RELATIONSHIP OF BODY-FAT TOPOGRAPHY TO INSULIN SENSITIVITY AND METABOLIC PROFILES IN PREMENOPAUSAL WOMEN
RELATIONSHIP OF BODY-FAT TOPOGRAPHY TO INSULIN SENSITIVITY AND METABOLIC PROFILES IN PREMENOPAUSAL WOMEN
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DOI：
10.1016/0026-0495(84)90164-1
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发表时间：
1984-01-01
影响因子：
9.8
通讯作者：
KISSEBAH, AH
中科院分区：
文献类型：
--
作者：
EVANS, DJ;HOFFMANN, RG;KISSEBAH, AH
在80名健康绝经前白色妇女中测定了体脂分布与代谢谱的关系，这些妇女的肥胖程度范围很广[理想体重百分比（% IBW）92-251]。从腰围/臀围比（WHR）（从0.64到1.02不等）评估上半身和下半身之间的脂肪分布。在23名妇女中，体内胰岛素敏感性也由稳态血浆葡萄糖（SSPG）水平确定，所述稳态血浆葡萄糖（SSPG）水平为通过生长激素抑制素、葡萄糖和胰岛素的静脉内输注获得的约100 μ U/ml的可比胰岛素水平。随着腰臀比的增加，空腹血浆胰岛素水平（r = 0.47，P < 0.001）、葡萄糖负荷后胰岛素和葡萄糖面积（分别为r = 0.53，P < 0.001; r = 0.50，P < 0.001）和空腹血浆甘油三酯浓度（r = 0.48，P < 0.001）逐渐增加。肥胖水平与这些代谢指标也存在类似的相关性。偏回归和多元回归分析和方差分析与线性对比模型显示，体脂地形的影响是独立的，和添加剂，肥胖水平。在单独的肥胖受试者中（%IBW：130），%IBW没有预测价值，但WHR仍然是血糖、胰岛素和甘油三酯浓度的重要预测因子。腰臀比也与血浆胆固醇水平相关，但这种相关性在很大程度上取决于其与%IBW的关系。腰臀比和%IBW与胰岛素抵抗指数SSPG均呈显著正相关（r = 0.60，P < 0.01; r = 0.61，P < 0.01）。在调整了%IBW的影响后，WHR与SSPG独立相关，在调整了WHR后，%IBW与SSPG显著相关。WHR和%IBW的综合效应呈加性。SSPG水平与空腹血浆胰岛素水平（r = 0.89，P < 0.001）、葡萄糖面积（r = 0.64，P < 0.01）、胰岛素面积（r = 0.52，P < 0.05）和空腹血浆甘油三酯浓度（r = 0.62，P < 0.01）相关。这些代谢变量之间也存在显著的相互作用。在调整WHR和%IBW的影响后，这些关联的强度大大减弱，但SSPG和空腹血浆胰岛素水平之间以及空腹血浆胰岛素水平、胰岛素面积和空腹血浆甘油三酯水平之间的关系仍然显著。显然，在绝经前肥胖妇女中，体脂定位的部位和肥胖程度影响胰岛素敏感性的程度，进而影响血糖、胰岛素和脂质水平。因此，识别脂肪优势部位可能会发现肥胖女性对胰岛素抵抗和代谢异常的易感性。但是，还必须考虑其他因素。
The relationship of body fat distribution to metabolic profiles was determined in 80 healthy premenopausal white women of a wide range of obesity levels [percentage of ideal body wt (% IBW) 92-251]. Distribution of fat between the upper and lower body was assessed from the waist/hips girth ratio (WHR), which varied from 0.64 to 1.02. In 23 women, in vivo insulin sensitivity was also determined from the steady-state plasma glucose (SSPG) level at comparable insulin levels of approximately 100 .mu.U/ml attained by the i.v. infusion of somatostatin, glucose and insulin. Increasing WHR was accompanied by progressively increasing fasting plasma insulin levels (r = 0.47, P < 0.001), insulin and glucose areas after glucose challenge (r = 0.53, P < 0.001; r = 0.50, P < 0.001, respectively) and fasting plasma triglyceride concentrations (r = 0.48, P < 0.001). Obesity level was similarly correlated with these metabolic indices. Partial and multiple regression analysis and analysis of variance with a linear contrast model revealed that the effects of body fat topography were independent of, and additive to, those of obesity level. Within obese subjects alone (%IBW: 130), %IBW had no predictive value, but WHR remained a significant predictor of plasma glucose, insulin and triglyceride concentrations. The WHR also correlated with the plasma cholesterol level, but this association was largely dependent on its relationship to %IBW. Both WHR and %IBW correlated with the insulin resistance index, SSPG (r = 0.60, P < 0.01; r = 0.61, P < 0.01, respectively). After adjustment for the effects of %IBW, WHR was independently correlated with SSPG and after adjustment for WHR, %IBW correlated significantly with SSPG. The combined effects of WHR and %IBW were additive. The SSPG level, in turn, correlated with the fasting plasma insulin level (r = 0.89, P < 0.001), glucose area (r = 0.64, P < 0.01), insulin area (r = 0.52, P < 0.05) and fasting plasma triglyceride concentration (r = 0.62, P < 0.01). Significant interactions among these metabolic variables were also present. After adjustment for the effects of WHR and %IBW, the strength of these associations was greatly diminished, but the relationship between the SSPG and fasting plasma insulin levels and between the fasting plasma insulin level, insulin area, and fasting plasma triglyceride level remained significant. Apparently in obese premenopausal women, the sites of body fat localization and obesity level influence the degree of insulin sensitivity and, in turn, plasma glucose, insulin and lipid levels. Recognition of the sites of fat predominance hence may identify the susceptibility of obese women to insulin resistance and metabolic aberrations. Other factors, however, must also be considered.