Promoter elements that are responsible for the polyunsaturated fatty acid repression colocalize with the promoter elements for SREBP-mediated regulation of the SCD genes.It is the goal of this review to provide an overview of the genetic regulation of the stearoyl-Co A desaturase in response to dietary polyunsaturated fatty acids and cholesterol.—Ntambi, J. Regulation of stearoyl-Co A desaturase by polyunsaturated fatty acids and cholesterol.A proper ratio of saturated to monounsaturated fatty acids contributes to membrane fluidity.Alterations in this ratio have been implicated in various disease states including cardiovascular disease, obesity, non-insulin-dependent diabetes mellitus, hypertension, neurological diseases, immune disorders, and cancer.A hyperlink is provided for those chemicals for which the basis for listing documentation is available electronically.
Oleic acid and palmitoleic acid are the major monounsaturated fatty acids in fat depots and membrane phospholipids.
Two mouse and rat genes (SCD1 and SCD2) and a single human SCD gene have been cloned and characterized (9–12).
Other SCD c DNAs and genes have been isolated from different species including yeast (13), ovine (14), and hamster (15), and the regulation of their expression is currently being studied by several research groups.
There appears to be a number of answers at different levels, i.e., special physico-chemical properties of oleic acid at body temperature, its effects on membrane fluidity, a readily available energy source, and the constraints of the intermediary metabolism of carbohydrates and fats.
During the de novo synthesis of fatty acids, the fatty acid synthase enzyme stops at palmitate but the end product of the pathway is usually oleic acid. High carbohydrate feeding also leads to high levels of palmitoleate as seen in neonates (2).