CIDE-A is expressed in liver of old mice and in type 2 diabetic mouse liver exhibiting steatosis

Bruce Kelder¹ , Keith Boyce²^,4 , Andres Kriete²^,5 , Ryan Clark¹ , Darlene E Berryman⁶ , Sheila Nagatomi² , Edward O List¹ , Mark Braughler²^,7 and John J Kopchick¹^,3

¹Edison Biotechnology Institute, Ohio University, Athens, OH 45701, USA

²Clinical Data Inc, Newton, MA 02458, USA

³Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, OH 45701, USA

⁴Immune Tolerance Network, Pittsburgh, PA 15238, USA

⁵Drexel University and Coriell Bioinformatics Initiative, School of Biomedical Engineering, Drexel University, Philadelphia, PA 19104, USA

⁶School of Human and Consumer Sciences, Ohio University, Athens, OH 45701, USA

⁷Rheogene, Norristown, PA 19403, USA

author email corresponding author email

Comparative Hepatology 2007, 6:4doi:10.1186/1476-5926-6-4


Published:	1 May 2007

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.

Conclusion

The corresponding increase in CIDE-A expression with hyperinsulinemia and liver steatosis suggests a novel pathway for lipid accumulation in the liver.