Anfossi Giovanni, Russo Isabella, Doronzo Gabriella, Trovati Mariella
Internal Medicine University Unit, San Luigi Gonzaga Faculty of Medicine and Department of Clinical and Biological Sciences, Turin University, San Luigi Gonzaga Hospital, 10043 Orbassano, Turin, Italy.
Arch Physiol Biochem. 2009 Oct;115(4):199-217. doi: 10.1080/13813450903136791.
Insulin is a vascular hormone, able to influence vascular cell responses. In this review, we consider the insulin actions on vascular endothelium and on vascular smooth muscle cells (VSMC) both in physiological conditions and in the presence of insulin resistance. In particular, we focus the relationships between activation of insulin signalling pathways of phosphatidylinositol-3 kinase (PI3-K) and mitogen-activated protein kinase (MAPK) and the different vascular actions of insulin, with a particular attention to the insulin ability to activate the pathway nitric oxide (NO)/cyclic GMP/PKG via PI3-K, owing to the peculiar relevance of NO in vascular biology. We also discuss the insulin actions mediated by the MAPK pathway (such as endothelin-1 synthesis and secretion and VSMC proliferation and migration) and by the interactions between the two pathways, both in insulin-sensitive and in insulin-resistant states. Finally, we consider the influence of free fatty acids, cytokines and endothelin on vascular insulin resistance.
胰岛素是一种血管激素，能够影响血管细胞反应。在本综述中，我们探讨胰岛素在生理条件下以及存在胰岛素抵抗时对血管内皮和血管平滑肌细胞（VSMC）的作用。特别地，我们关注磷脂酰肌醇-3激酶（PI3-K）和丝裂原活化蛋白激酶（MAPK）的胰岛素信号通路激活与胰岛素不同血管作用之间的关系，尤其关注胰岛素通过PI3-K激活一氧化氮（NO）/环磷酸鸟苷（cGMP）/蛋白激酶G（PKG）途径的能力，因为NO在血管生物学中具有特殊的相关性。我们还讨论了在胰岛素敏感和胰岛素抵抗状态下，由MAPK途径介导的胰岛素作用（如内皮素-1的合成与分泌以及VSMC的增殖和迁移）以及两条途径之间的相互作用。最后，我们考虑游离脂肪酸、细胞因子和内皮素对血管胰岛素抵抗的影响。
