Background: Diabetes mellitus (DM) is a strong predictor of in-stent restenosis after bare-metal stent (BMS) placement because of exaggerated neointima hyperplasia (NIH). Inhibition of vascular smooth muscle cell (VSMC) proliferation by paclitaxel-eluting stent (PES) has resulted in the amelioration of restenosis after BMS placement in patients with DM. We examined the effects of PES in Otsuka long-Evans Tokushima Fatty (OLETF) rat, which was discovered as an excellent animal model for human Type II DM. Methods: Thirty to thirty six week old OLETF and Long-Evans Tokushima Otsuka (LETO) (control) rats were utilized. Stents (3*13 mm sized in each group) were implanted in the thoracic aorta [1: cobalt-chromium stent (CC), 2: paclitaxel-eluting CC stent (PEC)] in a random fashion at 16 atm. Four weeks after stenting, the rats were sacrified and thoracic aorta were harvested for histologic analysis and scanning electron microscopy (SEM). Results: Average glucose level was 229짹4.2 mg/dl in LETO rats and 302짹33.7 mg/dl in OLETF rats. Body weight was 515짹21 g in LETO rats and 595짹17g in OLETF rats (p=NS) (n=6 in each group). After stenting, stent minimal luminal diameter was similar among the groups. NIH area with H&E in stent site was 242.6 關m2 for OLETF-1, 60.0짹2.5 關m2 for OLETF-2, and 36.5짹1.5 關m2 for LETO-2. Histologic area stenosis was 15.4 % for OLETF-1, 3.3짹1.4 % for OLETF-2, and 2.1짹0.03 % for LETO-2. All PEC in LETO and OLETF rats induced thrombus in stent site. In SEM analysis, stent covering area was over 80 % in OLETF-1 and less than 50% in OLETF-2. In immunohistochemisty analysis, increased expression of plasminogen activator inhibitor (PAI)-1 from NIH in OLETF-F1 was attenuated in OLETF-2. Conlusion: PEC significantly inhibited the NIH compared with that of CC and decreased expression of PAI-1 from NIH in type II DM rat model. However, increased thrombus and delayed re-endothelialization in stent site was observed. More specific effects of PEC will be soon elucidated.