In summary, despite LNA-antimiR-34a preventing a diabetes-induced increase in miR-34a in the mouse heart, inhibition of miR-34a was unable to improve diastolic function in a setting of established diastolic dysfunction, and only had a modest effect on attenuating diabetes-induced cardiac enlargement, cardiac fibrosis and elevation of ventricular BNP. This evidence concerns the gene NPPB and diabetes mellitus.