Stearoyl CoA desaturase (Δ9 desaturase) is an enzyme that participates in the de novo lipogenesis pathway. This pathway is tasked with the creation of new fatty acids from non-fat sources. The pathway operate primarily in the liver and the substrate most likely to be converted to fatty acids is glucose. In this way the cells of the body can create all the fatty acids they need with the exception of the two essential fatty acids alpha linolenic acid (ALA, C18:3 (n-3)) and linoleic acid (LA, C18:2 (n-3)) which are essential fatty acids and therefore must be derived from the diet. As a desaturation enzyme the stearoyl CoA desaturase enzyme adds a double bond to newly created saturated fatty acids to allow the creation of a number of unsaturated fatty acids such as palmitoleic acid (POA, C16:1 (n-7)). Palmitoleic acid has been investigated and been found to be an accurate marker of the activity of the de novo lipogenesis pathway, which in turn is upregulated by high intakes of dietary fructose and increased consumption of refined grains.
Evidence suggests that high levels of palmitoleic acid or a high ratio of monounsaturated to saturated fatty acids in erythrocyte plasma membranes are associated with an increased risk of breast cancer, gastric cancer and pancreatic cancer. High activity of stearoyl CoA desaturase is associated with shorter survival time from cancer and high levels of monounsaturated fatty acids have been observed in cancer cells. It is thought that a high endogenous synthesis of palmitoleic acid is required to sustain the neoplastic phenotype (those susceptible to abnormal tissue growth). High plasma levels of palmitoleic acid have been used as a marker of liver stearoyl CoA desaturase enzyme activity because the latter is difficult to measure. For example, researchers1 have assessed the cholesteryl ester proportion of palmitoleic acid and the palmitoleic acid to palmitic acid ratio, and investigated polymorphisms (different types of the same gene) in the stearoyl CoA gene, with relation to cancer.
The subjects in the study were 50 year old men that were followed prospectively for 40 years. Their plasma fatty acids measured at baseline and death and polymorphisms in their stearoyl coA desaturase gene were measured from DNA samples. The results of the study showed that the levels of palmitoleic acid and the ratio of palmitoleic acid to palmitic acid were associated with cancer mortality (a 37 % increased risk) when those with the highest palmitoleic acid and palmitoleic acid to palmitic acid ratios were compared to those with the lowest. Single nucleotide polymorphisms (SNP; variations in a gene that occur within a population) were associated to cancer death, especially if the subject had a low intake of polyunsaturated fatty acids in the diet. Therefore increased flux through the de novo lipogenesis pathway appears to increase the risk of cancer mortality in men. As de novo lipogenesis is upregulated with consumption of fructose and refined carbohydrates, this upregulation could be a marker of a poor quality diet.
1Byberg, L., Kilander, L., Lemming, E. W., Michaelsson, K. and Vessby, B. 2014. Cancer death is related to high palmitoleic acid in serum and to polymorphisms in the SCD-1 gene in healthy Swedish men. American Journal of Clinical Nutrition. 99: 551-558