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Lipid links inflammation, immunity and insulin resistance to cause epidemic diabetes

机译:脂质将炎症,免疫力和胰岛素抵抗联系在一起,导致流行性糖尿病

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摘要

Incidence of type 2 diabetes (T2D) is dramatically increasing in the past few decades and presently affecting more than 350 million people all over the globe. Oversupply of lipid is one of the major forces behind T2D. Excess of lipid decreases insulin sensitivity or activity that causes insulin resistance, a stage which occupies the centre of pathogenesis in T2D. Lipid induces adipose tissue inflammation that accompanies certain critical defects in adipocytes, a major cell in abdominal adipose tissue. These include increased population of hypertrophied adipocytes, decline in adipokines secretion, attenuation of adipogenesis, and increased lipotoxicity effecting greater deposition of fat which interferes with glucose uptake by insulin target cells. Inflammation of adipose tissue is further intensified due to the infiltration of macrophages, a member of the innate immune system, and their transformation from anti-inflammatory M2 to proinflammatory M1 phenotype. Hence, secretion of proinflammatory cytokines from both M1 macrophage and inflamed adipocytes is greatly elevated which adversely causes insulin resistance that leads to T2D. Association between lipid-induced inflammation and insulin resistance makes diabetes a critical disease.
机译:在过去的几十年中,2型糖尿病(T2D)的发病率急剧上升,目前影响着全球超过3.5亿人。脂质的过量供应是T2D背后的主要力量之一。脂质过多会降低胰岛素敏感性或引起胰岛素抵抗的活性,该阶段占据了T2D发病机理的中心。脂质诱导脂肪组织炎症,伴随着脂肪细胞(腹部脂肪组织中的主要细胞)的某些关键缺陷。这些包括肥大的脂肪细胞的增加,脂肪因子分泌的减少,脂肪形成的减弱以及脂毒性增加,从而影响脂肪的沉积,从而增加了脂肪的沉积,从而干扰了胰岛素靶细胞对葡萄糖的摄取。脂肪组织的炎症由于先天免疫系统成员巨噬细胞的浸润及其从抗炎M2到促炎M1表型的转化而进一步加剧。因此,来自M1巨噬细胞和发炎的脂肪细胞的促炎细胞因子的分泌大大增加,这不利地导致胰岛素抵抗,导致T2D。脂质引起的炎症和胰岛素抵抗之间的联系使糖尿病成为一种严重疾病。

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