The degree of hyperinsulinemia and impaired glucose tolerance predicts plasma leptin concentrations in women only: A new exploratory paradigm
The degree of hyperinsulinemia and impaired glucose tolerance predicts plasma leptin concentrations in women only: A new exploratory paradigm
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DOI：
10.1053/meta.2000.7745
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发表时间：
2000-08-01
影响因子：
9.8
通讯作者：
Maheux, P
中科院分区：
文献类型：
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作者：
Panarotto, D;Ardilouze, JL;Maheux, P
血浆瘦素已被证明与肥胖的许多指标以及胰岛素抵抗呈正相关。对于给定的体重，女性的这一水平高于男性，但造成这种差异的原因尚不清楚。在体内和体外，胰岛素已被证明能刺激脂肪组织产生瘦素。此前的研究报告称，糖尿病患者和非糖尿病患者的瘦素水平相似。然而，这些研究没有在新诊断的糖尿病患者中进行，其他变量(如性别)可能会混淆结果。因此，本横断面研究的目的是分别检测代谢变量(如血糖和胰岛素)对男性和女性血浆瘦素浓度的影响。我们测定了48名受试者(17名新诊断的2型糖尿病患者，13名糖耐量受损[IGT]患者和18名正常人)的瘦素水平。这三组在性别、年龄和体重指数(BMI)方面都很匹配。在调整了BMI和性别后，在3个糖耐量亚组中观察到了与性别相关的平均血浆瘦素差异(协方差分析P<；.03)。更具体地说，患有糖尿病或IGT的女性的血浆瘦素水平平均比正常女性低44%(P<；0.02)。在这些男性中，没有观察到这种组间差异。在同一女性亚组的单因素相关分析中，瘦素水平与空腹胰岛素呈正相关(r(S)=+.43，P&t；06)，与75g糖负荷后2小时血糖浓度呈负相关(r(S)=-.54，P&t；0.02)。在控制女性BMI的多元回归模型中，75g葡萄糖负荷后2小时的血胰岛素和血糖浓度是空腹血浆瘦素的良好预测因子(分别为r=+.38，P=0.02和r=-.70，P<0.01)。女性的瘦素水平似乎独立地并且在很大程度上受到环境血糖和血浆胰岛素浓度的影响。这些发现表明，女性脂肪组织合成瘦素比男性更容易受到胰岛素和葡萄糖体内调节的影响。IGT或2型糖尿病女性的血浆瘦素浓度也低于正常女性，这表明空腹和/或餐后高血糖仅在女性中干扰了血浆胰岛素对脂肪组织合成瘦素的刺激作用。版权所有(C)2000，由W.B.Saunders公司提供。
Plasma leptin has been shown to correlate positively with many indices of obesity, as well as insulin resistance. For a given body weight, the levels are higher in women than in men, but the reasons for this difference are not clear. Insulin has been shown to stimulate leptin production by adipose tissue in vivo and in vitro. Previous studies have reported that leptin levels are similar in diabetic and nondiabetic individuals. However, these studies were not performed in newly diagnosed diabetics, and other variables (such as gender) could have confounded the results. Therefore, the goal of the present cross-sectional study is to examine the effect of metabolic variables (such as glucose and insulin) on plasma leptin concentrations in men and women separately. We measured leptin levels in 48 subjects (17 with newly diagnosed type 2 diabetes mellitus, 13 with impaired glucose tolerance [IGT], and 18 normal individuals). The 3 groups were well matched for gender, age, and body mass index (BMI). When adjusted for the BMI and gender, a statistically significant gender-related difference in mean plasma leptin was observed across the 3 glucose tolerance subgroups (P < .03 by analysis of covariance [ANCOVA]). More specifically, plasma leptin levels were, on average, 44% lower in women with diabetes or IGT versus normal women (P < .02). No such between-group difference was observed in the men. In univariate analysis in the same female subgroup, plasma leptin correlated positively with fasting insulin (r(s) = +.43, P < .06) and negatively with 2-hour post-75-g glucose load plasma glucose concentration (r(s) = -.54, P < .02). In a multiple regression model controlling for the BMI in the female subgroup, circulating insulin and glucose concentrations 2 hours after the 75-g glucose load were good predictors of fasting plasma leptin (r = +.38, P = .02 and r = -.70, P < .001, respectively). Leptin levels in women appear to be influenced independently and to an important degree by ambient plasma glucose and plasma insulin concentrations. These findings suggest that the synthesis of leptin by adipose tissue is more susceptible to in vivo regulation by insulin and glucose in women than in men. Plasma leptin concentrations were also lower in women with IGT or type 2 diabetes versus normal women, suggesting that fasting and/or postprandial hyperglycemia interferes with the stimulatory effect of plasma insulin on the synthesis of leptin by adipose tissue in women only. Copyright (C) 2000 by W.B. Saunders Company.