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目的研究多囊卵巢综合征(polycystic Ovary Syndrome,PCOS)合并胰岛素抵抗(insulin resistance,IR)患者脂肪组织中瘦素受体下游信号转导分子-JAK2蛋白和STAT3蛋白的表达水平及其磷酸化程度,深入探讨PCOS患者合并胰岛素抵抗时存在瘦素抵抗的分子作用机制。方法采用酶联免疫吸附测定法(ELISA)检测PCOS伴随IR患者共23例(观察A组)、PCOS不伴随IR患者共18例(观察B组)以及因单纯性子宫肌瘤而就诊的患者共23例(对照组)的血清瘦素表达水平;采用放射免疫分析法(radioimmunoassay,RIA)检测各组患者空腹血清胰岛素(fasting insulin,FIN)水平;采用葡萄糖氧化酶法(glucose oxidase method)测定各组空腹血糖(fasting plasma glucose,FPG)水平,利用稳态模型(homeostasis model assessment,HOMA)评价并计算IR指数(HOMA-IR);采用蛋白质免疫印迹法(Western Blot,WB)测定各组患者脂肪组织中JAK2和STAT3的蛋白表达水平及其磷酸化程度。结果 1观察A组患者血清瘦素表达水平为(19.63±4.16)g/L,显著高于观察B组和对照组(P<0.01);与对照组相比较,观察B组血清瘦素表达水平未发现显著差异(P>0.05)。PCOS患者血清瘦素水平与HOMA-IR呈正相关(r=0.707,P<0.01);2观察A组JAK2和STAT3的蛋白表达分别为1.42±0.26和2.33±0.47,观察B组分别为1.36±0.18和2.10±0.24,对照组分别为1.29±0.11和2.45±0.36,3组间比较,差异均无统计学意义(P>0.05);3观察A组JAK2和STAT3蛋白酪氨酸磷酸化程度分别为1.87±0.16和3.32±0.17,均明显低于观察B组和对照组(P<0.01);观察B组与对照组比较,差异无统计学意义(P>0.05)。结论 PCOS合并IR患者可能同时存在瘦素抵抗,其原因可能与瘦素信号转导分子JAK2蛋白和STAT3蛋白磷酸化程度的降低有关。
Objective To investigate the expression of leptin receptor downstream signal transduction molecules-JAK2 and STAT3 in adipose tissue of patients with polycystic ovarian syndrome (PCOS) and insulin resistance (IR) and their phosphorylation To investigate the molecular mechanism of leptin resistance in PCOS patients with insulin resistance. Methods Twenty-three patients with PCOS accompanied by IR (Group A), 18 patients with PCOS without IR (Group B), and patients with simple myoma of uterus were enrolled in the study. The levels of serum leptin were detected in 23 patients (control group). Fasting insulin (FIN) levels were measured by radioimmunoassay (RIA) in each group. Glucose oxidase method The level of fasting plasma glucose (FPG) was measured and homeostasis model assessment (HOMA) was used to evaluate the IR index (HOMA-IR). The levels of adipocytes in each group were measured by Western Blot (WB) The protein expression and phosphorylation of JAK2 and STAT3 in tissues. Results 1 The level of serum leptin in group A was (19.63 ± 4.16) g / L, which was significantly higher than that in group B and control (P <0.01). Compared with the control group, the level of serum leptin No significant difference was found (P> 0.05). The level of serum leptin in PCOS patients was positively correlated with HOMA-IR (r = 0.707, P <0.01) .2 The protein expressions of JAK2 and STAT3 in group A were 1.42 ± 0.26 and 2.33 ± 0.47 respectively, and in group B it was 1.36 ± 0.18 And 2.10 ± 0.24 in the control group and 1.29 ± 0.11 and 2.45 ± 0.36 in the control group, respectively. There was no significant difference between the three groups (P> 0.05) .3 The levels of tyrosine phosphorylation of JAK2 and STAT3 in group A were 1.87 ± 0.16 and 3.32 ± 0.17, respectively, which were significantly lower than those in the observation group B and the control group (P <0.01). There was no significant difference between the observation group B and the control group (P> 0.05). Conclusions Leptin resistance may exist in patients with PCOS complicated with IR. The reason may be related to the decrease of the phosphorylation of JAK2 protein and STAT3 protein in leptin signaling transducers.