GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus
GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus
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DOI：
10.1054/plef.1998.0003
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发表时间：
1999-01-01
影响因子：
3
通讯作者：
Das, UN
中科院分区：
文献类型：
--
作者：
Das, UN
目前认为，GLUT-4受体、肿瘤坏死因子- α (tnf - α)、必需脂肪酸（EFAs）及其代谢物和daf-基因在肥胖和非胰岛素依赖型糖尿病（NIDDM）的发生发展中起重要作用。daf-2编码的蛋白与人胰岛素受体35%相同，daf-7编码转化生长因子- β (tgf - β)型信号，daf-16可以增强超氧化物歧化酶（SOD）的表达。EFAs及其代谢产物可以改变细胞膜流动性，提高GLUT-4和胰岛素受体的表达。脂肪酸可以抑制tnf - α的产生和分泌，这一机制可能与这些脂肪酸在胰岛素抵抗、肥胖和NIDDM发病机制中的作用有关。褪黑素具有与daf-16、tgf - β和SOD类似的抗氧化作用。基于这些证据，我们提出GLUT-4、tnf - α、EFAs、daf-基因、褪黑激素和瘦素之间的相互作用可能与胰岛素抵抗、肥胖、NIDDM、NIDDM并发症、寿命和衰老的发生或消除有关。
It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing.