Leptin and Mechanisms of Endothelial Dysfunction and Cardiovascular Disease
Leptin and Mechanisms of Endothelial Dysfunction and Cardiovascular Disease
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DOI：
10.1007/s11906-008-0082-2
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发表时间：
2008-12-01
影响因子：
5.6
通讯作者：
Tune, Johnathan D.
中科院分区：
文献类型：
--
作者：
Knudson, Jarrod D.;Payne, Gregory A.;Tune, Johnathan D.
瘦素是肥胖基因的产物，是自1994年克隆以来备受关注的分子。最初，大多数研究都围绕瘦素对饱腹感和能量平衡的影响展开。然而，近年来，由于瘦素与心血管系统有关，人们对它的关注越来越强烈。血浆瘦素浓度在肥胖和代谢综合征中显著升高，这两种疾病都与心血管疾病的发病率增加有关。在许多研究中，高瘦素血症与内皮功能障碍（已知的动脉粥样硬化性心血管疾病的前兆）和交感神经系统的激活有关。此外，最近的证据表明，从血管周围脂肪组织释放的瘦素也可能对潜在的血管系统，包括冠状动脉循环产生有害影响。本报告回顾了有关瘦素介导的内皮功能障碍、瘦素介导的交感神经激活以及瘦素作为血管周围脂肪衍生因子的相关文献。
Leptin, a product of the obesity gene, is a molecule that has received much attention since its cloning in 1994. Initially, most work centered around the effects of leptin on satiety and energy balance. However, in recent years there has been an intense focus on leptin as it relates to the cardiovascular system. Plasma leptin concentration is markedly elevated in obesity and the metabolic syndrome, both of which are associated with increased incidence of cardiovascular pathologies. In many studies, hyperleptinemia has been linked to endothelial dysfunction (a known precursor to atherosclerotic cardiovascular disease) and activation of the sympathetic nervous system. Additionally, recent evidence suggests that leptin released from perivascular adipose tissue may also have deleterious effects on the underlying vasculature, including the coronary circulation. This report reviews pertinent literature on leptin-mediated endothelial dysfunction, leptin-mediated sympathetic activation, and leptin as a significant perivascular adipose-derived factor.