University of California, Los Angeles, David Geffen School of Medicine, Division of Endocrinology, Diabetes and Hypertension, Los Angeles, CA 90095-7073, USA.
Obes Rev. 2010 Sep;11(9):635-44. doi: 10.1111/j.1467-789X.2009.00691.x.
Obesity is linked with many deleterious health consequences and is associated with increased risk of chronic disease including type 2 diabetes, atherosclerosis and certain forms of cancer. Recent work has highlighted the impact of obesity to activate inflammatory gene networks and suggests a causal function of inflammation in the pathogenesis of the metabolic syndrome. Since 2005, when Dr Gokhan Hotamisligil chaired the fourth Stock Conference in Istanbul, Turkey, entitled 'Obesity and Inflammation', there has been an explosion of studies investigating the relationship between obesity, inflammation and substrate metabolism. The exuberance surrounding this field of research is exemplified by the body of work that has been published in these past 4 years, including over 1400 publications. During this time, several novel mechanisms relating to cellular inflammation have been uncovered including the role of the hematopoietic system, toll-like receptor activation, endoplasmic reticulum stress and very recently T-cell activation in obesity-induced insulin resistance. These discoveries have led us to rethink cellular nutrient sensing and its role in inflammation and metabolic disease. Despite burgeoning investigation in this field, there still remain a number of unanswered questions. This review that evolved from the 2009 Stock Conference summarizes current research and identifies the deficiencies in our understanding of this topic. The overall goal of this Stock Conference was to bring together leading investigators in the field of inflammation and obesity research in the hope of fostering new ideas, thus advancing the pursuit of novel therapeutic strategies to reduce disease risk and or better treat chronic disease including type 2 diabetes, cardiovascular disease and cancer.
肥胖与许多有害的健康后果有关，并与慢性疾病风险增加相关，包括 2 型糖尿病、动脉粥样硬化和某些类型的癌症。最近的研究强调了肥胖激活炎症基因网络的影响，并表明炎症在代谢综合征发病机制中的因果作用。自 2005 年 Gokhan Hotamisligil 博士在土耳其伊斯坦布尔主持第四届题为“肥胖与炎症”的股票会议以来，已有大量研究调查肥胖、炎症和底物代谢之间的关系。在过去的 4 年中，该领域的研究工作蓬勃发展，发表了超过 1400 篇论文，这充分说明了这一点。在此期间，已经发现了与细胞炎症相关的一些新机制，包括造血系统、Toll 样受体激活、内质网应激以及最近 T 细胞激活在肥胖诱导的胰岛素抵抗中的作用。这些发现促使我们重新思考细胞营养感应及其在炎症和代谢性疾病中的作用。尽管该领域的研究不断增加，但仍有许多问题尚未得到解答。本次股票会议的综述总结了目前的研究，并指出了我们对这一主题理解的不足之处。本次股票会议的总体目标是汇集炎症和肥胖研究领域的领先研究人员，希望能激发新的想法，从而推进新的治疗策略的研究，以降低疾病风险，或更好地治疗慢性疾病，包括 2 型糖尿病、心血管疾病和癌症。
