多囊卵巢综合征胰岛素抵抗与瘦素关系的探讨

目的　探讨多囊卵巢综合征 (PCOS)妇女血清瘦素 (leptin)水平与胰岛素抵抗 (IR)的关系 ,为研究PCOS的发病机制和治疗新途径提供理论依据。方法　 5 1例PCOS患者及 2 3例正常妇女均测定体重指数(BMI)、腰臀比 (WHR)、血清生殖激素及leptin水平 ,同期行口服糖耐量 (OGTT)及胰岛素 (Ins)释放试验 ,OGTT示IR者给予二甲双胍 (1 5 g/d)治疗 3个月后复测上述指标。 结果　PCOS患者血清leptin水平高于相应对照组 ,且IR组显著高于NIR组 ;PCOS患者经二甲双胍治疗后血清Ins水平显著下降 ,胰岛素敏感指数 (ISI)显著上升 ,同时leptin水平下降。相关分析表明 ,PCOS患者血清leptin与BMI、WHR及T显著正相关 ,与ISI负相关 (r=0 6 7,P <0 0 1) ,多元回归显示leptin中有BMI、ISI引入。结论　PCOS患者血清leptin水平升高与胰岛素敏感性相关 ;二甲双胍治疗PCOS患者可提高其胰岛素敏感性 ,降低血清leptin水平。     

血清性激素结合球蛋白与多囊卵巢综合征糖代谢的相关研究

目的:探讨血清性激素结合球蛋白(SHBG)与多囊卵巢综合征(PCOS)患者糖代谢的关系及干预治疗对其影响。方法:以16例正常育龄妇女为对照组,69例PCOS患者分为3组:非胰岛素抵抗(NIR)组、高胰岛素血症(HI)组、异常糖代谢(AMG)组,其中6例患者接受12周二甲双胍联合体育锻炼干预治疗,免放法测定血清SHBG水平。分别比较4组SHBG水平,分析SHBG与BMI、腰围、血压、Homa-IR、胰岛素敏感指数(ISI)等因素的相关性。结果:SHBG水平:HI、AMG>NIR>对照组;BMI、Homa-IR:AMG>HI>NIR组(P<0.01);ISI:AMG相似文献   

二甲双胍/CC/HMG序贯用药治疗胰岛素抵抗PCOS患者的临床研究

目的 :探讨二甲双胍对胰岛素抵抗多囊卵巢综合征 (PCOS)患者的治疗效果及作用机理。方法 :随机将 69例胰岛素抵抗PCOS患者分为A、B两组。A组 34例用Diane 35治疗 3个周期后用CC +HMG促排卵 ;B组 35例用二甲双胍治疗 3个月后用CC +HMG促排卵。观察两组患者治疗前后的BMI、T、FINS、TNF α及排卵率。结果 :两组患者治疗后BMI及T差异无显著性(P >0 .0 5) ;FINS、TNF α及排卵率差异有显著性 (P <0 .0 5)。结论 :胰岛素抵抗PCOS患者治疗的关键是应用胰岛素增敏剂降低FINS ,二甲双胍对于PCOS合并不孕的治疗效果优于Diane 35。     

二甲双胍在多囊卵巢综合征促排卵治疗中的作用

目的　评估二甲双胍在多囊卵巢综合征 (PCOS)患者促排卵治疗中的作用。方法　以40例PCOS患者 (PCOS组 )为研究对象 ,其中 2 0例口服二甲双胍治疗 12周 ,治疗后 17例未孕者加用高纯度促卵泡激素 (FSH HP)治疗 1个周期 (A组 ) ,另 2 0例单用FSH HP治疗 1个周期 (B组 ) ;同时 ,以体重和月经周期均正常的 2 0例门诊患者为对照组。观察各组及A组患者口服二甲双胍前后血清FSH、黄体生成激素 (LH)、睾酮、瘦素、空腹血糖及空腹胰岛素水平 ;比较A、B两组促排卵治疗结果。结果　空腹胰岛素和瘦素水平 ,PCOS组显著高于对照组 (P <0 .0 5) ,PCOS肥胖者高于PCOS非肥胖者(P <0 .0 5) ,但PCOS非肥胖者与对照组相比 ,差异无显著性 (P >0 .0 5)。二甲双胍治疗后 ,LH、空腹胰岛素、睾酮及瘦素水平明显下降 (P <0 .0 5～ 0 .0 1)。PCOS组患者中有 3例服二甲双胍治疗期间妊娠 ,另外 3 7例行FSH HP促排卵治疗后有 7例妊娠 (A组 4例 ,B组 3例 ) ,总妊娠率为 19% ( 7 3 7) ;A组的排卵率 ( 88% ,15 17)和妊娠率 ( 2 4% ,4 17)虽高于B组 ( 70 % ,14 2 0 ;15% ,3 2 0 ) ,但差异无显著性 (P >0 .0 5)。结论　二甲双胍能降低胰岛素和瘦素水平 ,逆转PCOS患者性激素异常 ,使部分患者恢复排卵和妊娠 ,可增强PCOS患者对促性腺素的敏感     

二甲双胍联合枸橼酸氯米芬治疗多囊卵巢综合征伴胰岛素抵抗患者的疗效观察

目的　探讨二甲双胍联合枸橼酸氯米芬治疗多囊卵巢综合征 (PCOS)胰岛素抵抗性不孕症的疗效及二甲双胍对PCOS胰岛素抵抗伴假性黑棘皮病的治疗效果。方法　将 70例PCOS胰岛素抵抗性不孕症患者 (A组 ) ,按治疗方法不同分为Aa组、Ab组各 2 0例 ,Ac组 30例。Ac组口服二甲双胍 ,每日 3次 ,每次 5 0 0mg ,连用 3个月 ,从月经周期或撤退性出血第 5天开始口服枸橼酸氯米芬片 ,每日 1次 ,每次 5 0mg,连服 5d ,共用 3个周期 ;Aa组单用二甲双胍 ,Ab组单用枸橼酸氯米芬 ,Aa及Ab两组的用药方法分别同Ac组中二甲双胍和枸橼酸氯米芬的用法。 30例PCOS伴假性黑棘皮病和胰岛素抵抗的患者为B组 ,口服二甲双胍片治疗 3个月 ,用法同Aa组 ,观察各组患者治疗前后体重指数、腰臀比例、空腹胰岛素、空腹血糖、血浆胆固醇、甘油三酯、性激素 (卵泡刺激素、黄体生成素、催乳素、雌二醇、孕酮、睾酮 )水平的变化及B组的皮损变化。结果　 (1)Ac组治疗后胰岛素抵抗状态明显改善 ,妊娠率达 5 7% ,明显高于Aa组 (2 0 % )和Ab组 (15 % ) ,差异有极显著性 (P <0 0 1) ;Ac组治疗前 ,空腹胰岛素、体重指数、睾酮、血浆胆固醇、甘油三酯分别为 (4 9 7± 6 4 )mU/L、2 9 4± 2 2、(6 4± 2 2 )nmol/L、(6 3± 0 5 )mmol/L、(4 1± 1 0     

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。     

二甲双胍治疗耐克罗米酚多囊卵巢综合征23例临床分析

目的探讨二甲双胍在多囊卵巢综合征(PCOS)治疗中的作用.方法对23例耐克罗米酚PCOS患者的临床资料进行回顾性分析,比较二甲双胍治疗前后各项内分泌代谢指标的变化及其对恢复月经、促排结局及妊娠的影响.结果二甲双胍治疗前后比较,血清睾酮、空腹胰岛素水平下降,胰岛素敏感性指数上升(P<0.01).6例(26.09%)的患者恢复月经,4例(17.39%)恢复自然排卵,2例妊娠. 二甲双胍加促排治疗共26个周期,排卵周期率为61.54%(16/26),妊娠周期率为23.08%(6/26). 结论二甲双胍可以降低雄激素水平及胰岛素水平,改善PCOS妇女对克罗米酚促排的反应.     

二甲双胍对高胰岛素血症肥胖儿童糖代谢和血清脂源性激素的影响

目的观察二甲双胍治疗对高胰岛素血症肥胖患儿血清脂源性激素脂联素、抵抗素、瘦素水平的影响。 方法2004 01—2005 02将武汉市儿童医院和同济医院54例高胰岛素血症肥胖患儿分为轻、中度肥胖组及重度肥胖组,均以二甲双胍治疗12周，测量治疗前后体重、空腹血糖、空腹胰岛素及脂源性激素脂联素、瘦素、抵抗素的变化。 结果治疗前轻、中度肥胖组和重度肥胖组高胰岛素血症患儿空腹血糖水平与健康对照组比较差异无显著性(P>0.05)，血清胰岛素、瘦素、抵抗素及胰岛素抵抗指数(HOMA IR)均高于健康对照组(P<0.01)，脂联素水平明显低于健康对照组(P<0.01)。二甲双胍治疗12周后与治疗前相比,血清胰岛素水平、胰岛素抵抗指数明显降低(P<0.01)，轻、中度肥胖组及重度肥胖组血清瘦素水平分别由治疗前的(24.3±1.8)μg/L、(30.2±5.1)μg/L降低为治疗后的(19.6±6.3)μg/L、(24.7±5.3)μg/L，差异有统计学意义；抵抗素水平分别由治疗前的(16.5±6.0)μg/L、(22.3±5.2)μg/L升高为(22.0±5.1)μg/L、(30.6±11.7)μg/L，差异有统计学意义；轻、中度肥胖组和重度肥胖组血清脂联素水平治疗前分别为(8.4±3.2)mg/L、(6.5±1.2)mg/L，治疗后分别为(8.9±2.3)mg/L、(7.03±3.0)mg/L，治疗前后相比,P>0.05。体重指数(BMI)下降,但差异无显著性。 结论二甲双胍能显著改善肥胖患儿胰岛素抵抗。降低血清瘦素水平可能是其改善胰岛素抵抗机制之一，但在对脂源性激素脂联素、抵抗素水平的改善上，有其局限性。     

达英-35对非肥胖、非胰岛素抵抗多囊卵巢综合征胰岛素敏感性的影响

目的探讨达英-35[diane-35,每片含醋酸环丙孕酮(CAP)2 mg和乙炔雌二醇(EE)35 μg]对非肥胖、非胰岛素抵抗(IR)多囊卵巢综合征(PCOS)胰岛素敏感性的影响.方法选取32例非肥胖、非IR的PCOS患者作为研究对象,达英-35治疗3个月,治疗前后测定体重指数(BMI)、腰臀比(WHR)、血清促卵泡生成素(FSH)、促黄体生成素(LH)、睾酮(T)、瘦素(Leptin)和性激素结合球蛋白(SHBG),并进行口服糖耐量试验(OGTT)和胰岛素释放试验,计算游离雄激素指数(FAI)、葡萄糖和胰岛素曲线下面积、空腹血糖/胰岛素之比(GIR)、OGTT各时点的胰岛素/血糖比以及卵巢体积.结果①治疗前后BMI、WHR和FSH无改变,LH、LH/FSH值、FAI和卵巢体积明显下降(P＜0.01),T也较治疗前降低(P＜0.05),SHBG则明显升高(P＜0.01),血Leptin升高(P＜0.05).②治疗前后空腹血糖均在正常范围,葡萄糖曲线下面积(AUC葡萄糖)无改变,治疗后胰岛素曲线下面积(AUC胰岛素)、OGTT各时相的胰岛素/血糖比和胰岛素水平均升高(P＜0.01),GIR则从11.24±2.15 mg·L/dl·mU明显下降为3.77±0.60 mg·L/dl·mU (P＜0.01).结论达英-35在明显改善非肥胖、非IR PCOS高雄激素血症的同时有胰岛素抵抗的迹象,其原因可能与周围组织胰岛素敏感性下降有关.     

二甲双胍对多囊卵巢综合征患者胰岛素样生长因子-1的影响

目的探讨二甲双胍对多囊卵巢综合征（PCOS）患者血清胰岛素样生长因子-1（IGF-1）及胰岛素样生长因子结合蛋白-1（IGFBP-1）水平的影响及其作用机制，明确二甲双胍治疗的临床效果。方法2002年1—11月对山西医科大学第二医院24例PCOS患者给予二甲双胍500mg，一日3次，8～24周治疗，比较治疗前后血清IGF-1、IGFBP-1、空腹胰岛素及睾酮水平，并对月经恢复、排卵、妊娠情况进行分析。结果二甲双胍可降低血清空腹胰岛素及睾酮水平，能显著升高IGFBP-1水平，治疗前后血清IGF—1水平差异无显著性。单纯二甲双胍治疗后月经恢复率为41．67％（10／24）；自然排卵率为25．00％（6／24），自然妊娠率为12．50％（3／24）。二甲双胍加促排卵治疗共18个周期，排卵周期率66．67％（12／18），妊娠周期率为11．11％（2／18）。结论二甲双胍可以降低血清空腹胰岛素及睾酮水平，增高IGFBP-1水平，可以改善卵泡微环境，有助于月经恢复，提高促排卵和妊娠率．是治疗PCOS的重要手段。     

