This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The long-term goal of this application is to understand the role of stearoyl-CoA desaturase in metabolism. Stearoyl-CoA desaturase (SCD) is a critical regulator of lipogenesis that catalyzes the synthesis of monounsaturated fatty acids (MUFA), mainly oleoyl- (18:1n9) and palmitoleoyl-CoA (16:1n7). SCD expression is elevated in human and rodent obese and insulin resistant states, suggesting that excess 18:1n9 or 16:1n7 synthesis may contribute to metabolic disease development. Mice with a global deletion of the SCD1 isoform are remarkably resistant to diet- and genetically-induced obesity, insulin resistance and liver steatosis. In this project we will focus on two aims.
In Aim 1, we will determine the contribution of hepatic SCD1 expression to the ER stress response and ER stress-mediated lipogenesis.
In Aim 2, we will determine the mechanisms causing ER stress due to SCD1 deficiency. As the main metabolic culprits in diseases of the metabolic syndrome are lipids, understanding the role of stearoyl-CoA desaturase genes in hepatic metabolism and ER stress pathways might provide major insights
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