不同体重指数患者卵巢彩色多普勒参数与糖代谢的相关性分析

目的:探讨不同体重指数(BMI)的多囊卵巢综合征(PCOS)患者的彩色多普勒参数与糖代谢指标的相关性。方法:选取就诊的初诊PCOS患者108例,按BMI分为23kg/m2组(正常体重组,31例)、23~24.9kg/m~2组(肥胖前期组,19例)、≥25kg/m~2组(肥胖组,58例)。监测3组患者的糖代谢指标和彩色多普勒参数,分析各组患者超声参数与糖代谢各指标之间的相关性。结果:与正常体重组相比,肥胖前期组的胰岛素释放试验异常率显著增加(P0.05),而超声参数无差异;肥胖组的胰岛素释放试验异常率及糖耐量异常率(IGT)均显著增高,超声参数卵巢体积(OV)显著增高,搏动指数(PI)显著降低,差异有统计学意义(P0.05)。相关性分析显示,正常体重组患者的彩超参数与各糖代谢指标无显著相关;肥胖前期组的OV与卵泡个数(FN)均与2h血浆血糖(PG)呈正相关,PI与1h PG、葡萄糖曲线下面积(GAUC)、1h胰岛素(INS)、胰岛素曲线下面积(IAUC)呈负相关;肥胖组PCOS患者OV与1h PG、1h INS呈正相关,FN与FINS、1h INS、2h INS、IAUC呈正相关,Vs、Vd与2h PG呈正相关,PI、RI均与2h INS、IAUC呈负相关。结论:肥胖PCOS患者彩色多普勒超声参数与糖代谢指标具有明显的相关性。     

β细胞营养因子与多囊卵巢综合征相关性的临床研究

目的探讨β细胞营养因子与多囊卵巢综合征(PCOS)的相关关系。方法选取PCOS患者和非PCOS对照组各40名作为研究对象,测定性激素六项、生化指标及β细胞营养因子水平。PCOS患者给予屈螺酮炔雌醇及二甲双胍治疗3个月后复查上述各项指标,比较治疗前、后的变化。结果 (1)PCOS患者的体质量指数(BMI)、腰臀比(WHR)、甘油三酯(TG)、胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、空腹胰岛素(FINS)、胰岛素评价指数(HOMA-IR)、胰岛β细胞分泌指数(HOMA-β)、黄体生成素(LH)、睾酮(T)、β细胞营养因子水平均高于对照组。(2)PCOS肥胖者(BMI≥25 kg/m2)的空腹血糖(FBS)、1 h血糖(BS 60 min)、2 h血糖(BS 120 min)、FINS、1 h胰岛素(INS 60 min)、2 h胰岛素(INS 120 min)、3 h胰岛素(INS 180 min)、HOMA-IR、HOMA-β均高于非肥胖者。(3)PCOS肥胖组的β细胞营养因子水平明显高于PCOS非肥胖组及对照组。β细胞营养因子与年龄、BMI、T水平呈正相关(r=0.271,r=0.262,r=0.158,P=0.023,P=0.015,P=0.026),与WHR、FINS、HOMA-IR、HOMA-β水平呈负相关(r=-0.321,r=-0.076,r=-0.156,r=-0.027,P=0.021,P=0.003,P=0.006,P=0.012)。(4)PCOS患者应用屈螺酮炔雌醇及二甲双胍治疗后BMI、WHR、TG、TC、LDL-C、FINS、HOMA-IR、HOMA-β、LH、T、β细胞营养因子水平均比治疗前降低。结论 PCOS患者β细胞营养因子水平明显升高。屈螺酮炔雌醇与二甲双胍联合应用能有效地改善胰岛素抵抗,降低β细胞营养因子水平,是治疗PCOS较为有效的方法。     

