Insulin resistance is characterized by alterations of lipid metabolism, particularly elevated plasma triacylglycerol and decreased HDL-cholesterol concentrations and the presence of small, dense LDL particles. These observations are difficult to interpret in terms of cause and effect. In this review, the hypothesis is put forward that these changes stem from disruption of the normal precise co-ordination of postprandial lipid metabolism by insulin.
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Keith N. Frayn (1993) studied this question.