Insulin regulation of leptin synthesis and secretion in humans:: the model of myotonic dystrophy
Insulin regulation of leptin synthesis and secretion in humans:: the model of myotonic dystrophy
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DOI：
10.1046/j.1365-2265.1999.00675.x
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发表时间：
1999-05-01
影响因子：
3.2
通讯作者：
Soler, J
中科院分区：
文献类型：
--
作者：
Gómez, JM;Molina, A;Soler, J
目的 强直性肌营养不良 (MyD) 是一种众所周知的胰岛素抵抗全身性疾病。在本研究中，我们对 MyD 患者以及年龄、性别和体重指数 (BMI) 匹配的对照者的血浆瘦素水平进行了表征，并评估了瘦素对 MyD 临床表现的影响。 设计和患者 在 34 名 MyD 患者和 33 名对照者中研究了身体成分、血浆瘦素、空腹和口服葡萄糖耐量试验胰岛素、IGF-I 和 IGFBP3。通过IRMA或PIA测量胰岛素、瘦素、IGF-I、IGFBP3的水平。胰岛素敏感性根据稳态模型评估 (HOMA) 计算机求解模型进行建模。 结果 患者体脂百分比高于对照组（25.6 +/- 2.28% vs 18.8 +/- 1.53%，P=0.013）。患者的空腹和口服葡萄糖后的胰岛素水平均高于对照组，而患者的胰岛素敏感性低于对照组。患者的血清瘦素水平高于对照组（20.98 +/- 3.11% mu g/l vs 10.4 +/- 1.31 mu g/l，P = 0.004），并且无论是患者还是对照组，女性的血清瘦素水平均高于男性。在患者中，瘦素水平与年龄、体重指数、空腹胰岛素、胰岛素曲线下面积和较低的胰岛素敏感性相关，而瘦素水平与体脂或身体成分的其他参数不相关。在对照组中，瘦素水平与体重指数和体脂相关。使用逻辑回归模型对 2 个人群中的每一个人群的结果进行评估。在 MyD 模型中，87.88% 的患者中，胰岛素抵抗和年龄正确地识别出与对照组相比更高的瘦素水平；在与 BMI 呈负相关的对照男性模型中，84.33% 的患者正确识别了他们的瘦素水平。 结论 这些发现表明，MyD 为人类提供了不同的瘦素调节模型，并表明在 MyD 患者中，瘦素与胰岛素抵抗和年龄之间存在相关性，而与身体无关脂肪。相比之下，对照组的瘦素水平与性别和体重指数相关。该患者群体的瘦素数据在病因学上与肌肉疾病本身无关。
OBJECTIVE Myotonic dystrophy (MyD) is a systemic disorder in which insulin resistance is well recognized. In the present study we have characterized plasma leptin levels in patients with MyD and in age, sex and body mass index (BMI) matched controls and assessed the influence of leptin on the clinical manifestations of MyD.DESIGN AND PATIENTS Body composition, plasma leptin, fasting and post-oral glucose tolerance test insulin, IGF-I and IGFBP3 were studied in 34 MyD patients and 33 controls.MEASUREMENTS Body composition was measured using a bioelectrical impedance analyzer, and circulating levels of insulin, leptin, IGF-I, IGFBP3 were measured by IRMA or PIA. Insulin sensitivity was modelled according to a homeostasis model assessment (HOMA) computer-solved model.RESULTS Percentage body fat was higher in patients than in controls (25.6 +/- 2.28% vs 18.8 +/- 1.53%, P=0.013). Insulin levels, both fasting and after oral glucose were higher in patients than in controls, and insulin sensitivity was lower in patients than in controls. Serum leptin was higher in patients than in controls (20.98 +/- 3.11% mu g/l vs 10.4 +/- 1.31 mu g/l, P = 0.004), and higher in women than in men, both in patients and in controls. In patients, leptin levels were correlated with age, BMI, fasting insulin, insulin area under curve and lower insulin sensitivity, whereas leptin levels were not correlated with body fat or other parameters of body composition. In controls, leptin levels were correlated with BMI and body fat. The results were evaluated using logistic regression models for each of the 2 populations. In the model of MyD, insulin resistance and age correctly identified higher leptin levels in relation to controls out of 87.88% of patients, and in the model of controls male sex with a negative correlation and BMI correctly identified their leptin levels out of 84.33% cases.CONCLUSIONS These findings show that MyD provides a different model of leptin regulation in humans, and suggest that in MyD patients there are correlations between leptin and insulin resistance and age, irrespective of body fat. In contrast, leptin levels in controls, correlate with sex and BMI. The data on leptin in this population of patients can not be related aetiologically to the muscle disease itself.