Transcriptional Regulation of Glucose Sensors in Pancreatic β-Cells and Liver An Update 英文参考文献.docVIP

Sensors 2010, 10, 5031-5053; doi:10.3390/s100505031 OPEN ACCESS sensors ISSN 1424-8220 /journal/sensors Review Transcriptional Regulation of Glucose Sensors in Pancreatic β-Cells and Liver: An Update Jin-Sik Bae 1,2, Tae-Hyun Kim 1,2,3, Mi-Young Kim 1,2, Joo-Man Park 1,2,3 and Yong-Ho Ahn 1,2,3, * 1 Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, Seoul 120-752, Korea; E-Mails: baejinsik@yuhs.ac (J.-S.B.); taehyun@yuhs.ac (T.-H.K.); theresakim@yuhs.ac (M.-Y.K.); jjumans@yuhs.ac (J.-M.P.) 2 Center for Chronic Metabolic Disease Research, Yonsei University College of Medicine, Seoul, Korea 3 Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Korea * Author to whom correspondence should be addressed; E-Mail: yha111@yuhs.ac; Tel.: +82-2-2228-1674; Fax: +82-2-312-5041. Received: 1 February 2010; in revised form: 7 May 2010 / Accepted: 13 May 2010 / Published: 19 May 2010 Abstract: Pancreatic β-cells and the liver play a key role in glucose homeostasis. After a meal or in a state of hyperglycemia, glucose is transported into the β-cells or hepatocytes where it is metabolized. In the β-cells, glucose is metabolized to increase the ATP:ADP ratio, resulting in the secretion of insulin stored in the vesicle. In the hepatocytes, glucose is metabolized to CO2, fatty acids or stored as glycogen. In these cells, solute carrier family 2 (SLC2A2) and glucokinase play a key role in sensing and uptaking glucose. Dysfunction of these proteins results in the hyperglycemia which is one of the characteristics of type 2 diabetes mellitus (T2DM). Thus, studies on the molecular mechanisms of their transcriptional regulations are important in understanding pathogenesis and combating T2DM. In this paper, we will review a recent update on the progress of gene regulation of glucose sensors in the liver a