A Journey to Understand Glucose Homeostasis: Starting from Rat Glucose Transporter Type 2 Promoter Cloning to Hyperglycemia
Diabetes & Metabolism Journal
;
: 465-471, 2018.
Article
in English
| WPRIM
| ID: wpr-719116
ABSTRACT
My professional journey to understand the glucose homeostasis began in the 1990s, starting from cloning of the promoter region of glucose transporter type 2 (GLUT2) gene that led us to establish research foundation of my group. When I was a graduate student, I simply thought that hyperglycemia, a typical clinical manifestation of type 2 diabetes mellitus (T2DM), could be caused by a defect in the glucose transport system in the body. Thus, if a molecular mechanism controlling glucose transport system could be understood, treatment of T2DM could be possible. In the early 70s, hyperglycemia was thought to develop primarily due to a defect in the muscle and adipose tissue; thus, muscle/adipose tissue type glucose transporter (GLUT4) became a major research interest in the diabetology. However, glucose utilization occurs not only in muscle/adipose tissue but also in liver and brain. Thus, I was interested in the hepatic glucose transport system, where glucose storage and release are the most actively occurring.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Transcription Factors
/
Brain
/
Adipose Tissue
/
Promoter Regions, Genetic
/
Clone Cells
/
Cloning, Organism
/
Diabetes Mellitus, Type 2
/
Glucose Transport Proteins, Facilitative
/
Glucose Transporter Type 2
/
Adipogenesis
Limits:
Animals
/
Humans
Language:
English
Journal:
Diabetes & Metabolism Journal
Year:
2018
Type:
Article
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