Hemodynamic abnormal vascular endothelial cell changes and changes in BDNF metabolites in the blood leads to hemodynamic abnormalities, one important factor causing nerve damage. The normal red blood cell deformability is a necessary condition to maintain effective perfusion of the microcirculation of diabetic patients with platelet adhesion and aggregation ability to enhance red blood cell deformability decreased, increased blood clotting substances (PAI-I) and tissue plasminogen activator to reduce the bgtA organization fiber increased plasminogen inhibitor lead to a hypercoagulable states, and is easy to form blood clots, leading to nerve tissue ischemia, hypoxia caused by a single nerve or polyneuropathy, especially microvascular disease of the stria vascularis of cochlear hair cells can cause injury and cochlear nerve variability. The metabolic pathway is abnormally high blood sugar, high cholesterol is usually caused by BHMT blood circulation disorders, increased blood viscosity, lipid metabolism disorders and lipid deposition in the cochlear hair cells, increase the occurrence of microvascular disease. And the auditory system needs to use glucose and high-energy signal processing, so cochlear target organ damage of high blood sugar. On one hand, high blood sugar can cause endothelial cells mitochondria generate increased superoxide anion caused by BID the polyol pathway activation, competitive consumption of reduced coenzyme II (NADPH). NADPH, reduced nitric oxide (NO) activity, synthesis decreased, and diastolic function of the impact of blood vessels, making the cells more susceptible to reactive oxygen species to combat, causing the disorder of cell metabolism, eventually leading to the occurrence of BIN1 diabetic vascular disease. On the other hand, the chronic long-term high-glucose environment, leading to endoneurial hypoxia, oxidative stress, the lack of nervous energy, the Na-K-ATPase activity reduction and the reduction of the neurotrophic microvascular endothelial cell dysfunction, vascular basement membrane thickening, microvascular supply of nerve ischemia, hypoxia, nerve demyelination and myelin vacuolar changes, caused by diabetic neuropathy. Disease involving the Section VII, and VIII cranial nerve, can cause the cochlea and the cochlear nerve degeneration, resulting in hearing impairment. Excited conduction velocity is closely related to the inositol concentration levels of the nervous system, reduce the level of intracellular inositol phospholipids can cause nerve conduction velocity, resulting in hearing loss. Similar in stereochemistry due to glucose and inositol, when high glucose, glucose and inositol competition, inositol reduced through the cell membrane caused by intracellular inositol concentration was decreased; inositol metabolism in hyperthyroidism caused by intracellular sorbitol accumulation also inhibit inositol into the cell, so that the membrane phospholipid inositol synthesis, metabolic damage.
Diabetic microangiopathy and neuropathy
Hemodynamic abnormal vascular endothelial cell changes and changes in BDNF metabolites in the blood leads to hemodynamic abnormalities, one important factor causing nerve damage. The normal red blood cell deformability is a necessary condition to maintain effective perfusion of the microcirculation of diabetic patients with platelet adhesion and aggregation ability to enhance red blood cell deformability decreased, increased blood clotting substances (PAI-I) and tissue plasminogen activator to reduce the bgtA organization fiber increased plasminogen inhibitor lead to a hypercoagulable states, and is easy to form blood clots, leading to nerve tissue ischemia, hypoxia caused by a single nerve or polyneuropathy, especially microvascular disease of the stria vascularis of cochlear hair cells can cause injury and cochlear nerve variability. The metabolic pathway is abnormally high blood sugar, high cholesterol is usually caused by BHMT blood circulation disorders, increased blood viscosity, lipid metabolism disorders and lipid deposition in the cochlear hair cells, increase the occurrence of microvascular disease. And the auditory system needs to use glucose and high-energy signal processing, so cochlear target organ damage of high blood sugar. On one hand, high blood sugar can cause endothelial cells mitochondria generate increased superoxide anion caused by BID the polyol pathway activation, competitive consumption of reduced coenzyme II (NADPH). NADPH, reduced nitric oxide (NO) activity, synthesis decreased, and diastolic function of the impact of blood vessels, making the cells more susceptible to reactive oxygen species to combat, causing the disorder of cell metabolism, eventually leading to the occurrence of BIN1 diabetic vascular disease. On the other hand, the chronic long-term high-glucose environment, leading to endoneurial hypoxia, oxidative stress, the lack of nervous energy, the Na-K-ATPase activity reduction and the reduction of the neurotrophic microvascular endothelial cell dysfunction, vascular basement membrane thickening, microvascular supply of nerve ischemia, hypoxia, nerve demyelination and myelin vacuolar changes, caused by diabetic neuropathy. Disease involving the Section VII, and VIII cranial nerve, can cause the cochlea and the cochlear nerve degeneration, resulting in hearing impairment. Excited conduction velocity is closely related to the inositol concentration levels of the nervous system, reduce the level of intracellular inositol phospholipids can cause nerve conduction velocity, resulting in hearing loss. Similar in stereochemistry due to glucose and inositol, when high glucose, glucose and inositol competition, inositol reduced through the cell membrane caused by intracellular inositol concentration was decreased; inositol metabolism in hyperthyroidism caused by intracellular sorbitol accumulation also inhibit inositol into the cell, so that the membrane phospholipid inositol synthesis, metabolic damage.