title: MicroRNA dysregulation in liver and pancreas of CMP-Neu5Ac hydroxylase null mice disrupts insulin/PI3K-AKT signaling.
abstract: 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.
authors.affiliation: Department of Animal Biotechnology, Konkuk University, Hwayang-dong, Kwangjin-gu, Seoul 143-701, Republic of Korea.
authors.forename: Deug-Nam
authors.initials: DN
authors.lastname: Kwon
authors.affiliation: Department of Cosmetology, Hanseo University, Seosan, Chungnam 356-706, Republic of Korea.
authors.forename: Byung-Soo
authors.initials: BS
authors.lastname: Chang
authors.affiliation: Department of Animal Biotechnology, Konkuk University, Hwayang-dong, Kwangjin-gu, Seoul 143-701, Republic of Korea.
authors.forename: Jin-Hoi
authors.initials: JH
authors.lastname: Kim
mesh_terms: D000818:Animals; D003198:Computer Simulation; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D007328:Insulin / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008810:Mice, Inbred C57BL; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D006899:Mixed Function Oxygenases / Q000172:deficiency* / Q000378:metabolism; D010179:Pancreas / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015203:Reproducibility of Results; D015398:Signal Transduction / Q000235:genetics; D014158:Transcription, Genetic
chemical_list: D007328:Insulin; D035683:MicroRNAs; D006899:Mixed Function Oxygenases; C074383:CMPacetylneuraminate monooxygenase; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt