Expression data from hepatocyte specific Klf6 knockout mice vs. control on high fat diet

ABSTRACT: Dysregulated glucose homeostasis and lipid accumulation characterize non-alcoholic fatty liver disease (NAFLD), but underlying mechanisms are obscure. We report here that Krüppel-like factor 6 (KLF6), a ubiquitous transcription factor that promotes adipocyte differentiation, also provokes the metabolic abnormalities of NAFLD. Mice with either hepatocyte-specific knockdown of KLF6 (DeltaHepKlf6) or global KLF6 heterozygosity (Klf6 +/-) have reduced body fat content and improved glucose and insulin tolerance. Mice with KLF6 depletion, compared to wild type mice, are protected from high fat diet-induced steatosis. Three mice with a hepatocyte-specific knockdown of KLF6 (DeltaHepKlf6) on high fat diet and 3 littermate controls on the same diet were sacrificed after 8 weeks of diet. Liver tis

ORGANISM(S): Mus musculus

SUBMITTER: Weijia Zhang 

PROVIDER: E-GEOD-36724 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress