What are the causes of macroangiopathy due to diabetes mellitus Diabetic macroangiopathy mainly refers to atherosclerosis. The absolute or relative insufficiency of insulin secretion and the reduced sensitivity of target cells to insulin in diabetic patients cause disorders of sugar, protein and fat metabolism, resulting in a coordinated imbalance of hormones such as insulin, sex hormones, catecholamines and hyperglycemia within the body, and excessive blood, vascular endothelial dysfunction and abnormal platelet function can all lead to the development of atherosclerosis. For example, hypoglycemia can reduce lipids, lower lysosomal lipase activity in the vascular wall and accelerate the development of atherosclerosis; changes in hyperglycemia and disorders of fat metabolism also cause changes in hemodynamics, resulting in increased blood viscosity and hypercoagulability, poor microcirculatory blood flow, reduced cellular energy gain and hypoxia, which directly or indirectly cause endothelial cell damage and thus the development of atherosclerosis. Atherosclerosis can occur as a direct or indirect result of endothelial cell damage. After the formation of atherosclerosis, the plaque narrows the diameter of the originally open blood vessels, resulting in ischemia of the distal (foot) tissue and contributing to the development of diabetic foot. What are the causes of diabetic microangiopathy Diabetic microangiopathy is the pathological basis for organ complications and is often the direct cause of diabetic gangrene. In diabetic patients, under the effect of continuous hyperglycemia, the synthesis of glycated hemoglobin in the body is accelerated and deposited on the microvascular wall, as well as the damage to vascular endothelial cells by immune complexes, etc., resulting in increased microvascular permeability, thickened basement membrane, and abnormal proliferation of endothelial cells, leading to a reduction in microvascular diameter, rough inner membrane, increased body fluid permeability, and reduced vascular elasticity and contractility, which results in poor blood flow and increased blood viscosity. This leads to erythrocyte aggregation, platelet adhesion, especially at the endothelial injury, and finally microthrombosis and/or microvascular occlusion, which is called “thrombotic microangiopathy”. As a result of microvascular thrombosis, local tissue ischemia, hypoxia, and metabolite accumulation, diabetic gangrene occurs due to the combination of peripheral nerve dysfunction and infection. What are the causes of diabetic neuropathy The nerve nutrition relies on the trophoblastic vessels that run parallel to it, which also belong to the microvasculature. Diabetic microangiopathy makes the microvasculature that nourishes the nerves narrow and occlude, and the nerves become malnourished. Together with the long-term hyperglycemia, the metabolic dysregulation of the nerve cell membrane undergoes degenerative necrosis, which is the diabetic peripheral neuropathy. The incidence of diabetic peripheral neuropathy is as high as 60-90%, especially for those with disease duration of 10 years or more, almost all of them have damage to sensory, motor and autonomic nerves. The more the blood supply to the distal limb is poor, the heavier the nerve damage is. Once it occurs, its sensation and movement will be impaired, and its defense function against external damage will be reduced, which will easily lead to foot trauma, which is also an important factor in the occurrence of diabetic foot.