血清促生长激素释放激素受体配体与多囊卵巢综合征的相关性分析

目的:探讨血清促生长激素释放激素受体配体(Ghrelin)水平在多囊卵巢综合征(PCOS)中的意义.方法:选择我院PCOS患者48例作为研究对象(PCOS组),同期选择非PCOS患者40例作为对照(对照组),根据体重指数(IBM)将PCOS组、对照组患者分别分为肥胖与非肥胖,根据稳态模型胰岛素抵抗指数(HOMA-IR)将PCOS组及全部患者分为胰岛素抵抗(IR)与非IR.测定血清Ghrelin水平及内分泌代谢指标.结果:血清Ghrelin水平PCOS组低于对照组(P<0.05);肥胖组低于非肥胖组(P<0.05);非肥胖组低于非肥胖对照组(P<0.05);IR组低于非IR组(P<0.05).血清Ghrelin水平与BMI、空腹胰岛素(FINS)、HOMA-IR呈负相关(P<0.01,P<0.05,P<0.05),与胰岛素敏感指数(ISI)呈正相关(P<0.05).结论:PCOS患者存在血清低Ghrelin水平,Ghrelin水平与BMI、IR程度呈负相关.Ghrelin可能与PCOS的肥胖发生有相关性.血清Ghrelin检测可能作为预测PCOS患者IR的一个指标.     

多囊卵巢综合征患者脂联素、C反应蛋白水平的变化及其意义

目的:探讨脂联素(APN)、C反应蛋白(CRP)的变化对多囊卵巢综合征(PCOS)发病的意义。方法:按体重指数(BMI≥25kg/m2或<25kg/m2)分别将PCOS患者52例、对照组47例分为PCOS肥胖组(25例)、非肥胖组(27例)和对照肥胖组(23例)、对照非肥胖组(24例)4组。用ELISA法测定4组的APN水平、散射比浊法测CRP水平,葡萄糖氧化酶法测定空腹血糖(FPG)、化学发光法测空腹胰岛素(FIN)水平,并计算胰岛素抵抗指数(HOMA-IR)。结果:①PCOS组APN水平低于对照组(P<0.05),且同组肥胖者低于非肥胖者。②PCOS组CRP水平高于对照组(P<0.05),且肥胖者高于非肥胖者。③APN水平与BMI、HOMA-IR水平呈明显负相关(P<0.05)。结论:PCOS组APN水平降低,CRP水平升高,且以肥胖者明显。APN水平降低、CRP水平升高与PCOS患者胰岛素抵抗密切相关。     

肥胖与非肥胖多囊卵巢综合征患者血清肿瘤坏死因子-α(TNF-α)水平的比较

目的:比较肥胖与非肥胖多囊卵巢综合征(PCOS)患者血清肿瘤坏死因子-α(TNF-α)水平的差异。方法:55例PCOS患者,根据体质量指数(BMI)分为肥胖组(BMI>25,n=31)和非肥胖组(BMI≤25,n=24);同期选择50例非PCOS育龄妇女,分为肥胖对照组(BMI>25,n=25)和非肥胖对照组(BMI≤25,n=25)。应用酶联免疫吸附法(ELISA)测定血清TNF-α的含量,分析TNF-α与胰岛素抵抗指数(HOMA-IR)的相关性。结果:PCOS肥胖组与PCOS非肥胖组的TNF-α水平分别显著高于其相应的对照组(P<0.01),PCOS非肥胖组的TNF-α水平也显著高于肥胖对照组(P<0.05)。PCOS肥胖组与PCOS非肥胖组之间的TNF-α水平无显著差异(P>0.05)。PCOS组TNF-α与HOMA-IR呈显著正相关(P<0.05)。结论:肥胖与非肥胖PCOS患者的血清TNF-α水平均升高,可能存在肥胖以外升高TNF-α的途径;TNF-α与PCOS的IR发生有密切联系。     

妊娠期糖尿病患者血清网膜素水平与糖、脂代谢指标的相关性研究

目的:探讨妊娠期糖尿病(GDM)患者血清网膜素(Omentin)水平的变化及其与糖、脂代谢指标的相关性。方法:采用酶联免疫吸附法检测35例孕前肥胖的GDM孕妇(A组)、32例孕前非肥胖的GDM孕妇(B组)、36例正常健康孕妇(C组)的血清Omentin水平;同时测定所有受试者的糖、脂生化指标,并计算胰岛素抵抗指数(HOMA-IR)。结果:(1)GDM孕妇三酰甘油(TG)、空腹血糖(FPG)、空腹胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)水平均高于正常对照组,高密度脂蛋白(HDL-C)水平低于正常对照组(P均<0.05);(2)3组孕妇血清Omentin水平A组相似文献   