Nonobese women with polycystic ovary syndrome respond better than obese women to treatment with metformin

OBJECTIVE: To determine the clinical, hormonal, and biochemical effects of metformin therapy in obese and nonobese patients with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: Department of Gynecology of Federal University of S?o Paulo, S?o Paulo, Brazil. PATIENT(S): Twenty-nine patients with PCOS. INTERVENTION(S): Patients were treated with 500 mg of p.o. metformin t.i.d. for 6 months. MAIN OUTCOME MEASURE(S): Clinical data as well as serum concentrations of sex steroids, sex hormone-binding globulin (SHBG), gonadotropins, leptin, GH, lipids, insulin, and glucose levels were assessed before and after treatment. RESULT(S): In the metformin group of nonobese patients, the mean fasting serum insulin concentration decreased from a pretreatment value of 12.1 +/- 2.4 to 6.3 +/- 0.6 microU/mL after treatment, and the area under the curve of insulin decreased from 5,189.1 +/- 517.4 to 3,035.6 +/- 208.9 microU/mL per minute. Also in the metformin group of nonobese patients, the mean basal serum total testosterone, free testosterone, and androstenedione concentrations decreased by 38%, 58%, and 30%, respectively. In the obese patients treated with metformin, only free testosterone showed a statistically significant decrease (1.7 +/- 0.2). CONCLUSION(S): Our data suggest that nonobese patients respond better than obese patients to a 1.5 g/day metformin regimen.     

Metformin therapy increases insulin-like growth factor binding protein-1 in hyperinsulinemic women with polycystic ovary syndrome

OBJECTIVES: Polycystic ovary syndrome (PCOS) is associated with hyperandrogenism, insulin resistance, compensatory hyperinsulinemia, and increased levels of free insulin-like growth factor-I (IGF-I), presumably due to a decline in IGF binding protein 1 (IGFBP-1). This study was designed to evaluate effects of metformin therapy on serum levels of IGFBP-1 and IGF-I. STUDY DESIGN: Twenty-seven obese, hyperandrogenic PCOS women with elevated fasting insulin were treated for 12 weeks with metformin (500 mg p.o., t.i.d.). Serum levels of insulin, testosterone, sex hormone binding globulin (SHBG), IGF-I, and IGFBP-1 were measured before and after treatment. Body mass index (BMI) and waist-to-hip ratio (WHR) were assessed at baseline and at the end of therapy. RESULTS: Metformin therapy significantly increased IGFBP-1 concentration by 38% (P = 0.05) but had no demonstrable effect on the total IGF-I levels. Fasting insulin levels declined by 38% (P = 0.0001) while the glucose/insulin ratio increased by 72% (P = 0.0001) and quantitative insulin sensitivity check index (QUICKI) increased by 8% (P = 0.0001). Metformin treatment also significantly decreased testosterone (by 37%, P = 0.0001) and increased SHBG concentration (by 16%, P = 0.04). Multiple linear regression analysis revealed that baseline IGFBP-1 levels correlated inversely and independently with two baseline parameters: WHR (P = 0.003) and free testosterone index (P = 0.04). CONCLUSIONS: The present study shows that metformin therapy not only restores normal levels of insulin and testosterone, but also decreases the pool of free-bioactive IGF-I by increasing the levels of circulating IGFBP-1. We provide further arguments in favor of metformin therapy in hyperinsulinemic women with PCOS.     

