Rizvi Ali A
Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of South Carolina School of Medicine, Columbia, South Carolina 29203, USA.
Am J Med Sci. 2009 Oct;338(4):310-8. doi: 10.1097/MAJ.0b013e3181a4158c.
In recent years, an explosion of research related to the cellular and vascular accompaniments of the metabolic syndrome has generated intense interest and controversy. Attention has focused on the vascular endothelium, where heightened, low-grade inflammatory processes lead to a continuum of vascular insults ranging from early endothelial derangements to advanced atherosclerosis. Inflammatory biocytokines, such as C-reactive protein, have been speculated to be both markers and mediators of oxidative stress and endovascular toxicity. Adipocytokines originating from fatty tissue have reinforced the concept that fat is a metabolically active organ rather than inert tissue. To fully elucidate its complex pathogenetic mechanisms, further inquiry into the inflammatory components of the metabolic syndrome is warranted. Unraveling the role of emerging proinflammatory markers has the promising potential to shed light into the underlying pathophysiology of the epidemic of obesity and the metabolic syndrome and thus help devise effective therapies.
近年来,与代谢综合征的细胞和血管伴随现象相关的研究激增,引发了强烈的兴趣和争议。注意力集中在血管内皮上,在那里,增强的低度炎症过程会导致一系列血管损伤,从早期内皮紊乱到晚期动脉粥样硬化。炎症生物细胞因子,如C反应蛋白,被推测是氧化应激和血管内毒性的标志物和介质。源自脂肪组织的脂肪细胞因子强化了脂肪是一个代谢活跃器官而非惰性组织的概念。为了充分阐明其复杂的发病机制,有必要进一步探究代谢综合征的炎症成分。阐明新兴促炎标志物的作用有望揭示肥胖和代谢综合征流行的潜在病理生理学,从而有助于设计有效的治疗方法。