Simply put, diabetes is caused by insulin deficiency. Such as sudden weight gain, the body's original insulin secretion is not enough to deal with the huge body fat and sugar metabolism, sugar metabolism disorders, blood glucose concentration rises, the amount of sugar excreted in the urine increases, causing diabetes. Diabetes mellitus is categorized into type 1 and type 2. The medical causes and mechanisms are as follows:

Type 1 diabetes

Type 1 diabetes is caused by immune-mediated selective destruction of pancreatic islet B cells. Lymphokines and free radicals also recruit CIM4 T-lymphocytes to the site of damage and activate them. Macrophages also present viral antigens or self-antigens of damaged B cells to CD4 lymphocytes, and activated CD4 cells further activate B lymphocytes to produce antiviral antibodies and anti-B-cell auto-antibodies, which contribute to the destruction of B cells.

Type 2 diabetes mellitus

Numerous studies have shown that free radicals are generated in large quantities in the human body under the stimulation of high blood glucose and high free fatty acid (FFA) levels, which in turn initiates oxidative stress. Activation of the oxidative stress signaling pathway leads to insulin resistance (IR), impaired insulin secretion, and diabetic vasculopathy. Thus, oxidative stress is not only involved in the pathogenesis of type 2 diabetes, but also constitutes the pathogenesis of late diabetic complications. Oxidative stress and diabetes are mutually reinforcing, forming a circle that is difficult to break.

Insulin resistance can precede the onset of diabetes, and under its effect, compensatory insulin secretion increases early in the disease to maintain normal glucose tolerance. When insulin resistance increases, compensatory insulin secretion decreases, or both*** occur together, the disease gradually progresses to hypoglycemia and diabetes, and blood glucose begins to rise. The combination of high blood glucose and high FFA*** leads to high ROS production and oxidative stress, as well as activation of stress-sensitive signaling pathways, which in turn exacerbates insulin resistance, and clinically manifests itself in the continued progression and worsening of diabetes. In vitro studies have shown that ROS and oxidative stress can cause a cascade of activation of multiple serine kinases. Recent trials of antioxidants to improve glycemic control have also confirmed that ROS and oxidative stress cause insulin resistance.

Oxidative stress is central to the pathogenesis of diabetes

β-cells are also an important target of oxidative stress, and β-cells are sensitive to ROS because of their low levels of antioxidant enzymes. β-cells are directly damaged by ROS, which promote apoptosis of β-cells, and indirectly inhibit the function of β-cells by affecting insulin signaling pathways. β-cells are damaged, and the secretion of insulin is lowered, and peak secretion is delayed, and glucose fluctuations are increased, When β-cells are damaged, the level of insulin secretion decreases, the peak of secretion is delayed, and the fluctuation of blood glucose is intensified, which makes it difficult to control the rapid rise of postprandial blood glucose, and causes more significant damage to the cells.