2 diabetic patients, and the effects of an HMG-CoA reductase inhibitor, simvastatin, were studied.
Methods: Messenger RNA (mRNA) expression in circulating mononuclear cells was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), focusing on the following factors: liver X receptor α (LXR α), ATP-binding cassette A1 (ABCA1), scavenger receptor class B type 1 (SR-B1), apolipoprotein E (ApoE), apolipoprotein A-1 (ApoA-1), caveolin, and cholesterol ester transfer protein (CETP). Type 2 diabetic subjects (n=29) were divided into three subgroups: patients with normolipidemia (DM group, n=11), patients with untreated hyperlipidemia (DMHL group, n=10), and those with hyperlipidemia treated with simvastatin 5-10mg/day (DMST group, n=8). The control group (CNT group) included seven healthy volunteers.
Results: Simvastatin treatment significantly increased plasma levels of ApoA-I compared to the other three groups. Simvastatin treatment improved the expression of mRNA for LXRα, ABCA1, and ApoA-I compared with DMHL or control groups.
Conclusion: Our data suggest that RCT may be reduced in type 2 diabetic patients with hyperlipidemia, and simvastatin may be able to improve reverse cholesterol transport for this population of diabetic patients.