Tchernof A, Labrie F, Bélanger A, Després J P
Liptd Research Center, Clinical Research Center, Sle foy, Quebec, Canada.
J Endocrinol. 1996 Sep;150 Suppl:S155-64.
Obesity is a heterogeneous condition and not every obese patient is at increased risk of cardiovascular diseases (CVD). It is now well established that the regional distribution of body fat is a critical correlate of the metabolic complications of obesity. Studies that have assessed adipose tissue distribution by imaging techniques such as computed tomography have demonstrated the importance of the intra-abdominal (visceral) fat depot as a marker of a cluster of metabolic abnormalities which include glucose intolerance, insulin resistance, hyper-insulinemia, hypertriglyceridemia, elevated number of apo B-carrying lipoproteins as well as hypoalphalipoproteinemia. Although the association between visceral obesity and metabolic complications can hardly be questioned, it has been suggested that it may not necessarily represent a causal relationship. For instance, concomitant alterations in sex steroid levels have been found in both men and women with abdominal (visceral) obesity which have also been reported to be significantly correlated with the insulin resistant-dyslipidemic state found in abdominal obese subjects. In women, abdominal obesity is associated with increased free testosterone concentrations and reduced sex hormone binding globulin (SHBG) levels, whereas in men this condition is associated with reduced testosterone and adrenal C12 steroid (dehydroepiandrosterone, androstenedione, androstene-3 beta, 17 beta-diol) levels as well as decreased SHBG concentrations. These altered steroid and SHBG; levels have been reported to be independent correlates of the metabolic complications of visceral obesity although they cannot solely account for the increased CVD risk found in these patients. In this regard, intervention studies are clearly warranted to better quantity the respective contribution of excess visceral adipose tissue and of the concomitant alterations in sex steroid levels as modulators of metabolic disturbances increasing CVD risk in obesity.
肥胖是一种异质性疾病，并非每个肥胖患者患心血管疾病（CVD）的风险都会增加。现在已经明确，体脂的区域分布是肥胖代谢并发症的关键相关因素。通过计算机断层扫描等成像技术评估脂肪组织分布的研究表明，腹内（内脏）脂肪库作为一组代谢异常的标志物具有重要意义，这些代谢异常包括葡萄糖不耐受、胰岛素抵抗、高胰岛素血症、高甘油三酯血症、载脂蛋白B的脂蛋白数量增加以及低α脂蛋白血症。虽然内脏肥胖与代谢并发症之间的关联几乎毋庸置疑，但有人认为这不一定代表因果关系。例如，在患有腹部（内脏）肥胖的男性和女性中都发现了性类固醇水平的伴随变化，据报道这些变化也与腹部肥胖受试者中发现的胰岛素抵抗性血脂异常状态显著相关。在女性中，腹部肥胖与游离睾酮浓度升高和性激素结合球蛋白（SHBG）水平降低有关，而在男性中，这种情况与睾酮和肾上腺C12类固醇（脱氢表雄酮、雄烯二酮、雄烯 - 3β，17β - 二醇）水平降低以及SHBG浓度降低有关。据报道，这些改变的类固醇和SHBG水平是内脏肥胖代谢并发症的独立相关因素，尽管它们不能完全解释这些患者中增加的CVD风险。在这方面，显然有必要进行干预研究，以更好地量化内脏脂肪组织过多以及性类固醇水平的伴随变化作为肥胖中增加CVD风险的代谢紊乱调节因素的各自贡献。
