This deficiency affects not only fatty acid synthesis, but also secondary activation of fatty acid oxidation. Matsuzaka et al suggest that the reduction in insulin resistance in Elovl6 deficient mice could take place via restoration of hepatic insulin sensitivity by phosphorylation of Akt in the liver. Elovl6 deficiency alters hepatic fatty acid composition;SI-2 changes in fatty acid chain length and the ratio of fatty acids could reduce SREBP-1 and PPARa in the liver. Reduction in SREBP-1 leads to decreased fatty acid synthesis via reduction of lipogenic gene expression and increases in IRS-2 levels expression and insulin sensitivity. Reduction in lipogenesis could lead to decreased hepatic diacylglycerol content, which would lead to decreased PKCe activity and increased insulin sensitivity. Several studies have shown that Elovl6 expression is regulated by many dietary, hormonal and developmental factors. This elongase is also regulated by SREBP-1, which in turn is regulated by the PUFA. SREBP-1c plays a crucial role in the dietary regulation of most hepatic lipogenic genes. Matsuzaka et al showed that the mRNA levels of fatty acyl-CoA elongase were suppressed in livers from fasted SREBP-1 wild-type mice and markedly activated by refeeding in the wild-type mice, showing nutritional regulation of FACE as a lipogenic enzyme. Similar results were reported by Wang et al in Elovl6 expression levels in the liver of fasted rats that were later refed. Like Matsuzaka, these authors also saw that the PUFA suppressed the expression of lipid enzymes, DPBQ including Elovl6. FACE mRNA levels are markedly increased in a refed state after fasting in the liver and adipose tissue. This refeeding response is significantly reduced in SREBP-1 deficient mice. Dietary PUFAs caused a profound suppression of this gene expression, which could be restored by SREBP-1c overexpression. The diet in our study population is characterized by a high intake of monounsaturated fatty acids. In this study we found an interaction between the intake of fat and some of the polymorphisms of the ELOVL6 gene in relation to insulin sensitivity.