Instances of
obesity and related metabolic abnormalities are increasing across the world.
Non-alcoholic fatty liver disease (
NAFLD) is a common disorder in obese people and is becoming the leading cause of
hepatocellular carcinoma. Recently, long non-coding RNAs (lncRNAs) have been proven to play remarkable roles in numerous biological processes and human diseases, including
NAFLD. However, the function of
lncRNA in
NAFLD pathogenesis remains largely unknown. The aim of this study was to explore the
lncRNA expression profile in
NAFLD mice and to identify novel lncRNAs involved in the pathogenesis of
NAFLD. We performed microarray analysis to compare the expression profiles of lncRNAs and mRNAs in the liver of diabetic db/db mice with
NAFLD and normal mice. A total of 3360 lncRNAs (2048 up-regulated and 1312 down-regulated) and 2685 mRNAs (1195 up-regulated and 1490 down-regulated) were found to be differentially expressed between the
NAFLD and control groups. Real-time PCR validation of five differentially expressed lncRNAs in the liver samples was consistent with the microarray results. Besides, the up-regulated
lncRNA, AK012226, was also significantly increased in an NCTC1469
NAFLD cellular model. Thus, the up-regulated
lncRNA, AK012226, was chosen for subsequent studies. A co-expression network of AK012226-mRNAs was constructed and bioinformatic analysis of these co-expressed mRNAs indicated that they were enriched in the
PPAR signaling pathway. Furthermore,
Nile red staining and flow cytometry analysis revealed that knockdown of AK012226 by
siRNA significantly reduced the
lipid accumulation in the NCTC1469 cells treated with
free fatty acids. In conclusion, the present study identifies the dysregulated lncRNAs and mRNAs involved in
NAFLD, and in particular, a novel
lncRNA, AK012226, was identified to be associated with
lipid accumulation in
NAFLD.