title: CIDE-A is expressed in liver of old mice and in type 2 diabetic mouse liver exhibiting steatosis.
abstract: BACKGROUND
  Increased levels of circulating fatty acids caused by insulin resistance and increased adipocyte lipolysis can accumulate within the liver resulting in steatosis. This steatosis sensitizes the liver to inflammation and further injury which can lead to liver dysfunction. We performed microarray analysis on normal mouse liver tissue at different ages and type 2 diabetic liver exhibiting steatosis to identify differentially expressed genes involved in lipid accumulation and liver dysfunction.
  
  
  RESULTS
  Microarray analysis identified CIDE-A as the most differentially expressed gene as a function of age. Mice fed a high fat diet developed hyperinsulinemia, hyperglycemia and liver steatosis, all features of the human metabolic syndrome. Increased CIDE-A expression was observed in type 2 diabetic liver and the elevated CIDE-A expression could be reversed by weight loss and normalization of plasma insulin. Also, CIDE-A expression was found to be correlated with hepatic lipid accumulation.
  
  
  CONCLUSIONS
  The corresponding increase in CIDE-A expression with hyperinsulinemia and liver steatosis suggests a novel pathway for lipid accumulation in the liver.
authors.affiliation: Edison Biotechnology Institute, Ohio University, Athens, OH 45701, USA. kelder@ohio.edu
authors.forename: Bruce
authors.initials: B
authors.lastname: Kelder
authors.forename: Keith
authors.initials: K
authors.lastname: Boyce
authors.forename: Andres
authors.initials: A
authors.lastname: Kriete
authors.forename: Ryan
authors.initials: R
authors.lastname: Clark
authors.forename: Darlene E
authors.initials: DE
authors.lastname: Berryman
authors.forename: Sheila
authors.initials: S
authors.lastname: Nagatomi
authors.forename: Edward O
authors.initials: EO
authors.lastname: List
authors.forename: Mark
authors.initials: M
authors.lastname: Braughler
authors.forename: John J
authors.initials: JJ
authors.lastname: Kopchick