The Role of Inflammatory Cytokines in Diabetes and Its Complications
The Role of Inflammatory Cytokines in Diabetes and Its Complications
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DOI：
10.1902/jop.2008.080246
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发表时间：
2008-08-01
影响因子：
4.3
通讯作者：
King, George L.
中科院分区：
文献类型：
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作者：
King, George L.
随着肥胖症的增加，全世界糖尿病的患病率正在迅速增加。并发症是糖尿病患者的主要恐惧。糖尿病并发症影响许多组织和器官，引起视网膜病变、肾病、神经病变、心血管疾病、外周血管疾病、中风和牙周病变。免疫异常与1型和2型糖尿病及糖尿病并发症有关。T细胞异常被认为是1型糖尿病中自身免疫性疾病的主要原因，导致胰岛的破坏。在2型糖尿病中，炎症和单核细胞的活化被认为对于增强胰岛素抵抗是重要的，并且可能导致胰岛细胞胰岛素分泌功能的丧失。许多因素可以增强胰岛素抵抗，包括遗传、久坐不动的生活方式、肥胖和其他疾病，如慢性炎症或感染。炎症增加，如单核细胞活化和炎症标志物水平增加，C-反应蛋白、纤溶酶原激活物抑制剂-1和其他细胞因子在无糖尿病的胰岛素抵抗状态中有报道。一种可能的机制是代谢物的异常水平，例如来自脂肪组织的脂质、脂肪酸和各种细胞因子，激活单核细胞并增加炎性细胞因子的分泌，从而增强胰岛素抵抗。根据这一模型，肥胖激活单核细胞，增强胰岛素抵抗，增加2型糖尿病的风险。先天免疫功能低下也可能参与糖尿病并发症的发生。一般而言，高血糖是糖尿病视网膜病变、肾病和神经病变的主要引发因素，并参与糖尿病心血管疾病的发展。虽然炎症在糖尿病微血管疾病发展中的确切作用尚不清楚，但糖尿病和胰岛素抵抗诱导的炎症可能会加速糖尿病患者的动脉粥样硬化。此外，研究表明，具有炎症基础的疾病，如肥胖和2型糖尿病，可能导致牙周病，这表明牙周异常可能部分受到炎症变化的影响。需要进一步的研究来确认炎症和糖尿病，微血管疾病和牙周病的发病的作用。牙周病学杂志2008;79：7527-1534。
The prevalence of diabetes worldwide is increasing rapidly in association with the increase in obesity. Complications are a major fear of patients with diabetes. Complications of diabetes affect many tissues and organs, causing retinopathy, nephropathy, neuropathy, cardiovascular diseases, peripheral vascular diseases, stroke, and periodontal pathologies. Immunologic abnormalities are associated with type 1 and type 2 diabetes and diabetic complications. T cell abnormalities are believed to be the major cause of autoimmune disease in type 1 diabetes, leading to the destruction of pancreatic islets. In type 2 diabetes, inflammation and activation of monocytes are postulated to be important for enhancing insulin resistance and may contribute to the loss of insulin secretory function by islet cells. Many factors can enhance insulin resistance, including genetics, a sedentary lifestyle, obesity, and other conditions, such as chronic inflammation or infection. Increases in inflammation, such as activation of monocytes and increased levels of inflammatory markers, e.g., C-reactive protein, plasminogen activator inhibitor-1, and other cytokines, were reported in insulin-resistant states without diabetes. One possible mechanism is that abnormal levels of metabolites, such as lipids, fatty acids, and various cytokines from the adipose tissue, activate monocytes and increase the secretion of inflammatory cytokines, enhancing insulin resistance. According to this model, obesity activates monocytes and enhances insulin resistance, increasing the risk for type 2 diabetes. Abnormalities in innate immunity might also participate in the development of diabetic complications. In general, hyperglycemia is the main initiator of diabetic retinopathy, nephropathy, and neuropathy, and it participates in the development of diabetic cardiovascular diseases. Although the precise role of inflammation in the development of diabetic microvascular diseases is still unclear, it is likely that inflammation induced by diabetes and insulin resistance can accelerate atherosclerosis in patients with diabetes. Also, it was shown that conditions with an inflammatory basis, such as obesity and type 2 diabetes, can contribute to periodontal disease, suggesting that periodontal abnormalities may be partly influenced by inflammatory changes. Further research is required to confirm the role of inflammation and the onset of diabetes, microvascular diseases, and periodontal pathologies. J Periodontoi 2008;79:7527-1534.