Adiponectin and resistin serum levels in women with polycystic ovary syndrome during oral glucose tolerance test: A significant reciprocal correlation between adiponectin and resistin independent of insulin resistance indices

Adiponectin and resistin serum levels in women with polycystic ovary syndrome during oral glucose tolerance test: A significant reciprocal correlation between adiponectin and resistin independent of insulin resistance indices
复制标题

DOI:
10.1016/j.ymgme.2004.12.014
复制
发表时间:
2005-05-01
影响因子:
3.8
通讯作者:
Lewinski, A
Lewinski, A
中科院分区:
生物学2区
文献类型:
--
作者:
Lewandowski, KC;Szosland, K;Lewinski, A

文献摘要

被引文献

相似文献

多囊卵巢综合征(PCOS)与胰岛素抵抗(IR)、肥胖和2型糖尿病的发病率增加有关。抵抗素,一种脂肪细胞因子,可能代表肥胖和这些代谢紊乱之间的联系。也有证据表明,炎症是人类的一种高抵抗状态,抵抗素的细胞因子诱导可能导致内毒素血症、肥胖和其他炎症状态下的胰岛素抵抗。相反,在动脉粥样硬化小鼠模型中,脂联素增加胰岛素敏感性,改善葡萄糖耐量,抑制炎症途径,而腺病毒表达的脂联素减少动脉粥样硬化病变。我们的目的是评估PCOS女性患者脂联素和抵抗素与IR指标之间是否存在关系,以及这些脂肪细胞因子的血清水平是否会因葡萄糖诱导的高胰岛素血症而改变。19例PCOS女性,年龄36.3 +/- 11.4岁(平均+/- SD),体重指数(BMI) 29.3 +/- 7.7 kg/m(2),在75 g口服糖耐量试验(OGTT)进行0、60和120 min时测定血清抵抗素和脂联素水平,并与HOMA-IR、QUICKI等IR指标及OGTT期间葡萄糖和胰岛素水平计算的胰岛素抵抗指数相关。抵抗素浓度在OGTT 0、60和120 min时分别为7.31 +/- 4.58、7.47 +/- 5.40、7.22 +/- 5.12 pg/ml, P = 0.77),但脂联素浓度在OGTT 120 min时从基线的11.32 +/- 4.64 μ g/ml增加到14.78 +/- 7.41 μ g/ml (P < 0.01)。在60 ~ 120 min,脂联素的总体上升幅度更大(从12.31 +/- 5.72到14.78 +/- 7.41 μ g/ml, P < 0.006)。抵抗素和脂联素与多囊卵巢综合征的IR、脂质指数或其他激素参数均无相关性。然而,血清抵抗素和脂联素之间存在显著的负相关(P = 0.001)。总之,我们观察到血清脂联素和抵抗素之间存在很强的负相关,尽管与IR指标缺乏直接相关性。鉴于抵抗素和脂联素在炎症过程中的相反作用,我们推测脂联素与抵抗素的相对比例可能独立于IR参数影响PCOS女性的心脏代谢风险。OGTT期间观察到的脂联素增加需要进一步研究。(c) 2005爱思唯尔公司版权所有。
Polycystic ovary syndrome (PCOS) is associated with an increased incidence of insulin resistance (IR), obesity, and type 2 diabetes. Resistin, an adipocytokine, may represent a link between obesity, and these metabolic disorders. There is also evidence that inflammation is a hyperresistinemic state in humans, and cytokine induction of resistin may contribute to insulin resistance in endotoxemia, obesity, and other inflammatory states. In contrast, adiponectin, increases insulin sensitivity, improves glucose tolerance, inhibits inflammatory pathways, while adenovirus-expressed adiponectin reduces atherosclerotic lesions in a mouse model of atherosclerosis. We aimed to assess, in women with PCOS, whether there is a relationship between adiponectin and resistin and the indices of IR, and whether serum levels of these adipocytokines are altered by glucose-induced hyperinsulinaemia. Serum levels of resistin and adiponectin were measured at 0, 60, and 120 min during 75 g oral glucose tolerance test (OGTT), in 19 women with PCOS, age 36.3 +/- 11.4 years (mean +/- SD), body mass index (BMI) 29.3 +/- 7.7 kg/m(2), and correlated with the indices of IR, such as HOMA-IR, QUICKI, and the insulin resistance index calculated from glucose and insulin levels obtained during OGTT. There was no change in resistin concentrations (7.31 +/- 4.58, 7.47 +/- 5.40, 7.22 +/- 5.12 pg/ml, at 0, 60, and 120 min of OGTT, respectively, P = 0.77), but there was an increase in adiponectin from 11.32 +/- 4.64 mu g/ml at baseline to 14.78 +/- 7.41 gg/ml, at 120 min of OGTT (P < 0.01). The magnitude of the overall rise in adiponectin was greater from 60 to 120 min (from 12.31 +/- 5.72 to 14.78 +/- 7.41 mu g/ml, P < 0.006). Neither resistin, nor adiponectin correlated with the indices of IR, lipids, or other hormonal parameters of the PCOS. There was, however, a significant negative correlation between serum resistin and adiponectin (P = 0.001). In conclusion, we observed a strong negative correlation between serum adiponectin and resistin, despite the lack of direct correlation with the indices of IR. Given the opposite effects of resistin and adiponectin on the inflammatory process, we speculate that relative proportion of adiponectin-to-resistin might potentially influence cardiometabolic risk in women with the PCOS independently of IR parameters. The observed increase in adiponectin during OGTT requires further study. (c) 2005 Elsevier Inc. All rights reserved.