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Prescription Diabetes Drugs
Posted by admin in Prescription Diabetes Drugs on July 01st, 2009
Glycation of low-density lipoprotein (LDL) cholesterol is likely to be atherogenic and the concentration of glycated LDL or apolipoprotein (apo) B is positively correlated with plasma levels of small dense-LDL particles, but not glycated hemoglobin (HbA1c), report researchers.
The results of two studies of glycated LDL were presented at the Heart UK 23rd Annual Conference in Liverpool in the UK by Nahla Younis and Handrean Soran from Zagazig University in Egypt and the University of Manchester in the UK.
Younis presented data showing that macrophage cells incubated with glycated LDL as opposed to non-glycated LDL took up a significantly higher amount of cholesterol, suggesting that glycation of LDL might be an important atherogenic mechanism.
Younis and her colleagues also found that small dense-LDL was more susceptible to glycation than more buoyant forms and that high-density lipoproteins (HDL) with high paraoxenase-1 activity opposed LDL glycation.
In another study involving 111 Type 2 diabetic patients (statin treated and untreated) and 11 healthy controls without diabetes, Soran and colleagues assessed possible links among glycated apolipoprotein (apo)B, small dense LDL, and HbA1c.
The researchers reported that average levels of glycated apoB were 5.8, 3.5, and 2.9 mg/dl in Type 2 diabetics not treated with a statin, Type 2 diabetics treated with a statin, and controls, respectively.
In the corresponding three groups 69.0%, 39.0%, and 37.5% of the glycated apoB was found in small dense-LDL.
Plasma concentration of glycated apoB was observed to be positively correlated with small dense-LDL, but not HbA1c.
“This may explain why statins are more effective than glycemic control in decreasing cardiovascular disease risk in patients with diabetes and suggests that other means of decreasing small dense-LDL will decrease cardiovascular risk,” concluded Soran.
MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009
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