These cardiorenal protective effects may be attributed largely to the prevention of db/db mice from the development of diabetic phenotypes such as hyperglycaemia, hyperlipidaemia, hypertension, glucose intolerance, insulin resistance and obesity in Smad3 KO‐db/db, but not in Smad3+/−db/db and Smad3 WT‐db/db mice as seen in this and other studies.10, 19. This evidence concerns the gene SMAD3 and hypertensive disorder.