Transcription profiling of livers from SCD1 knockout and wild type mice to elucidate the molecular basis of protection against adiposity in mice lacking of stearoyl-CoA desaturase-1 function

ABSTRACT: Stearoyl-CoA desaturase (SCD) is a central lipogenic enzyme catalyzing the synthesis of monounsaturated fatty acids, mainly oleate (C18:1) and palmitoleate (C16:1), which are components of membrane phospholipids, triglycerides, wax esters, and cholesterol esters. Several SCD isoforms (SCD1-3) exist in the mouse. Here we show that mice with a targeted disruption of the SCD1 isoform have reduced body adiposity, increased insulin sensitivity, and are resistant to diet-induced weight gain. The protection from obesity involves increased energy expenditure and increased oxygen consumption. Compared with the wild-type mice the SCD1-/- mice have increased levels of plasma ketone bodies but reduced levels of plasma insulin and leptin. In the SCD1-/- mice, the expression of several genes of lipid oxidation are up-regulated, whereas lipid synthesis genes are down-regulated. These observations suggest that a consequence of SCD1 deficiency is an activation of lipid oxidation in addition to reduced triglyceride synthesis and storage. Experiment Overall Design: RNA was isolated from livers of 10 individual 6-week-old female mice by using a standard method. Mouse genome U74A arrays were used to monitor the expression level of approximately 10,000 genes and expressed sequence tags (Affymetrix). Genes differentially expressed were identified by comparing expression levels in SCD1-/- and wild-type mice.

ORGANISM(S): Mus musculus

SUBMITTER: Alan Attie 

PROVIDER: E-GEOD-2926 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress