Letters to the Editor |
UCLA School of Medicine, Department of Medicine, Microbiolog, and Human Genetics, Los Angeles, Calif
UCLA School of Medicine, Human Genetics, Los Angeles, Calif
In response:
The justification of using the desaturation index as a measure of SCD was based primarily on studies with mouse models, including a hypertriglyceridemic model.1 Also, because the individuals were fasted, the effect of fatty acids from the diet would be minimized. However, we do not disagree with the points made by Drs Karpe and Hodson. Clearly, the desaturation index is not a very accurate measure of SCD activity. Our primary objective was not to estimate SCD activity but rather to find novel genetic markers for analysis of familial combined hyperlipidemia. For example, it is interesting that one suggestive quantitative trait locus for the desaturation index overlaps with a locus for fatty liver in the same group of patients.2
References
1. Attie AD, Krauss RM, Gray-Keller MP, Brownlie A, Miyazaki M, Kastelein JJ, Lusis AJ, Stalenhoef AF, Stoehr JP, Hayden MR, Ntambi JM. Relationship between stearoyl-coenzymeA (CoA) desaturase activity and plasma triglycerides in human and mouse hypertriglyceridemia. J Lipid Res. 2002; 43: 1899–1907.
2. Brouwers MC, Cantor RM, Kono N, Yoon JL, van der Kallen CJ, Bilderbeek-Beckers MA, van Greevenbroek MM, Lusis AJ, de Bruin TW. Heritability and genetic loci of fatty liver in familial combined hyperlipidemia. J Lipid Res. 2006; 47: 2799–2807.
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