PCOS患者血清HSP70、炎症-氧化应激指标表达及与胰岛素抵抗的关系

目的探讨多囊卵巢综合征(PCOS)患者血清热休克蛋白-70(HSP-70)、炎症-氧化应激指标表达及与胰岛素抵抗(IR)的关系。方法选取PCOS患者126例为PCOS组,根据体重指数(BMI)分为PCOS-A组(BMI25 kg/m~2,n=60)和PCOS-B组(BMI≥25 kg/m~2,n=66),同期健康体检者60例为正常对照组(NC组)。检测并比较两组的BMI、腰臀比(WHR)、糖代谢指标、血清HSP-70、炎症标记物、氧化应激标记物。结果 PCOS组的血清HSP-70、MCP-1、IL-6、IL-18、TNF-α、MDA水平显著高于NC组,SOD、GSH-Px显著低于NC组(P0.05)。血清HSP-70与FPG、2 h PG、FINS、HOMA-IR、MCP-1、IL-6、IL-18、TNF-α、MDA呈显著正相关性,与SOD、GSH-Px呈显著负相关性(P0.05);且HOMA-IR与MCP-1、IL-6、IL-18、TNF-α、MDA呈显著正相关性,与SOD、GSH-Px呈显著负相关性(P0.05)。结论 PCOS患者存在血清HSP-70高表达,且与糖代谢紊乱、IR、慢性炎症及氧化应激反应密切相关,可能参与PCOS的发生及发展过程。     

妊娠糖尿病患者血清Omentin-1、IRS-1、IRS-2与胰岛素抵抗的关系

目的探讨妊娠糖尿病(GDM)患者血清Omentin-1、IRS-1、IRS-2水平变化及与胰岛素抵抗(IR)的关系。方法 92例GDM患者(GDM组)根据体重指数(BMI)分为肥胖组(OB组,n=55)与非肥胖组(NOB组,n=37),同期健康妊娠糖耐量(NGT)正常孕妇(NGT组)分为OB组(n=52)和NOB组(n=40)。检测比较各组的HOMA-IR、Omentin-1、IRS-1、IRS-2。结果① GDM-OB组孕前BMI、糖代谢指标与GDM-NOB组比较差异显著(P0.05);GDM-OB组FINS、HOMA-IR、IRS-2显著高于GDM-NOB组(P0.05),GDM-NOB组显著高于NGT组(P0.05),Omentin-1、IRS-1及IRS-1/2则显著降低(P0.05);② Pearson相关性分析及校正年龄和BMI后偏向关系分析显示,Omentin-1仍与FPG、FINS、HOMA-IR、IRS-2呈显著负相关性(P0.05),与IRS-1、IRS-1/2呈显著正相关性(P0.05)。结论 Omentin-1与GDM及其IR密切相关,Omentin-1低表达提示糖代谢紊乱及IR,其作用机制可能与IRS-1/IRS-2信号通路有关。     

