By IANS,
Washington : A variation in the way a single protein is processed by the body might account for some people’s failure to respond to drugs that lower “bad” cholesterol, according to a new study.
The gene variation, called alternative splicing, has helped explain the drugs’ decreased power to reduce low-density lipoprotein (LDL) in some participants.
The study is the first to show that a change in a biological process substantially modifies the effectiveness of cholesterol-lowering drugs, known as statins.
“The implications could go well beyond the efficacy of statins by helping us to understand the differences among individuals in how cholesterol is metabolised,” said Ronald Krauss, co-author of the study.
The discovery could lead to improved cholesterol treatment and new therapy for other chronic ailments.
Simvastatin is one of several statin drugs that can effectively reduce the risk of heart attacks in people with high cholesterol.
They work by blocking a key enzyme required for the production of cholesterol called HMGCR. However, all people don’t have the same response to statins.
Krauss and his team, seeking a genetic explanation for this variability, analysed differences in how the gene responsible for producing HMGCR was processed – or spliced – among more than 900 participants enrolled in the study.