MicroRNA Dysregulation in Liver and Pancreas of CMP-Neu5Ac Hydroxylase Null Mice Disrupts InsulinPI3K-AKT Signaling

الملخص EN

CMP-Neu5Ac hydroxylase (Cmah)-null mice fed with a high-fat diet develop fasting hyperglycemia, glucose intolerance, and pancreatic β-cell dysfunction and ultimately develop characteristics of type 2 diabetes.

The precise metabolic role of the Cmah gene remains poorly understood.

This study was designed to investigate the molecular mechanisms through which microRNAs (miRNAs) regulate type 2 diabetes.

Expression profiles of miRNAs in Cmah-null mouse livers were compared to those of control mouse livers.

Liver miFinder miRNA PCR arrays (n=6) showed that eight miRNA genes were differentially expressed between the two groups.

Compared with controls, seven miRNAs were upregulated and one miRNA was downregulated in Cmah-null mice.

Specifically, miR-155-5p, miR-425-5p, miR-15a-5p, miR-503-5p, miR-16-5p, miR-29a-3p, and miR-29b-3p were significantly upregulated in the liver and pancreas of Cmah-null mice.

These target miRNAs are closely associated with dysregulation of insulin/PI3K-AKT signaling, suggesting that the Cmah-null mice could be a useful model for studying diabetes.