PCOS合并糖代谢异常患者内脏脂肪与脂联素及肿瘤坏死因子-α的相关性研究

目的:探讨多囊卵巢综合征(PCOS)合并糖代谢异常患者内脏脂肪与血清脂肪因子脂联素(APN)、肿瘤坏死因子α(TNF-α)的相关性。方法:选择在我院门诊确诊PCOS患者37例,其中合并糖代谢异常患者20例(P-IGT组),糖代谢正常患者17例(P-NGT组),另选18例健康同龄女性作为正常对照组,检测其空腹血糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、血清胰岛素(FINS)、APN、TNF-α、白介素6(IL-6)水平等;按稳态模型计算胰岛素抵抗指数(HOMA-IR);采用双能X线骨密度仪检测全身脂肪含量及内脏脂肪面积(VATA)。结果:1P-IGT组血清FINS及HOMA-IR水平明显高于P-NGT组及正常对照组(P0.01);P-IGT组APN水平明显低于P-NGT组及正常对照组(P0.01);P-IGT组TNF-α明显高于P-NGT组及正常对照组(P0.05,P0.01);IL-6在3组之间差异无统计学意义(P0.05)。2P-IGT组的全身脂肪含量明显高于P-NGT组及正常对照组(P0.01);P-IGT组与P-NGT组VATA均显著高于正常对照组(均P0.01)。APN与FINS、体质量指数(BMI)、腰臀比(WHR)、HOMA-IR、全身脂肪含量、VATA呈负相关(r=-0.306,-0.617,-0.356,-0.343,-0.520,-0.405,均P0.05);TNF-α与FINS、BMI、HOMA-IR、TG、全身脂肪含量、VATA呈正相关(r=0.309,0.351,0.255,0.268,0.465,0.362,均P0.05)。APN、TNF-α是VATA的重要影响因素。结论:PCOS患者无论有否糖代谢异常均出现VATA明显增加,而合并糖代谢异常者全身脂肪含量及VATA均增加。PCOS患者合并糖代谢异常与内脏脂肪组织分泌肿瘤坏死因子-α增多及APN分泌减少有关。     

不同胰岛素增敏剂对多囊卵巢综合征代谢异常的疗效比较

目的:比较二甲双胍与罗格列酮治疗多囊卵巢综合征(PCOS)内分泌、代谢异常的疗效。方法:将89例PCOS患者分成A、B两组,A组予二甲双胍,B组予罗格列酮,均连用6个月。观察患者用药前后的体重、生殖激素、血糖和胰岛素水平的变化。结果:用药6月A组患者体重下降,B组体重上升,两组LH、LH/FSH、T均下降,治疗前后比较差异有显著性(P<0.05);B组T的下降幅度比A组明显(P<0.05)。A、B组空腹胰岛素(FINS)、餐后2小时胰岛素、胰岛素抵抗指数(Homa IR)均下降,治疗前后比较差异有显著性(P<0.05)。FINS、2小时INS以及Homa IR下降程度均表现为:罗格列酮>二甲双胍(P<0.05)。结论:罗格列酮比二甲双胍更能改善PCOS患者的胰岛素抵抗,而且无胃肠副反应,但价格较贵、起效较慢和引起体重增加,而二甲双胍有减轻体重的作用。     

The relationship between metabolic status and levels of adiponectin and ghrelin in lean women with polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is commonly associated with insulin resistance, obesity, dyslipidemia and hypertension. Adiponectin, an adipocyte-specific protein with important roles in glucose and lipid homeostasis, possesses antidiabetic and insulin-sensitizing properties. Ghrelin, a protein ligand for the growth hormone secretagog receptor, has been shown to stimulate food intake and to influence energy balance, insulin signaling and glucose metabolism. We aimed to evaluate the relationships between metabolic alterations and adiponectin and ghrelin levels in lean PCOS women, compared with lean and obese women. The study was carried out on 20 non-obese PCOS women aged 20 – 48 years and age-matched groups of 45 healthy lean and 37 obese women. Hormonal and biochemical parameters, adiponectin and ghrelin concentrations and anthropometric data were determined. In PCOS subjects, we found increased homeostasis model assessment – insulin resistance index (HOMA-IR) with non-significant differences in adiponectin and ghrelin concentrations compared with healthy women, although the PCOS group showed a tendency to lower adiponectin levels. However, ghrelin levels in PCOS women were significantly higher than in obese women. Moreover, we observed a negative correlation between adiponectin and testosterone, cholesterol, triglycerides, glucose and diastolic blood pressure in PCOS. In conclusion, it can be suggested that higher values of HOMA-IR with lower adiponectin levels may indicate future development of metabolic syndrome or other metabolic disturbances in lean PCOS women.     

