摘要
The incidence of obesity has increased dramatically during recent decades. Obesity will cause a decline in life expectancy for the first time in recent history due to numerous co-morbid disorders. Adipocyte and adipose tissue dysfunction belong to the primary defects in obesity and may link obesity to several health problems including increased risk of insulin resistance, type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, atherosclerosis, dementia, airway disease and some cancers. However, not all obese individuals develop obesity related metabolic or cardiovascular disorders potentially due to a preserved normal adipose tissue architecture and function. The majority of patients with obesity have an impaired adipose tissue function caused by the interaction of genetic and environmental factors which lead to adipocyte hypertrophy, hypoxia, a variety of stresses and inflammatory processes within adipose tissue. Ectopic fat accumulation including visceral obesity may be considered as a consequence of adipose tissue dysfunction, which is further characterized by changes in the cellular composition, increased lipid storage and impaired insulin sensitivity in adipocytes, and secretion of a proinflammatory, atherogenic, and diabetogenic adipokine pattern. This review focuses on the discussion of mechanisms causing or maintaining impaired adipose tissue function in obesity and potentially linking obesity to its associated disorders. A model is proposed how different pathogenic factors and mechanisms may cause dysfunction of adipose tissue.
摘要译文
在最近的几十年中，肥胖症的发病率急剧上升。由于多种合并症，肥胖症将导致最近寿命的首次预期寿命下降。脂肪细胞和脂肪组织功能障碍是肥胖症的主要缺陷，并且可能将肥胖症与一些健康问题联系起来，包括胰岛素抵抗，2型糖尿病，脂肪肝疾病，高血压，血脂异常，动脉粥样硬化，痴呆，气道疾病和某些癌症的风险增加。然而，并非所有肥胖者都可能由于保留的正常脂肪组织结构和功能而发展出与肥胖有关的代谢或心血管疾病。大多数肥胖患者的脂肪组织功能受损是由遗传和环境因素的相互作用引起的，这些因素导致脂肪细胞肥大，缺氧，多种压力和脂肪组织内的炎症过程。包括内脏肥胖在内的异位脂肪堆积可能被认为是脂肪组织功能障碍的结果，其特征还在于细胞组成的变化，脂肪细胞中脂质存储的增加和胰岛素敏感性的降低以及促炎，动脉粥样硬化和糖尿病形成的脂肪因子的分泌。这篇综述着重讨论了引起或维持肥胖中脂肪组织功能受损的机制，并可能将肥胖与其相关疾病联系起来。提出了一个模型，说明不同的致病因素和机制如何引起脂肪组织功能障碍。
M. Blüher. Adipose Tissue Dysfunction in Obesity[J]. Experimental and Clinical Endocrinology & Diabetes, 2009,117(06): 241-250