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Summary
Toplak H et al.  
BMI and lipid lowering - is there a relation

Journal of Clinical and Basic Cardiology 2000; 3 (2): 115-117

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Fig. 1: Nahrung - Metabolismus



Keywords: AdipositasAtorvastatinHMG-CoA-ReduktasehemmerWirkungAtorvastatindrug actionHMG-CoA-reductase inhibitorsobesity

Lipid lowering has become one of the major and efficient tools in cardiovascular primary and secondary disease prevention. The best understood causes of hyperlipidaemias are specific genetic changes such as "familial hypercholesterolaemia", the inherited LDL-receptor defect, and mutations like ApoB3500 leading to decreased binding of ApoB containing lipoprotein particles to their eliminating receptors. But that does not explain hyperlipidaemia in most of our patients. We assume that present changes in the understanding of the "metabolic syndrome" will prove to be more important for that purpose. Obesity and especially visceral adipose tissue seem to play a central role in generating an increased "fatty acid flux" and a resulting "lipoprotein flux" towards the periphery which might increase the importance of minor underlying genetic variants and "weaknesses" in lipoprotein metabolism. In the present paper we outline the pathophysiological background of the importance of obesity and visceral fat and describe an increasing response to atorvastatin in hyperlipidaemic patients grouped by BMI. J Clin Basic Cardiol 2000; 3: 115-7.
 
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