|
Objective: Polycystic ovary syndrome (PCOS) is common in women of childbearing age, endocrine and reproductive function disorders, insulin resistance is a key part of its incidence the PCOS pathogenesis of familial aggregation suggesting that genetic factors play an important role in its pathogenesis . Adiponectin is an adipocytokine, has the role of improving insulin sensitivity. The purpose of this study is ① explore PCOS patients the relationship of serum adiponectin levels and insulin resistance, and the significance of determination of serum adiponectin levels in patients with PCOS; ② explore of Shandong Han adiponectin gene exons 2 rs2241766 45G15G (G / T) single nucleotide polymorphism (SNP) and the second intron rs1501299 276 (A / C) single nucleotide polymorphisms in the pathogenesis of PCOS. Method: select 48 cases of patients with PCOS according to the Rotterdam revised diagnostic criteria, 40 cases of the same period Select control, divided into obese group and non-obese group, as well as insulin resistance group with non-insulin-resistant group, determination of serum adiponectin levels and indicators of Endocrinology and Metabolism. The same diagnostic criteria to select 120 cases of PCOS patients concurrently choose to control the 120 cases, the use of the polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) method of adiponectin gene SNP 45G15G (G / T) and SNP 276 ( A / C) polymorphism genotyping analysis, comparing different genotypes between adiponectin levels and sugar, lipid metabolism indicators differences. Results: comparison of serum adiponectin levels: PCOS group than the control group (6.56 ± 3.30μg/ml vs 8.92 ± 4.99μg/ml, P <0.05); PCOS non-obese group than the control non-obese group (8.05 ± 3.49 μg / ml vs 11.52 ± 5.24μg/ml, P <0.05); insulin resistance group than in the non-insulin-resistant group (5.45 ± 3.24μg/ml vs 7.42 ± 3.14μg/ml, P <0.05). Serum adiponectin levels and body mass index (r = -0.491, P <0.01), fasting insulin levels (r = -0.516, P <0.01), HOMA-IR (r = -0.449, P <0.01), waist to hip ratio (r = -0.296, P <0.05), HOMA-IS (r = -0.242, P <0.05), triglycerides (r = -0.365, P <0.05) was negatively correlated with glucose insulin ratio (r = 0.390 , P <0.01), insulin sensitivity index (r = 0.463, P <0.01) were positively correlated. To control the influence of BMI, serum adiponectin levels are still with fasting insulin levels (r = -0.225, P <0.05), HOMA-IR (r = -0.283, P <0.05), triglycerides (r = -0.382, P <0.05) was negatively associated with glucose insulin ratio (r = 0.366, P <0.01), insulin sensitivity index (r = 0.372, P <0.01) were positively correlated. Adiponectin gene SNP 45G15G (G / T) and SNP 276 (A / C) with PCOS correlation (P = 0.021, OR = 1.629,95% CI = 1.074-2.469; P = 0.015, OR = 1.576, CI = 1.091-2.279). The PCOS patients adiponectin gene SNP 45G15G (G / T) point of G / G genotype compared with T / T and T / G genotype insulin area under the curve was significantly higher (250.78 ± 207.11 vs 154.84 ± 95.32, P <0.05); PCOS patients SNP 276 (A / C) the locus C / C and C / A genotype compared with A / A genotype serum adiponectin levels (6.05 ± 3.16μg/ml vs 8.96 ± 3.21μg/ml, P <0.05) and glucose insulin ratio (vs18.93 ± 12.32, 13.00 ± 6.85, P <0.01) significantly reduced fasting insulin levels (8.82 ± 5.54 vs 6.00 ± 2.77mIU / L, P <0.05) and HOMA-IR (1.95 ± 1.30 vs 1.25 ± 0.53, P <0.05) were significantly higher. Conclusion: ① PCOS patients hypoadiponectinemia adiponectin levels and insulin resistance were negatively correlated. ② adiponectin gene SNP 45G15G (G / T) and SNP 276 (A / C) Polymorphism and people pathogenesis of PCOS correlation, SNP 276 (A / C) be affected by the change of serum adiponectin levels PCOS the patient's insulin sensitivity, the genetic susceptibility of insulin resistance in the pathogenesis of PCOS. ③ adiponectin may be a predictor of long-term complications of type 2 diabetes in patients with PCOS, low adiponectin levels and the presence of adverse genotypes PCOS patients should strengthen the follow-up, to prevent abnormal glucose metabolism and Progress.
|