The relationship between metabolic status and levels of adiponectin and ghrelin in lean women with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is commonly associated with insulin resistance, obesity, dyslipidemia and hypertension. Adiponectin, an adipocyte-specific protein with important roles in glucose and lipid homeostasis, possesses antidiabetic and insulin-sensitizing properties. Ghrelin, a protein ligand for the growth hormone secretagog receptor, has been shown to stimulate food intake and to influence energy balance, insulin signaling and glucose metabolism. We aimed to evaluate the relationships between metabolic alterations and adiponectin and ghrelin levels in lean PCOS women, compared with lean and obese women. The study was carried out on 20 non-obese PCOS women aged 20 - 48 years and age-matched groups of 45 healthy lean and 37 obese women. Hormonal and biochemical parameters, adiponectin and ghrelin concentrations and anthropometric data were determined. In PCOS subjects, we found increased homeostasis model assessment - insulin resistance index (HOMA-IR) with non-significant differences in adiponectin and ghrelin concentrations compared with healthy women, although the PCOS group showed a tendency to lower adiponectin levels. However, ghrelin levels in PCOS women were significantly higher than in obese women. Moreover, we observed a negative correlation between adiponectin and testosterone, cholesterol, triglycerides, glucose and diastolic blood pressure in PCOS. In conclusion, it can be suggested that higher values of HOMA-IR with lower adiponectin levels may indicate future development of metabolic syndrome or other metabolic disturbances in lean PCOS women.     

Can adiponectin predict abnormal glucose tolerance in Thai women with polycystic ovary syndrome?

AIM: To evaluate whether adiponectin levels could predict abnormal glucose tolerance (AGT) in Thai women with polycystic ovary syndrome (PCOS). METHODS: A 75-g oral glucose tolerance test (OGTT) with fasting adiponectin and insulin (FI) blood sampling in 170 women with PCOS were performed consecutively. RESULTS: The prevalence of AGT was 45.9%. The body mass index (BMI), waist-to-hip ratio (WHR), fasting glucose and 2-h postload glucose were greater in the PCOS women with AGT than those without AGT (P<0.001). In addition, the PCOS women with AGT had more severe insulin resistance (IR) and lower adiponectin levels than those without AGT. However, the area under the ROC curve of adiponectin and insulin in predicting AGT was smaller than that of homeostatic model of IR (HOMA-IR) (P<0.01). The arbitrary cut-off values at 12 ug/mL of adiponectin, 10 microiu/mL of FI and 2 of HOMA-IR showed the sensitivity and specificity of 80.8% and 33.7%; 87.2% and 34.8%; and 89.7% and 31.5%, respectively. With these cut-off points, 46 (27.1%), 42 (24.7%) and 37 (21.8%) women, respectively, could be eliminated from performing OGTT. However, 15 (19.2%), 10 (12.8%) and 8 (10.3%), respectively, missed the diagnosis. In addition, with WHR and acanthosis nigricans adjustment, HOMA-IR, but not adiponectin, was a significant predictor of AGT. CONCLUSION: Our study demonstrated that almost half of the women with PCOS had AGT. Adiponectin levels were significantly lower in the PCOS women with AGT than those without AGT. However, adiponectin was not shown to be as strong a predictive factor and might not be such an excellent screening test as FI and HOMA-IR.     

Frequency of adiponectin gene polymorphisms in polycystic ovary syndrome and the association with serum adiponectin,androgen levels,insulin resistance and clinical parameters

Aim.?Although the association between adiponectin gene polymorphisms and insulin resistance has been investigated in many studies, there are only a few studies, which have investigated adiponectin gene polymorphisms in patients with polycystic ovary syndrome (PCOS). The objectives of this study were to determine the frequency of T45G polymorphisms localised in exon 2 of the adiponectin gene in a Turkish population with PCOS and to determine the association of T45G polymorphisms with insulin resistance and serum adiponectin levels in PCOS.

Materials and methods.?Ninety-six patients with PCOS and 93 healthy control subjects were included in the study. Insulin resistance was estimated via HOMA-IR. Serum adiponectin levels were measured by ELISA. For determination of adiponectin gene polymorphisms, PCR was performed with appropriate primers after genomic DNA was obtained from the peripheral blood of the patients and control subjects.

Results.?Adiponectin levels were low in patients with PCOS than control subjects. There was no significant statistical difference between the PCOS and control groups with respect to the frequency of polymorphisms and the genotype distribution. Adiponectin gene polymorphisms were not associated with the anthropometric parameters, hyperandrogenism and adiponectin levels in PCOS. However, the fasting insulin level and insulin resistance were significantly higher and more frequent, respectively, in the polymorphic group compared to the other genotypes among patients with PCOS.

