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首页> 外文期刊>RSC Advances >Prediabetes: grounds of pitfall signalling alteration for cardiovascular disease
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Prediabetes: grounds of pitfall signalling alteration for cardiovascular disease

机译：糖尿病前期：心血管疾病的陷阱信号改变的理由

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Impaired glucose metabolism either in prediabetes or diabetes mellitus is one of the detrimental root causes of premature mortality throughout the world. Uncontrolled prediabetes coincides with the induction of diabetic mellitus and associated cardiovascular diseases (CVDs). Needless to mention, impaired glucose metabolism, including impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), have been known individually or in combination as the prediabetic stage but by itself it is not diabetes mellitus. Impaired beta-cell function, insulin resistance, increased level of free fatty acids, hyperinsulinemia and down-regulation of GLUT-4 are critical impairments during prediabetes. The vascular endothelium sustains the free flow of blood in vessels by normalizing vascular tone by releasing numerous endothelial-derived factors. However, in recent studies a marked impairment in endothelial-derived factors has been observed in prediabetes. Thus, the impaired endothelial-derived factors could make prediabetic patients more vulnerable to cardiovascular disease pathology. Nobel laureates, Robert Furchgott, Louis Ignarro and Ferid Murad (1998) discovered a novel signalling molecule, nitric oxide (NO), identified as an endothelium-derived relaxing factor. This imperative mediator has potent vasodilatory, anti-platelet, anti-proliferative, and anti-inflammatory actions in vessels. Endothelium-derived NO generation is mediated through the activation of PI3-K-Akt-eNOS-NO signalling pathways. Therefore, conspicuous destruction in PI3-K-Akt-eNOS-NO signalling has been revealed in prediabetes and renders individuals more susceptible to CVDs. Several research reports have defined prediabetes as a platform for diabetes mellitus and associated CVDs. But the molecular alteration during prediabetes is unclear; however, the signalling modulator may be an imperative issue and may open a prerequisite new vista for novel research. In this review, we have critically discussed the possible signalling alteration in prediabetes.
机译：糖尿病前期或糖尿病中葡萄糖代谢受损是全世界过早死亡的有害根源之一。不受控制的糖尿病前期与糖尿病和相关心血管疾病（CVD）的诱发同时发生。不用说，已知的糖代谢受损，包括空腹血糖受损（IFG）和葡萄糖耐量受损（IGT），已被单独或综合称为糖尿病前期，但其本身并不是糖尿病。 β细胞功能受损，胰岛素抵抗，游离脂肪酸水平升高，高胰岛素血症和GLUT-4的下调是糖尿病前期的关键损害。血管内皮通过释放多种内皮衍生因子来使血管张力正常化，从而维持血管中的血液自由流动。然而，在最近的研究中，在糖尿病前期中已观察到内皮源性因子的显着损伤。因此，内皮源性因子受损可能使糖尿病前期患者更容易患心血管疾病。诺贝尔奖获得者Robert Furchgott，Louis Ignarro和Ferid Murad（1998）发现了一种新的信号分子，一氧化氮（NO），被确定为内皮源性舒张因子。这种命令性介质在血管中具有有效的血管舒张，抗血小板，抗增殖和抗炎作用。内皮来源的NO生成是通过PI3-K-Akt-eNOS-NO信号通路的激活来介导的。因此，在糖尿病前期中已经揭示了PI3-K-Akt-eNOS-NO信号中的明显破坏，并使个体更易患CVD。一些研究报告已将前驱糖尿病定义为糖尿病和相关CVD的平台。但是尚不清楚糖尿病前期的分子变化。然而，信号调制器可能是当务之急，并且可能为新颖的研究打开先决条件。在这篇综述中，我们严格地讨论了前驱糖尿病中可能的信号改变。

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