Role of Peroxisome Proliferator-Activated Receptor-γ in the Glucose-Sensing Apparatus of Liver and β-Cells
- 1Department of Biochemistry and Molecular Biology, Center for Chronic Metabolic Disease Research, Yonsei University College of Medicine, Seoul, Korea
- 2Brain Korea 21 Project for Medical Sciences, Yonsei University College of Medicine, Seoul, Korea
- Address correspondence and reprint requests to Yong-ho Ahn, Department of Biochemistry and Molecular Biology, Center for Chronic Metabolic Disease Research, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemoon-gu, Seoul 120-752, Korea. E-mail: yha111{at}yumc.yonsei.ac.kr
Abstract
Type 2 diabetes develops in the context of both insulin resistance and β-cell failure. Thiazolidinediones are a class of antidiabetic agents that are known to improve insulin sensitivity in various animal models of diabetes. The improved insulin sensitivity may be achieved either by systemic insulin sensitization or by direct action of peroxisome proliferator-activated receptor (PPAR)-γ on the transcription of genes involved in glucose disposal. Evidence supporting the direct action of PPAR-γ on glucose metabolism is observed in the genes involved in insulin-stimulated glucose disposal. We already showed that GLUT2 and β-glucokinase were directly activated by PPAR-γ. Recently, we have identified and characterized the functional PPAR response element in the GLUT2 and liver type glucokinase (LGK) promoter of the liver. It is well known that adipose tissue plays a crucial role in antidiabetic action of PPAR-γ. In addition, PPAR-γ can directly affect liver and pancreatic β-cells to improve glucose homeostasis.
- GK, glucokinase
- GSIS, glucose-stimulated insulin secretion
- LGK, liver type glucokinase
- PPAR, peroxisome proliferator-activated receptor
- PPRE, PPAR response element
- TZD, thiazolidinedione
Footnotes
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This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Les Laboratoires Servier.
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- Accepted June 2, 2003.
- Received March 17, 2003.
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