Conclusion.?The risk of PCOS, hyperandrogenism in patients with PCOS and low serum adiponectin levels cannot be directly attributed to T45G adiponectin gene polymorphisms in exon 2, rather these polymorphisms may be associated with insulin resistance and hyperinsulinemia in PCOS.     

Adiponectin is an independent determinant of insulin resistance in women with polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCOS) is frequently associated with insulin resistance and a consequent increased risk of metabolic diseases. The aim of the present study was to investigate the role of adiponectin in insulin resistance in PCOS women. MATERIALS AND METHODS: Forty-seven patients with PCOS and 23 control subjects, matched for age and body mass index (BMI), were enrolled in the study. Clinical, metabolic and hormonal parameters and adiponectin levels were measured, and HOMA-IR score (homeostasis model assessment-insulin resistance index) was calculated for each subject. RESULTS: There was no difference in adiponectin levels between PCOS patients and the control group. However, adiponectin levels were negatively correlated with obesity-associated parameters and HOMA-IR score in PCOS patients and controls. As adiponectin is modulated by BMI we adjusted for BMI among the PCOS patients, and found a negative correlation between adiponectin levels and HOMA-IR score (r = -0.51, p < 0.001). Adiponectin and BMI were independent determinants of insulin resistance in PCOS patients (adjusted R2 = 0.66, p < 0.001). CONCLUSION: Adiponectin did not seem to be actively involved in the pathogenesis of PCOS. However, adiponectin levels were independently associated with insulin resistance in PCOS patients, suggesting that adiponectin might play a role in the complicated metabolic abnormalities of PCOS.     

Adiponectin levels in women with polycystic ovary syndrome and severe insulin resistance

OBJECTIVE: Adiponectin is an adipokine that is decreased in obesity and type 2 diabetes. Women with polycystic ovarian syndrome (PCOS) are obese and are at risk for type 2 diabetes. The objective of the current study was to investigate the relationship of adiponectin to obesity and insulin resistance in women with PCOS and severe insulin resistance. METHODS: Thirty women with PCOS and acanthosis nigricans indicating severe insulin resistance were included in the study. Eleven body mass index (BMI)-matched women with normal ovulatory cycles served as controls. Fasting glucose, insulin, and adiponectin levels were measured, and a standard oral glucose tolerance test (OGTT) with insulin levels was performed. To further investigate the role of insulin sensitivity on adiponectin levels, 10 women with PCOS were treated with 4 mg rosiglitazone daily for 6 months and adiponectin levels were measured before and after treatment. RESULTS: Fasting insulin levels (33.5 +/- 3.8 microU/mL; P <.001) and insulin area under the curve (AUC) during OGTT (536.2 +/- 70.5 microU/mL; P <.01) were higher in women with PCOS, while glucose levels were similar to controls. Adiponectin levels were lower (P <.01) in women with PCOS (5.6 +/- 2.6 microg/mL) compared with controls (8.5 +/- 3.9 microg/mL). There was a significant negative correlation between adiponectin levels and fasting insulin levels (r = -0.40, P = .02), insulin AUC during OGTT (r = -0.47, P = .008), fasting glucose levels (r = -0.45, P = .01), and glucose AUC during OGTT (r = -0.51, P = .003). There was no correlation between BMI and serum adiponectin (r = -0.12, P = .508) in women with PCOS, while there was a negative correlation (r = -0.746, P = .013) in controls. There was a significant (P <.01) increase in adiponectin levels when treated with rosiglitazone, despite unchanged BMI. CONCLUSION: These results indicate that in women with PCOS and severe insulin resistance, insulin sensitivity appears to be the major determinant of adiponectin levels rather than adiposity. Low adiponectin levels may predict women with PCOS who are at high risk for developing type 2 diabetes.     

