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Should not yet change dyslipidemia practice; leaves open C10 compounds as hypothesis-generating LPL agonists.
Lipoprotein lipase has long been known to hydrolyse triglycerides from triglycerides-rich lipoproteins. It also the ability to promote the binding of lipoproteins to the wide variation of lipoprotein receptors. There are some studies that suggest the possible atherogenic role of lipoprotein lipase. In theory, lipoprotein lipase deficiency should help to clarify this question. However, the rarity of this condition means that it has not been possible to conduct epidemiological studies. During the last decade it became obvious that elevated plasma TG and low HDL-cholesterol are part of CVD residual risk. Thus LPL is an attractive target for correcting dyslipidemia and reduction of CVD residual risk.
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Dorovsky et al. (2016) studied this question.
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