Letters to the Editor |
Oxford Centre for Diabetes, Endocrinology, and Metabolism, University of Oxford, UK
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
Recently, Aldons Lusis and coworkers suggested a relationship between stearoyl-coenzyme A (CoA) desaturase-1 (SCD1) activity and familial combined hyperlipidemia (FCH).1 The relationship between SCD1 and metabolic features related to FCH has attracted interest because it was shown that the SCD1 knockout mouse is obesity-resistant on high-fat feeding and has increased insulin sensitivity.2
The surrogate marker used for SCD1 activity is often the ratio of the product and precursor for the SCD1 enzymatic step, ie, either the ratio between 16:1n-7 and 16:0 or that of 18:1n-9 and 18:0 in plasma samples. Not only is this ratio very much dependent on previous food intake, it is also influenced by the fraction of lipids in plasma in which it is analyzed.3 The main plasma lipid fractions containing fatty acids are triglycerides, phospholipids, cholesteryl esters, and nonesterified fatty acids. Phospholipids, which have typical plasma concentrations of 2 to 3 mmol/L, show clear signs of fatty acid partitioning. They are enriched in long-chain polyunsaturated fatty acids, mainly 18:2n-6, but are relatively poor in, for example, 16:1n-7.3 Compared with plasma triglycerides, the plasma phospholipids are also poor in 18:1n-9 and rich in 18:0.3 Typical molar % of 16:1n-7 and 16:0 in plasma phospholipids are 2 and 30, whereas the average values for plasma triglycerides are 5% and 30%.3 The corresponding values for 18:1n-9 and 18:0 in plasma triglycerides are 28% and 4.5%, respectively, whereas the relative values are 10% and 14% for phospholipids. Importantly, the abundance of plasma phospholipids does not increase in
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