Inhibition of fatty acid translocase cluster determinant 36 (CD36), stimulated by hyperglycemia, prevents glucotoxicity in INS-1 cells
- Inhibition of fatty acid translocase cluster determinant 36 (CD36), stimulated by hyperglycemia, prevents glucotoxicity in INS-1 cells
- 원규장; 김용운; 문준성; 서예진; 박소영; 김종연; 윤지성; 이인규[이인규]; 이형우
- PANCREATIC BETA-CELLS; INSULIN-SECRETION; GENE-EXPRESSION; LIPOTOXICITY; FAT/CD36; OBESE; MEN; SENSITIVITY; DYSFUNCTION; PALMITATE
- Issue Date
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.420, no.2, pp.462 - 466
- The purpose of the present study was to determine whether exposure of pancreatic islets to glucotoxic conditions changes fatty acid translocase cluster determinant 36 (CD36) and examine the role of CD36 on the induction of glucotoxicity. We measured the changes of CD36 and insulin secretion in high glucose (30 mM) exposed INS-1 cells and CD36 suppressed INS-1 cells by transfection of CD36 siRNA. The intracellular peroxide level of INS-1 cells increased in the high glucose media compared to normal glucose (5.6 mM) media. The mRNA levels of insulin and PDX-1, as well as glucose stimulated insulin secretion (GSIS) were decreased in INS-1 cells exposed to high glucose media compared to normal glucose media, while CD36 and palmitate uptake were significantly elevated with exposure to high glucose media for 12 h. The inhibition of CD36 reversed the decreased GSIS and intracellular peroxide level in INS-1 cells. These results suggest that high glucose may exacerbate glucotoxicity via increasing fatty acid influx by elevation of CD36 expression, and that CD36 may be a possible target molecule for preventing glucotoxicity in pancreatic beta-cells. (C) 2012 Elsevier Inc. All rights reserved.
- Appears in Collections:
- 의과대학 > 내과학교실 > Articles
의과대학 > 생리학교실 > Articles
- Files in This Item:
There are no files associated with this item.
- RIS (EndNote)
- XLS (Excel)