In our obese animal model, cardiac hypertrophy is present in spite of miR-499 being down regulated, showing that miR-208a/miR-499 pathway is not the driving force to generate the increase of heart mass and leaving open this possibility to other signal pathways like IGF-1, TGF-β or inflammatory cytokines related to diabetic cardiomyopathy (Table 1)48,49. This evidence concerns the gene TGFB1 and diabetic cardiomyopathy.