Most diabetic patients do not know the danger of hyperglycemia, they think it is just a matter of urinating more, they can eat and sleep, so they belittle the timely treatment, and many of them only consider going to hospital for treatment when they have complications or see other diabetic patients have complications, which is already too late at this time. Forgive me for not knowing that high blood sugar has already caused greater harm to the blood vessels, even if the blood sugar is well controlled afterwards, still prone to vascular complications, this is the so-called “metabolic memory effect”. Conversely, if intensive glucose-lowering therapy is administered early, the benefits to the diabetic patient can still be seen several years after intensive glucose-lowering therapy is stopped. In patients with type 2 diabetes, the residual islet β-cell function is about 50%. Persistent hyperglycemia can further aggravate the damage to β-cells, and as the disease progresses, β-cell function declines at a rate of 4.5% per year, and the progression of destructive β-cell function determines the natural course of type 2 diabetes. Evidence suggests that islet β-cell function is partially reversible at the time of initial diagnosis and that intensive insulin therapy can reverse and repair β-cell function. The earlier the insulin therapy can better protect the β-cells and reduce their gradual decompensation from exposure to hyperglycemia, which not only gives the patient good glycemic control, but also interrupts the metabolic memory imprint of the patient’s β-cells, thus facilitating the patient’s endpoint prognosis. Intensive treatment at the beginning of the disease can significantly intervene throughout the disease, making subsequent glycemic control easier, and even some can enter the honeymoon phase and stop insulin, thus improving the prognosis. A Swedish study comparing insulin therapy and gliphenylurea therapy in the early stage of diabetes showed that insulin therapy group not only had better glycemic control than gliphenylurea group, but also had good protection of pancreatic β-cell function, which may suggest that stimulation of endogenous insulin secretion is not as beneficial as exogenous insulin therapy. The development of late β-cell function decline to loss of function is irreversible, mainly related to β-cell depletion, islet amyloid deposition and increased β-cell apoptosis, in which glucotoxicity and lipotoxicity caused by chronic hyperglycemia and dyslipidemia play a major role. Currently, it is advocated that patients with fasting blood glucose over 13.0 mmol/L should be treated with intensive insulin therapy, which can be considered as subcutaneous premixed insulin, or 3 short and 1 long regimen, or insulin pump if available.