Forst T, Hohberg C, Pfützner A
Institute for Clinical Research and Development, Mainz, Germany.
Horm Metab Res. 2009 Feb;41(2):123-31. doi: 10.1055/s-0028-1119378. Epub 2009 Feb 12.
The metabolic syndrome is associated with an excess of increase in cardiovascular complications. Disturbances in insulin efficacy and insulin secretion are major features of the metabolic syndrome and might precede the development of diabetes mellitus by decades. Recent investigations highlighted the link between disturbances in insulin physiology and subsequent mechanisms of atherosclerosis. Insulin resistance is an early feature of increasing visceral adipose tissue and is directly associated to the activation of a couple of atherogenic pathways, including inflammation and the activation of the mitogen-activated proteinkinase pathway accelerating the atherogenic process. In patients with normal beta-cell function, insulin resistance is compensated by increased insulin release from the beta cells to keep blood glucose levels compensated. In those patients, genetically predisposed to type 2 diabetes, beta-cell function deteriorates with the development of timely, qualitative and quantitative insulin secretion disorders, and the development of overt diabetes mellitus. The coexistence of insulin resistance with functional beta cell failure results in loss of blood glucose control especially after a meal and increases the cardiovascular risk of these patients far beyond the increased glucose levels.
代谢综合征与心血管并发症的过度增加有关。胰岛素效能和胰岛素分泌紊乱是代谢综合征的主要特征，可能在糖尿病发生前数十年就已出现。最近的研究突出了胰岛素生理紊乱与动脉粥样硬化后续机制之间的联系。胰岛素抵抗是内脏脂肪组织增加的早期特征，与包括炎症和丝裂原活化蛋白激酶途径激活在内的多种致动脉粥样硬化途径的激活直接相关，这些途径加速了动脉粥样硬化进程。在β细胞功能正常的患者中，胰岛素抵抗通过β细胞增加胰岛素释放得到代偿，以维持血糖水平。在那些遗传易患2型糖尿病的患者中，随着适时、定性和定量胰岛素分泌紊乱的发展以及显性糖尿病的发生，β细胞功能会恶化。胰岛素抵抗与功能性β细胞功能衰竭并存会导致血糖控制丧失，尤其是在进食后，并使这些患者的心血管风险远远超过血糖升高所带来的风险。
