Background: Imparired isulin mediated glucose trans- port at fat and muscle is a major feature of insulin resistandce in NIDDR. One kind of facilitative glucose transporter protein, the so ealled inmdin responsive facilitative glucose transporter (GLUT4) is a important candidate gene for NIDDM. Although many study already done that decreased GLUT4 gene expression fat tissue in insulin resistance NIDDM or abesity. But, there is possible genetic defect in the codirig regions of GLUT4 gene cou1d contribute to impaired expression or function of GLUT4 molecule in patients with NJDDM. The purpose of this study was to analysis of GLUT4 gene in Korean NIDDM patients. Method: We purified genomic DNA of peripberal leukocyte for 50 patients of Korean NIDDM patients. The technique af SSCP-PCR was used for screening the variation of GLUT4 gene. Direct sequencing was done after detected variable mobility shifting band on non- denaturing polyacrylamide gel. 11 pairs of primer whieh include the all coding region of GLUT4 gene, Result. Although this result has not amino acid substitution due to mutated nucleotides. We get a one polymorphism (Asm 130) which sequence were AAC to AAC/T, heterozygote allele in 40% of NIDDM patienta We tried more 80 NIDDM patients genomic DNA for detect the variation of exon 9 lle 383, but we could not find any variatioo for SSCP-PCR analysis. Conelusion: Hhe finding of this study suggest that coding region of GLUT4 gene is normal in most patients with NIDDM. The defect in insulin regulated glucose transporter, this is characteristic of this disease is like to be secondary to inherited defect in molecules important mediating insulin stimulation of glucose transport acquire abnormalities of glucose transporter function. Noninsulin dependent diabetes mellitus,