Both insulin resistance and chronic hyperglycaemia contribute to impaired cardiac contractility and structure via reduced Ca2+ influx through L‐type Ca2+ channels, impaired PI3K/Akt pathway, accumulated reactive oxygen species (ROS), increased advanced glycation end products (AGEs) formation, increased lipotoxicity, and multiple potential mechanisms such as autophagy, chronic inflammation, and epigenetic mechanisms [10]. This evidence concerns the gene AKT1 and Hyperglycemia.