DM aggravates left ventricular (LV) remodeling and failing after MI. We hypothesized that DM-related imbalance between TGFb and Bone Morphogenetic Protein (BMP) is a crucial factor in LV remodeling. We induced MI in control (n=19) and streptozotocin-induced DM (n=27) mice. Peri-operative mortality was 10% in control and 40% in DM mice. At 4 weeks after MI, echocardiography showed a 50% increase in LV diameter and significantly decreased fractional shortening (FS) in both control and DM mice. However, the reduction in FS after MI tended to be larger in DM mice (DM n=8, 33±8% versus control n=10, 24±11%, mean±SD, p=0.057). WB-analysis of pSmads revealed increased TGFb and BMP signaling after MI. However, the ratio of TGFb/BMP signaling remained constant and no differences were observed between control and DM mice. Thus, in contrast to previous studies in more severe DM models, we observed no clear aggravation of structural and functional deterioration of the heart in mild DM, as compared to control mice. We suggest that mild DM is insufficient for induction of TGFb/BMP signaling imbalance, adverse remodeling, and early decompensation after experimental MI. Supported by DFN-grant 2003-11-022