Dandona Paresh, Mohanty Priya, Chaudhuri Ajay, Garg Rajesh, Aljada Ahmad
Division of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo, and Kaleida Health, Buffalo, New York, New York, USA.
J Clin Invest. 2005 Aug;115(8):2069-72. doi: 10.1172/JCI26045.
The discovery of the antiinflammatory effect of insulin and the proinflammatory effect of glucose has not only provided novel insight into the mechanisms underlying several disease states but has also provided a rationale for the treatment of hyperglycemia in several acute clinical conditions. Van den Berghe et al. previously showed the benefits of intensive glycemic control with insulin in patients admitted to intensive care units. In this issue of the JCI, the same group of investigators now demonstrates that infusion of insulin to restore euglycemia in these patients results in a marked reduction in inflammatory indices such as adhesion molecules, hepatic iNOS, and plasma NO metabolites. The reduction in the mediators of inflammation may thus be responsible for the impressive improvement in clinical outcomes following insulin therapy, and the results suggest a new paradigm in which glucose and insulin are related not only through their metabolic actions but also through their opposite effects on inflammatory mechanisms.
胰岛素抗炎作用和葡萄糖促炎作用的发现，不仅为深入了解多种疾病状态的潜在机制提供了新视角，也为多种急性临床病症中高血糖的治疗提供了理论依据。范登伯格等人此前已表明，在重症监护病房住院患者中强化胰岛素血糖控制具有益处。在本期《临床研究杂志》中，同一组研究人员现在证明，对这些患者输注胰岛素以恢复正常血糖会导致炎症指标显著降低，如黏附分子、肝脏诱导型一氧化氮合酶和血浆一氧化氮代谢产物。因此，炎症介质的减少可能是胰岛素治疗后临床结果显著改善的原因，这些结果提示了一种新的范式，即葡萄糖和胰岛素不仅通过其代谢作用相关联，还通过它们对炎症机制的相反作用相关联。
