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A Journey to Understand Glucose Homeostasis: Starting from Rat Glucose Transporter Type 2 Promoter Cloning to Hyperglycemia
Yong Ho Ahn
Diabetes Metab J. 2018;42(6):465-471.   Published online November 2, 2018
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  • 51 Download
  • 7 Web of Science
  • 6 Crossref
AbstractAbstract PDFPubReader   

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.


Citations to this article as recorded by  
  • Physiological functions of glucose transporter-2: From cell physiology to links with diabetes mellitus
    Zhean Shen, Yingze Hou, Guo Zhao, Libi Tan, Jili Chen, Ziqi Dong, Chunxiao Ni, Longying Pei
    Heliyon.2024; 10(3): e25459.     CrossRef
  • Missense mutation of ISL1 (E283D) is associated with the development of type 2 diabetes
    Juan Zhang, Rong Zhang, Chanwei Liu, Xiaoxu Ge, Ying Wang, Fusong Jiang, Langen Zhuang, Tiantian Li, Qihan Zhu, Yanyan Jiang, Yating Chen, Ming Lu, Yanzhong Wang, Meisheng Jiang, Yanjun Liu, Limei Liu
    Diabetologia.2024;[Epub]     CrossRef
  • Estimation and implications of the genetic architecture of fasting and non-fasting blood glucose
    Zhen Qiao, Julia Sidorenko, Joana A. Revez, Angli Xue, Xueling Lu, Katri Pärna, Harold Snieder, Peter M. Visscher, Naomi R. Wray, Loic Yengo
    Nature Communications.2023;[Epub]     CrossRef
  • Umbilical Cord-Mesenchymal Stem Cell-Conditioned Medium Improves Insulin Resistance in C2C12 Cell
    Kyung-Soo Kim, Yeon Kyung Choi, Mi Jin Kim, Jung Wook Hwang, Kyunghoon Min, Sang Youn Jung, Soo-Kyung Kim, Yong-Soo Choi, Yong-Wook Cho
    Diabetes & Metabolism Journal.2021; 45(2): 260.     CrossRef
  • Aging-related modifications to G protein-coupled receptor signaling diversity
    Jaana van Gastel, Hanne Leysen, Jan Boddaert, Laura vangenechten, Louis M. Luttrell, Bronwen Martin, Stuart Maudsley
    Pharmacology & Therapeutics.2021; 223: 107793.     CrossRef
  • Glucose transporters in the small intestine in health and disease
    Hermann Koepsell
    Pflügers Archiv - European Journal of Physiology.2020; 472(9): 1207.     CrossRef
Original Article
Development of Proinsulin-secreting Non-endocrine Cell.
Do Jun Yoon, Seok Hyun Kim, Jae Woo Kim, Yu Kyong Kim, Young Duk Song, Yong Ho Ahn
Korean Diabetes J. 1998;22(4):467-474.   Published online January 1, 2001
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  • 16 Download
AbstractAbstract PDF
Recently, the advent of genetic engineering technics enabled. us to transfer foreign genes of interests into various cells and establish an "artificial b-cells" capable of secreting insulin in response to plasma glucose level. In this study, we have designed a study to establish an "artificial b-cells" by transfecting liver/pancreatic b-cell type glucose transporter 2(GLUT2) cDNA and genomic DNA of proinsulin into non-endocrine cell. Because GLUT2 molecules on the plasma membranes act as a sensor of glucose outside the cell and promote the secretion of proinsulin from the cells, cotransfection of GLUT2 cDNA along with insulin gene will translate the GLUT2 molecules necessary for glucose transport into the cells and hence leading to insulin secretion. METHODS: We have subcloned GLUT2 cDNA and proinsulin gene into separate eukaryotic expression vectors and transfected them to Chinese hamster ovary cells. The stable cell lines harboring GLUT2 cDNA and proinsulin gene were selected by G418, neomycin analogue. The surviving clones were harvested and subjected to Southem blot analysis by digesting the chromosomal DNA either with BamHI for insulin gene detection or Xho I/Sma I double digestion for GLUT2 gene detection. The amount of proinsulin secretion into the medium was measured by the insulin radioimmunoassay(DPC, Coat-A-Count insulin, LA, USA) which detected proinsulin with 40% cross-reactivity. RESULTS: 1) We were able to find out 3 clones positive for both GLUT2 gene and insulin gene. 2) Of these clones, clone 5 cells secreted proinsulin 3 times as much as that of the control CHO cells. CONCLUSION: There was some increase of proinsulin secretion in artificial g-cells compared to control cells. But this increased proinsulin secretion was not enough to be used as therapeutics. We need more expriments to find out more efficient way of proinsulin secretion and to identify the glucose-regulated insulin secretion in these artificial b-cells.

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