Daly P A, Landsberg L
Department of Medicine, Harvard Medical School, Boston, Massachusetts.
Diabetes Care. 1991 Mar;14(3):240-8. doi: 10.2337/diacare.14.3.240.
An important link exists between obesity, noninsulin-dependent diabetes mellitus (NIDDM), and hypertension. Most patients with NIDDM are obese; the incidence of hypertension in obesity and NIDDM is substantial, approaching 50% in some studies. Furthermore, hypertension is known to contribute to the increased cardiovascular morbidity and mortality in patients with obesity and NIDDM. Despite the obvious clinical importance, the pathogenesis of hypertension in obesity and NIDDM remains poorly understood. Recent studies have identified hyperinsulinemia and insulin resistance as important threads that tie hypertension, obesity, and NIDDM together. The hypothesis is developed that insulin-mediated sympathetic stimulation contributes to blood pressure elevation in both obesity and NIDDM. Recruited as a mechanism to limit weight gain and restore energy balance, insulin resistance and sympathetic stimulation increase blood pressure by enhancing renal Na+ reabsorption and stimulating the cardiovascular system. In this article, we review the evidence on which this hypothesis is based.
肥胖、非胰岛素依赖型糖尿病(NIDDM)和高血压之间存在着重要联系。大多数NIDDM患者都肥胖;肥胖和NIDDM患者中高血压的发病率相当高,在一些研究中接近50%。此外,已知高血压会导致肥胖和NIDDM患者心血管发病率和死亡率增加。尽管具有明显的临床重要性,但肥胖和NIDDM患者高血压的发病机制仍知之甚少。最近的研究已将高胰岛素血症和胰岛素抵抗确定为将高血压、肥胖和NIDDM联系在一起的重要线索。由此提出的假说认为,胰岛素介导的交感神经刺激会导致肥胖和NIDDM患者血压升高。作为限制体重增加和恢复能量平衡的一种机制,胰岛素抵抗和交感神经刺激通过增强肾脏对钠离子的重吸收和刺激心血管系统来升高血压。在本文中,我们回顾了这一假说所依据的证据。