Why visceral fat is bad: Mechanisms of the metabolic syndrome
Why visceral fat is bad: Mechanisms of the metabolic syndrome
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DOI：
10.1038/oby.2006.277
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发表时间：
2006-02-01
期刊：
影响因子：
6.9
通讯作者：
Ader, Marilyn
中科院分区：
文献类型：
--
作者：
Bergman, Richard N.;Kim, Stella P.;Ader, Marilyn
人们已经达成共识，储存在身体中央部位的脂肪特别有害，因为它预示着糖尿病，心血管疾病，高血压和某些癌症的风险更大（1 - 3）。胰岛素抵抗是一个相关的特征，可能是中心脂肪和疾病风险之间的重要联系。此外，在非糖尿病但有风险的个体中伴随胰岛素抵抗的高胰岛素血症可能会放大甚至介导内脏肥胖的一些有害影响（4 - 6）。然而，关于内脏脂肪与疾病风险之间可能联系的机制的信息较少。例如，关于内脏隔室中的脂肪比皮下脂肪赋予更大风险的具体机制存在争议。许多研究者认为内脏脂肪细胞分泌的一种或多种成分可能介导胰岛素抵抗。在所谓的"坏因素"中，有游离脂肪酸（FFA）1本身（"门户理论"）（7 - 9）或脂肪组织释放的细胞因子（脂肪因子），如白细胞介素-1、白细胞介素-6、肿瘤坏死因子-α、β-内酰胺酶或脂联素的减少，已反复显示脂联素与胰岛素抵抗降低相关（10 - 13）。当然，胰岛素本身也可能参与其中，因为其他脂肪分泌的蛋白质化合物还没有被发现。但为什么是内脏脂肪呢？这是因为内脏脂肪储存库的独特解剖位置，流出物进入肝脏，还是因为内脏脂肪本身的分子特征，这可能有利于释放有害分子进入体循环？这些问题仍然没有答案。然而，在我们的实验室里，我们已经开发了肥胖狗模型，这导致了一些
A consensus has emerged that fat stored in the central segment of the body is particularly damaging in that it portends greater risk for diabetes, cardiovascular disease, hypertension, and certain cancers (1–3). It is also accepted that insulin resistance is a related characteristic that may be an essential link between central fat and disease risk. Additionally, it is possible that the hyperinsulinemia that accompanies insulin resistance in non-diabetic but at-risk individuals may magnify, or even mediate, some of the detrimental effects of visceral adiposity (4–6). However, there is less information regarding the mechanisms that may link visceral fat with risk for disease. For example, there is controversy regarding the specific mechanisms by which fat in the visceral compartment confers greater risk than subcutaneous fat. Many investigators have suggested that one or more moieties secreted by the visceral adipocyte might mediate insulin resistance. Among the socalled “bad actors” are free fatty acids (FFAs) 1 themselves (“portal theory”)(7–9) or the adipose tissue–released cytokines (adipokines) such as interleukin-1, interleukin-6, tumor necrosis factor-, resistin, or a reduction in adiponectin, which has been repeatedly shown to be associated with reduced insulin resistance (10–13). Of course, insulin itself could be involved, as other adipose-secreted protein compounds not yet identified.But why visceral fat? Is it because of the unique anatomical position of the visceral fat depot, with effluent entering the liver, or is it because of molecular characteristics of visceral fat itself, which may favor release of damaging molecules into the systemic circulation? These questions remain unanswered. However, in our laboratory, we have developed the obese dog model, which has led to some