Insulin resistance and body fat distribution - Contribution of visceral fat accumulation to the development of insulin resistance and atherosclerosis
Insulin resistance and body fat distribution - Contribution of visceral fat accumulation to the development of insulin resistance and atherosclerosis
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DOI：
10.2337/diacare.19.3.287
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发表时间：
1996-03-01
期刊：
影响因子：
16.2
通讯作者：
Matsuzawa, Y
中科院分区：
文献类型：
--
作者：
Yamashita, S;Nakamura, T;Matsuzawa, Y
体脂分布可通过计算机断层扫描（CT）评估。采用脐部水平的内脏脂肪面积与皮下脂肪面积之比（V/S比）将肥胖受试者分为内脏脂肪肥胖（VFO）或皮下脂肪肥胖（SFO）。口服葡萄糖耐量试验中，VFO患者的血清甘油三酯和总胆固醇水平以及血浆葡萄糖面积高于SFO患者。V/S比与血浆葡萄糖面积、血清甘油三酯水平、总胆固醇水平以及收缩压和舒张压呈显著正相关。VFO常与冠状动脉疾病相关。此外，VFO比SFO更常伴有多种危险因素。VFO患者的稳态血浆葡萄糖（SSPG）水平明显高于SFO患者，提示VFO患者的胰岛素抵抗可能比SFO患者更为显著。此外，即使在非肥胖受试者中，内脏脂肪堆积也与这些并发症有关。内脏脂肪面积（VFA）与空腹血糖、血清甘油三酯和总胆固醇水平显著相关。下丘脑腹内侧（VMH）病变的Goto-Kakizaki （GK）大鼠和otsuka - long - evans - tokusima - fatty （OLETF）大鼠等动物模型均伴有内脏脂肪堆积和早期主动脉粥样硬化。衰老、性激素、遗传和饮食因素以及缺乏运动都可能诱发内脏脂肪堆积。内脏脂肪的特点是其高脂肪生成活性和加速脂肪分解活性。高水平的游离门脉脂肪酸（FFAs）可能最终导致肝脏甘油三酯合成增强，引起高脂血症。高的门脉FFA水平也会诱发胰岛素抵抗，从而引起葡萄糖耐受不良、高血压，最终导致动脉粥样硬化。我们提出一个术语，“内脏脂肪综合征”，作为一种高度动脉粥样硬化状态，包括内脏脂肪积累，葡萄糖耐受不良（胰岛素抵抗），高脂血症和高血压。
Body fat distribution can be assessed by computed tomography (CT). The ratio of visceral fat area to subcutaneous fat area (V/S ratio) at the level of umbilicus was used to classify obese subjects as having visceral fat obesity (VFO) or subcutaneous fat obesity (SFO). Serum triglyceride and total cholesterol levels and plasma glucose area in an oral glucose tolerance test were higher in patients with VFO than in those with SFO. Significant positive correlations were demonstrated between V/S ratio and plasma glucose area, serum triglyceride level, and total cholesterol level as well as systolic or diastolic blood pressure. VFO was more frequently associated with coronary artery disease. Moreover, VFO was more often accompanied by multiple risk factors than was SFO. Steady-state plasma glucose (SSPG) level was significantly higher in patients with VFO than with SFO, suggesting that insulin resistance may be more remarkable in VFO than in SFO.Furthermore, visceral fat accumulation was also associated with these complications even in nonobese subjects. Visceral fat area (VFA) was significantly correlated with fasting plasma glucose, serum triglyceride, and total cholesterol levels. Animal models such as Goto-Kakizaki (GK) rats with ventromedial hypothalamus (VMH) lesions and Otsuka-Long-Evans-Tokushima-Fatty (OLETF) rats were accompanied by visceral fat accumulation and an early stage of aortic atherosclerosis. Aging, sex hormone, genetic, and dietary factors and physical inactivity may induce visceral fat accumulation. Visceral fat is characterized by its high lipogenic activity as well as its accelerated lipolytic activity. High levels of portal free fatty acids (FFAs) may eventually result in an enhancement of hepatic triglyceride synthesis, causing hyperlipidemia. High portal FFA levels would also induce insulin resistance, thereby causing glucose intolerance, hypertension, and finally atherosclerosis. We propose a term, ''visceral fat syndrome,'' as a highly atherogenic state, which includes visceral fat accumulation, glucose intolerance (insulin resistance), hyperlipidemia, and hypertension.