Matsuzawa Y
Sumitomo Hospital, Professor Emeritus Osaka University, Kita-Ku, Osaka, Japan.
Int J Obes (Lond). 2008 Dec;32 Suppl 7:S83-92. doi: 10.1038/ijo.2008.243.
Clustering of multiple risk factors such as impaired glucose metabolism, lipid disorders and hypertension has been shown to be the major background of atherosclerotic diseases, and disease entities such as the metabolic syndrome represent a highly atherogenic state. Although these common risks may generally co-exist by accident in one individual, clustering of multiple risk factors in the metabolic syndrome does not occur by accident, and there should be a key player for the syndrome. In 1983, we reported the method for fat analysis using computed tomography scan, which enables us to analyze intra-abdominal visceral adiposity as well as subcutaneous fat. Visceral fat accumulation has been shown to cause impaired glucose metabolism, lipid disorders, and hypertension, and therefore it is considered to be a key player in the metabolic syndrome. To clarify the mechanism by which visceral fat accumulation causes a variety of metabolic and vascular diseases, we studied the molecular characteristics of adipose tissue and adipocytes by investigating expressed genes in visceral and subcutaneous adipocytes and revealed that adipocytes, especially visceral adipocytes, secrete a variety of bioactive substances, the so-called adipocytokines. We showed that visceral fat accumulation causes abnormalities in adipocytokine secretion, such as hypersecretion of plasminogen activator inhibitor 1, which is related to thrombogenic vascular diseases. More importantly, we discovered an important benign adipocytokine named adiponectin, which protects against the development of diabetes mellitus, hypertension, inflammation, and atherosclerotic vascular diseases. Plasma levels of adiponectin decreased in individuals with visceral fat accumulation, and hypoadiponectinemia caused by visceral fat accumulation might be one of the major causes of metabolic syndrome.
多种风险因素的聚集，如糖代谢受损、脂质紊乱和高血压，已被证明是动脉粥样硬化疾病的主要背景，而代谢综合征等疾病实体代表了一种高度致动脉粥样硬化的状态。虽然这些常见风险通常可能偶然同时存在于一个个体中，但代谢综合征中多种风险因素的聚集并非偶然发生，该综合征应该存在一个关键因素。1983年，我们报道了使用计算机断层扫描进行脂肪分析的方法，该方法使我们能够分析腹部内脏脂肪以及皮下脂肪。内脏脂肪堆积已被证明会导致糖代谢受损、脂质紊乱和高血压，因此被认为是代谢综合征的关键因素。为了阐明内脏脂肪堆积导致各种代谢和血管疾病的机制，我们通过研究内脏和皮下脂肪细胞中表达的基因，研究了脂肪组织和脂肪细胞的分子特征，发现脂肪细胞，尤其是内脏脂肪细胞，会分泌多种生物活性物质，即所谓的脂肪细胞因子。我们发现内脏脂肪堆积会导致脂肪细胞因子分泌异常，比如纤溶酶原激活物抑制剂1分泌过多，这与血栓形成性血管疾病有关。更重要的是，我们发现了一种名为脂联素的重要良性脂肪细胞因子，它可以预防糖尿病、高血压、炎症和动脉粥样硬化性血管疾病的发生。内脏脂肪堆积个体的血浆脂联素水平降低，内脏脂肪堆积引起的低脂联素血症可能是代谢综合征的主要原因之一。
