Abstract
Despite clinical evidence that postprandial lipemia and chylomicrons could contribute to atherosclerosis, direct evidence is lacking. The study by Weinstein et al(1) provides evidence to suggest that intact chylomicrons might be atherogenic by using genetically altered mice lacking Gpihbp1 protein, which may play a major role in the lipolysis of triglyceride-rich lipoproteins. However, the study does not rule out a contribution by remnants or limited lipolysis by other potential enzymes or pathways. It might be intriguing to determine the contribution of cholesterol derivatives in the chylomicrons to the lesions and the nature of the lesions.
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