达英-35联合不同胰岛素增敏剂对PCOS伴IR患者的临床疗效比较

目的:比较吡格列酮和二甲双胍分别配伍达英-35治疗多囊卵巢综合征(P-COS)的内分泌异常以及对卵巢生殖功能恢复的疗效。方法:随机将91例PCOS合并胰岛素抵抗(IR)患者分为两组,吡格列酮配伍组47例口服达英-35和盐酸吡格列酮,二甲双胍配伍组44例口服达英-35和盐酸二甲双胍,两组均于治疗3个月后进行诱导排卵治疗3个周期。检测治疗前后性激素、IR程度、血脂水平以及观察诱导排卵的效果。结果:二甲双胍配伍组治疗后BM I明显降低(P<0.05)。两组治疗后F-G评分均显著降低(P<0.05),卵泡总数及卵巢体积均显著降低(P<0.01),LH、LH/FSH、A2均显著降低(P<0.01)。两组治疗后IR明显改善(P<0.01),吡格列酮配伍组FIN水平降低的更为显著(P<0.05)。吡格列酮配伍组治疗后TC显著下降(P<0.05),TG、LDL-C显著下降(P<0.01),HDL-C显著升高(P<0.05),二甲双胍配伍组治疗前后血脂无明显改变(P>0.05)。两组的周期排卵率、单卵泡发育率、妊娠结局无明显差异(P>0.05)。结论:达英-35与吡格列酮配伍或与二甲双胍联合应用,均能改善PCOS患者的IR和高雄激素症状,对于异常的糖脂代谢,吡格列酮的疗效要优于二甲双胍。     

脂联素基因多态性与妊娠期糖尿病的相关性研究

目的:探讨脂联素基因启动子区单核苷酸多态性与妊娠期糖尿病(GDM)的相关性。方法:采用基质辅助激光解吸电离飞行时间质谱(MALDI-TOFMS)技术,检测103例GDM孕妇和97例正常孕妇脂联素基因启动子区-11426A>G及-11377C>G多态位点,并测定40例未经任何治疗的GDM孕妇FINS、FPG、TC、TG、HDL-C、LDL-C、脂联素水平,同时计算稳态模型的胰岛素抵抗指数。结果:(1)GDM孕妇脂联素基因-11426A>G位点的AG、GG基因型频率显著高于对照组(χ2=8.822,P=0.012),G等位基因频率明显高于对照组(χ2=10.283,P=0.001)。-11377C>G位点基因型频率及等位基因频率在二组孕妇中分布无显著差异(P>0.05)。(2)GDM孕妇脂联素-11426A>G多态性位点AG+GG基因型组甘油三酯水平高于AA基因型组(P=0.023),血清脂联素水平低于AA基因型组(P=0.024)。结论:脂联素基因-11426A>G位点多态性可能与GDM的发生有关,G等位基因在GDM孕妇中分布频率增加,A→G突变可能通过降低血清脂联素水平参与GDM的发生。     

resistin在妊娠期糖尿病患者胎盘组织的表达及意义

目的:探讨妊娠期糖尿病(GDM)患者胎盘组织抵抗素(resistin)的表达及在妊娠期糖尿病发病过程中的意义。方法:用逆转录聚合酶链反应(RT-PCR)及免疫印迹法(Western blot)检测18例妊娠期糖尿病患者(妊娠期糖尿病组)和18例正常晚期妊娠妇女(正常对照组)胎盘组织resistin mRNA和resistin蛋白的表达,同时检测体重指数(BMI)、空腹血糖水平(FPG)、空腹胰岛素水平(FINS)、血脂水平和胰岛素抵抗指数(HO- MA-IR)。结果:(1)GDM组甘油三酯(TG)、FPG、FINS及HOMA-IR的水平明显高于对照组(P<0.05或P<0.01);(2)两组胎盘组织中均可检测到resistin mRNA和resistin蛋白表达。GDM组的resistin mRNA表达水平及蛋白表达水平均高于对照组(P<0.01,P<0.05);(3)GDM组HOMA-IR水平与胎盘组织resistin mRNA表达水平(r=0.621,P<0.05)、resistin蛋白表达水平(r=0.739,P<0.01)及TG(r=0.786,P<0.01)呈正相关;GDM组TG水平与胎盘组织resistin mRNA表达水平(r=0.592,P<0.05)、resistin蛋白表达水平(r=0.546,P<0.05)呈正相关。正常妊娠组则无相关性。结论:胎盘组织分泌的resistin与GDM胰岛素抵抗密切相关,胎盘resistin表达异常可能参与了GDM的发病过程。