High fat diet induced downregulation of microRNA-467b increased lipoprotein lipase in hepatic steatosis
► MicroRNA-467b (miR-467b) is downregulated in high fat diet induced hepatic steatosis. ► Lipoprotein lipase is a direct target of miR-467b. ► MiR-467b – lipoprotein lipase pathway is involved in the insulin resistance of hepatocytes. Non-alcoholic fatty liver disease (NAFLD) is characterized by hep...
Saved in:
Published in | Biochemical and biophysical research communications Vol. 414; no. 4; pp. 664 - 669 |
---|---|
Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
04.11.2011
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | ► MicroRNA-467b (miR-467b) is downregulated in high fat diet induced hepatic steatosis. ► Lipoprotein lipase is a direct target of miR-467b. ► MiR-467b – lipoprotein lipase pathway is involved in the insulin resistance of hepatocytes.
Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic fat accumulation and is presently the most common chronic liver disease. However, the mechanisms underlying the development of steatosis remain unclear. MicroRNAs (miRNAs) are small non-coding RNAs that modulate a variety of biological functions. We have investigated the role of miRNA in the development of steatosis. We found that miR-467b expression is significantly downregulated in liver tissues of high-fat diet fed mice and in steatosis-induced hepatocytes. The downregulation of miR-467b resulted in the upregulation of hepatic lipoprotein lipase (LPL), the direct target of miR-467b. Moreover, the interaction between miR-467b and LPL was associated with insulin resistance, a major cause of NAFLD. These results suggest that downregulation of miR-467b is involved in the development of hepatic steatosis by modulating the expression of its target, LPL. |
---|---|
Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2011.09.120 |