Effects of metformin on serum insulin and anti-mullerian hormone levels and on hyperandrogenism in patients with polycystic ovary syndrome

Objective: To evaluate the relationship between serum anti-mullerian hormone levels (AMH) and insulin resistance (IR) before and after meformin treatment and to compare AMH levels of polycystic ovary syndrome (PCOS) women in the early follicular phase. Methods: Twenty PCOS women with IR, taking metformin 1500?mg/day for 8 weeks, and 16 non-PCOS controls were enrolled in this longitudinal study. Serum levels of AMH, insulin, glucose, testosterone, and quantitative insulin check index (QUICKI), were assessed before and after treatment in PCOS group. Results: AMH levels were higher in untreated PCOS (p < 0.0001), as were luteinizing hormone (LH) (p = 0.0004), testosterone (p = 0.0017) as well as 17-hydroxyprogesterone (p = 0.03). PCOS women show positive correlation between AMH and testosterone (R = 0.83; p < 0.0001) only prior to treatment. Metformin treatment, lead to a significant decrease in serum insulin (p = 0.0132) and testosterone (p = 0.0017) levels. However, no alteration in AMH levels was observed after treatment. Conclusion: Despite the improvement of metabolic parameters and the reduction of androgen levels, AMH levels did not change after metformin treatment. Maybe, the dose, and possibly the time of use, of metformin are factors associated with the reduction of AMH levels.     

Increased insulin-like growth factor-I levels in women with polycystic ovary syndrome, and beneficial effects of metformin therapy.

We aimed to investigate whether metformin would reverse the endocrinopathy of polycystic ovary syndrome (PCOS), allowing resumption of cyclic ovulation and regular menses, and whether metformin causes any change in the serum concentration of insulin-like growth factor-I (IGF-I) in patients with PCOS. Fifty-eight women with PCOS participated in the study and received metformin at a dose of 850 mg three times a day (total 2550 mg) for 16 weeks. Serum concentrations of luteinizing hormone, follicle stimulating hormone, estradiol, free testosterone, total testosterone, 17-hydroxyprogesterone, dehydroepiandrosterone sulfate, fasting insulin, IGF-I, sex hormone binding globulin and insulin-like growth factor binding protein-1 (IGFBP-1) were evaluated before and after metformin treatment. Patients were divided into two groups as responders and non-responders according to the achievement of regular menstrual periods. The mean IGF-I levels decreased significantly on metformin therapy. After 16 weeks of metformin treatment, 55.17% of PCOS patients achieved regular menses. Only the change in serum levels of progesterone and IGF-I on metformin were statistically significant between responders and non-responders; metformin-induced decremental change in IGF-I levels were greater in responders. In conclusion, we observed that elevated IGF-I levels may have a crucial role in many consequences of PCOS in addition to hyperinsulinemia. By decreasing insulin and IGF-I levels, metformin therapy offers additional beneficial effects in resumption of regular menses. Thus, in PCOS patients with elevated levels of IGF-I, metformin may be considered as an appropriate agent to be used for the regulation of menstrual cycles.     

高胰岛素血症在多囊卵巢综合征发病中的作用及抗胰岛素的治疗

目的探讨高胰岛素（ＩＮＳ）血症在多囊卵巢综合征（ＰＣＯＳ）发病中的作用及二甲双胍对ＰＣＯＳ的治疗效果。方法将２３例ＰＣＯＳ病人分为肥胖组（１２例）和非肥胖组（１１例）,于服二甲双胍前及服二甲双胍８～１２周后,应用放射免疫法测定基础状态下雄激素、黄体生成素（ＬＨ）、性激素结合球蛋白及促性腺激素释放激素激动剂（ＧｎＲＨａ）刺激后,血１７α羟孕酮（１７ＯＨＰ）和ＬＨ的水平、口服糖耐量试验（ＯＧＴＴ）中血ＩＮＳ水平。结果用药后肥胖组空腹血ＩＮＳ水平和非肥胖组ＯＧＴＴ时血ＩＮＳ反应曲线下面积均明显下降;两组基础状态下的血１７ＯＨＰ、雄烯二酮（Ａ）、睾酮（Ｔ）水平均显著下降、性激素结合蛋白水平显著增加;ＬＨ基值及ＧｎＲＨａ刺激后的ＯＨＰ和ＬＨ值均无明显变化。结论高ＩＮＳ血症在ＰＣＯＳ的高雄激素血症起重要作用,二甲双胍可用于ＰＣＯＳ的治疗     

Clinical and endocrinological effects of 6 months of metformin treatment in young hyperinsulinemic patients affected by polycystic ovary syndrome.

