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Submitted on March 24, 2005
Accepted on December 1, 2005
Laboratory for Diabetic Nephropathy, SNP Research Center, The Institute of Physical and Chemical Research, Kanagawa, Japan; Department of Medicine, Metabolism & Endocrinology, School of Medicine, Juntendo University, Tokyo, Japan
* To whom correspondence should be addressed. E-mail: smaeda{at}src.riken.jp.
We have identified Kruppel-like factor 7 (KLF7) as a new candidate for conferring susceptibility to type 2 diabetes. To ascertain the possible involvement of KLF7 in the pathogenesis of type 2 diabetes, we examined the functional roles of KLF7 in various types of cells. In human adipocytes overexpressing KLF7, the expression of adiponectin and leptin was decreased compared with that in control cells, whereas expression of IL-6 was increased. In the insulin secreting cell line (HIT-T15 cells), the expression and glucose-induced secretion of insulin were significantly suppressed in KLF7 overexpressed cells compared with control cells, accompanied by the reduction in the expression of GLUT2, SUR1, Kir6.2 and PDX1. We also found that the overexpression of KLF7 resulted in the decrease of hexokinase 2 expression in smooth muscle cells, and of GLUT2 expression in the HepG2 cells. These results suggest that KLF7 may contribute to the pathogenesis of type 2 diabetes through an impairment of insulin biosynthesis and secretion in pancreatic beta cells, and a reduction of insulin sensitivity in peripheral tissues. Therefore, we suggest that KLF7 plays an important role in the pathogenesis of type 2 diabetes, and may be a useful target for new drugs to aid in the prevention and treatment of this disease.
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