如你有此疾病,請遵照閣下醫生的完整醫療方案;而是否使用多學科復康方案前,你必須咨詢主診醫生的意見,如果閣下的主診醫生不建議您加入補充劑調理組合,請你不要使用。如果你需要尋求其他醫生作第二咨詢,閣下可聯絡我們線上<無邊界醫生>或你自己城市內的其他專業醫生的再診斷。
糖尿血管病
糖尿病慢性高血糖的後遺症分為微血管併發症和大血管併發症。微血管疾病導致失明、腎功能衰竭和神經病變，糖尿病加速的大血管疾病導致心肌梗死、中風和下肢截肢的風險過高。慢性高血糖與血管損傷之間的聯系已由四個獨立的生化异常建立：多元醇途徑流量新增、晚期糖基化終產物（AGEs）形成新增、蛋白激酶C（PKC）啟動和己糖胺途徑流量新增。這些看似不相關的途徑有一個潜在的共同點：線粒體電子傳遞鏈產生過多的超氧物。線粒體活性氧（ROS）部分抑制糖酵解酶甘油醛-3-磷酸脫氫酶，將新增的底物流量從糖酵解轉移到葡萄糖過度利用途徑。初步的體內實驗證據表明，這一新範式為研究和藥物開發提供了新的基礎。
Diabetic Angiopathy
The sequelae of chronic hyperglycemia in diabetes of all phenotypes aredivided into microvascular and macrovascular complications. Microvascular disease causes blindness, renal failure, and neuropathy, and diabetes-accelerated macrovascular disease causes excessive risk for myocardial infarction, stroke, and lower limb amputation. The link between chronic hyperglycemia and vascular damage has been established by four independent biochemical abnormalities: increased polyol pathway flux, increased formation of advanced glycation end-products (AGEs), activation of protein kinase C (PKC), and increased hexosamine pathway flux. These seemingly unrelated pathways have an underlying common denominator: overproduction of superoxide by the mitochondrial electron transport chain. Mitochondrial reactive oxygen species (ROS) partially inhibit the glycolytic enzymes glyceraldehyde-3-phosphate dehydrogenase, which diverts increased substrate flux from glycolysis to pathways of glucose overutilization. Preliminary experimental evidence in vivo suggests that this new paradigm provides a novel basis for research and drug development.
If you have this disease, please follow your doctor's complete medical plan. You must consult the attending doctor before using the multidisciplinary rehabilitation plan. If your attending doctor does not recommend you to join the supplement conditioning combination, please do not use it. If you need to seek second opinion from other doctors, you can contact our online "Doctors Without Borders", or another professional doctor in your own city.