Details

Autor(en) / Beteiligte

• Nakhjavani, Manouchehr, MD
• Asgharani, Firouzeh, MD
• Khalilzadeh, Omid, MD, MPH
• Esteghamati, Alireza, MD
• Ghaneei, Azam, MD
• Morteza, Afsaneh, MD, MPH
• Anvari, Mehdi, MD

Titel

Oxidized Low-Density Lipoprotein Is Negatively Correlated With Lecithin-Cholesterol Acyltransferase Activity in Type 2 Diabetes Mellitus

Ist Teil von

• The American journal of the medical sciences, 2011-02, Vol.341 (2), p.92-95

Ort / Verlag

Hagerstown, MD: Elsevier Inc

Erscheinungsjahr

2011

Quelle

MEDLINE

Beschreibungen/Notizen

• Abstract Introduction It is now believed that the oxidative modification of plasma lipoproteins enhance their atherogenicity in patients with type 2 diabetes. Because a variety of highly reactive lipid peroxidation products can transfer from oxidized low-density lipoprotein (ox-LDL) to high-density lipoprotein -cholesterol, the authors evaluated the association between ox-LDL and lecithin-cholesterol acyl-transferase (LCAT) activity, a key enzyme in reverse cholesterol transport and HDL remodeling. Methods A total of 45 patients with diabetes and 45 age-, sex- and body mass index-matched healthy adult volunteers were enrolled. Fasting blood samples were obtained, and plasma glucose, lipid profile, creatinine, insulin, ox-LDL and LCAT activity were measured. Homeostasis model assessment of insulin resistance was also calculated. Results Patients with diabetes, compared with healthy participants, had a significantly higher ox-LDL (17.16 ± 3.75 U/L versus 7.93 ± 1.92 U/L, P < 0.001) and lower LCAT activity (73.7 ± 9.1 μ mol/L/hr versus 88.7 ± 4.5 μ mol/L/hr, P < 0.001). The higher level of LCAT activity completely disappeared after adjustment for ox-LDL. LCAT activity had a significant ( P < 0.001) inverse correlation with ox-LDL ( r = -0.77) in patients with diabetes and healthy participants ( r =-0.75). Conclusion LCAT activity is significantly decreased in type 2 diabetes. The lower LCAT activity in type 2 diabetes might be through ox-LDL mechanism. ox-LDL may adversely affect high-density lipoprotein -cholesterol metabolism by reducing LCAT activity.