In 1921, insulin was discovered by Frederick Banting, an orthopaedic surgeon in Ontario, Canada, after he had noticed, during a patient autopsy with no history of glycosuria, that a pancreatic stone had destroyed the enzyme-producing acinar cells of the pancreas but left the islets of Langerhans intact. 1 In 1922, after developing a method to extract the islets without damage from digestive enzymes, he administered the newly identified and purified hormone and successfully treated a 14-year-old boy with type 1 diabetes in ketoacidosis. 1 Subsequently, insulin has largely been known for its critical role in glucose metabolism by acting on peripheral tissues, such as the liver and muscle, to maintain glycaemia by regulating glucose production and disposal. In this way, insulin is crucial for treating many types of diabetes (types 1 and 2, gestational, latent autoimmune diabetes in adults or type 1.5, maturity onset diabetes of the young). 2,3 At the cellular level, insulin mediates its actions via the insulin receptor (IR) in which binding results in receptor autophosphorylation and phosphorylation of IR substrate (IRS). Activation of IRS triggers the phosphoinositide 3-kinase (PI3K)-Akt pathway and facilitates many metabolic functions, including glucose transport via glucose transporter type 4 (GLUT4), glycogen and lipid synthesis, and the mitogen-activated protein kinase pathway, involved in gene transcription and cell proliferation. 4,5 Insulin is well known as a metabolic hormone for its control of blood glucose, by regulating peripheral glucose transport in muscle and adipose tissue, suppressing gluconeogenesis and adipose tissue lipolysis. 6,7 A lack of IRs in skeletal muscle (MIRKO mouse model) results in symptoms of metabolic syndrome, including increased fat mass, triglycerides and free