Most patients with polycystic ovary syndrome (PCOS) have hyperinsulinemia; thus it has been postulated that insulin-lowering drugs, such as metformin, might be a useful long-term choice. We evaluated the effects of 6 months' administration of metformin on clinical and endocrine indices in PCOS patients. Forty-two hyperinsulinemic women with PCOS were continuously treated with metformin for 6 months. Gonadotropins, androgens (testosterone and androstenedione), insulin, sex hormone binding globulin (SHBG), lipid profile and clinical indices (menstrual length, body mass index (BMI), Ferriman-Gallwey score and waist/hip ratio (WHR)) were studied before and after metformin treatment. All women experienced a normalization of menstrual cycle length (reduction rate, 36.9%), a significant decrease in luteinizing hormone, insulin and androgen levels and an increase in SHBG plasma concentrations, with a concomitant decrease in cycle length and WHR. Significant changes were observed in the lipid profile. According to baseline androgen levels, patients were divided into two groups: 20 normoandrogenic and 17 hyperandrogenic women. The greatest decline of androgens, BMI and Ferriman-Gallwey score was observed in hyperandrogenic patients. Lowering of androgenicity was independent of BMI. Significant changes in lipid profile were observed in both groups after metformin treatment. These results suggest that metformin is effective in decreasing hyperandrogenism, mainly by reducing insulin levels. This leads to an improvement of clinical manifestations of PCOS and, in particular, of hyperandrogenism.     

罗格列酮联合二甲双胍治疗多囊卵巢综合征的临床疗效观察

目的 :探讨罗格列酮联合二甲双胍治疗多囊卵巢综合征 (PCOS)的临床疗效。方法 :10 0例临床上有PCOS表现的肥胖不育患者通过口服葡萄糖耐量试验 (OGTT)、胰岛素及C肽释放试验 ,检出胰岛素抵抗 (IR)患者 80例 ,随机分为A、B、C 3组 ,分别给予促排卵药 ,促排卵药加二甲双胍 ,促排卵药加二甲双胍加罗格列酮 ,共治疗 2个月经周期 ,比较 3组用药前后及 3组间体重指数 (BMI)、胰岛素抵抗指数 (HomaIR)、游离脂肪酸(FFA)、肿瘤坏死因子α(TNFα)、纤溶酶原激活抑制物 1(PAI 1)和排卵率的变化。结果 :C组患者治疗后的BMI、HomaIR、FFA、TNFα、PAI 1较治疗前明显下降 (P <0 .0 5 )。C组的排卵率明显优于A组 (P <0 .0 1)和B组 (P <0 .0 5 )。结论 :罗格列酮联合二甲双胍治疗PCOS效果显著。     

Effects of metformin therapy on hyperandrogenism in women with polycystic ovarian syndrome.

Polycystic ovarian syndrome (PCOS) is one of the most common endocrine diseases in women. This syndrome is characterized by hyperandrogenism, chronic anovulation, infertility and obesity. The association between PCOS-related hyperandrogenemia and insulin resistance is well documented in the literature. Insulin resistance and the resulting raised plasma levels of insulin are reported to be responsible for the high androgen concentration observed in patients with PCOS. In this prospective study, blood samples for levels of testosterone (T), dehydroepiandrosterone sulfate (DHEAS), luteinizing hormone (LH), follicle-stimulating hormone (FSH), LH/FSH, prolactin and fasting blood sugar (FBS) before starting metformin administration were obtained randomly from 40 women who were apparently obese, had PCOS and had been referred to a university hospital. Metformin was then given at a dose of 500 mg three times a day for 8 weeks, after which time the pretreatment study was repeated. Clinical symptoms of PCOS, including acne and hirsutism score and body mass index (BMI), were assessed before and after the treatment cycle. Metformin therapy resulted in a significant decrease in total testosterone levels and FBS. There was also a significant decline in BMI, length of the menstrual cycle, acne and hirsutism score. There were no significant changes in the levels of DHEAS, prolactin, FSH or LH, or in LH/FSH. The effect of metformin on subjects with elevated DHEAS levels was different to that on individuals with normal DHEAS levels. In the latter group there were only significant improvements in the length of the menstrual cycle, BMI and testosterone and DHEAS levels. It is concluded that metformin therapy in subjects with PCOS results in a decrease in fasting blood sugar and testosterone levels, and leads to a significant improvement in the clinical manifestation of hyperandrogenism. These responses also related to the level of adrenal function.