Transcriptional Regulation of Glucose Sensors in Pancreatic β-Cells and Liver: An Update

被引：38

作者：

Bae, Jin-Sik ^{[1
,2
]}

Kim, Tae-Hyun ^{[1
,2
,3
]}

Kim, Mi-Young ^{[1
,2
]}

Park, Joo-Man ^{[1
,2
,3
]}

Ahn, Yong-Ho ^{[1
,2
,3
]}

机构：

[1] Yonsei Univ, Coll Med, Dept Biochem & Mol Biol, Seoul 120752, South Korea

[2] Yonsei Univ, Coll Med, Ctr Chron Metab Dis Res, Seoul 120752, South Korea

[3] Yonsei Univ, Coll Med, Brain Korea Project Med Sci 21, Seoul 120752, South Korea

来源：

SENSORS | 2010年 / 10卷 / 05期

关键词：

glucose sensor; solute carrier family 2 (SLC2A2); glucokinase (GCK); transcription; liver; pancreatic beta-cell; GLUCOKINASE GENE-EXPRESSION; ELEMENT-BINDING PROTEIN-1C; ACTIVATED-RECEPTOR-GAMMA; NUCLEAR FACTOR 3-BETA; SMALL HETERODIMER PARTNER; INDUCED INSULIN-SECRETION; PEROXISOME PROLIFERATOR; GLUT2; GENE; TRANSPORTER GENE; FASTING GLUCOSE;

D O I：

10.3390/s100505031

中图分类号：

O65 [分析化学];

学科分类号：

070302 ; 081704 ;

摘要：

Pancreatic beta-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 beta-cells or hepatocytes where it is metabolized. In the beta-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 and beta-cells.

引用

页码：5031 / 5053

页数：23

共 131 条

[1] β-cell-specific inactivation of the mouse Ipf1/Pdx1 gene results in loss of the β-cell phenotype and maturity onset diabetes [J].