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1.
观察吡格列酮对2型糖尿病患者胰岛素抵抗的治疗作用,对30例2型糖尿患者予吡格列酮30mg/d口服,12周后发现餐后2小时血糖(PC2hPG)、糖化血红蛋白(GHbA1c)、空腹血糖(FPG)、胰岛素抵抗指数(Homa—IR)与用药前比较明显降低(P〈0.01)。提示吡格列酮可降低FPG、PC2hPG、GHbA1c及血浆胰岛素水平,明显减轻胰岛素抵抗。  相似文献   

2.
目的观察国产吡格列酮对2型糖尿病(T2DM)病人血糖、血脂代谢和胰岛素抵抗(IR)的作用,并检测治疗前后血清脂联素水平的变化。方法用随机双盲法、与安慰剂平行对照,比较48例T2DM病人用吡格列酮30mg和安慰剂(1:1)干预治疗12w后的血糖、血脂、IR、血清脂联素水平改变。结果吡格列酮治疗12w后,空腹血糖和餐后2h(2hPG)血糖、糖化血红蛋白(HbA1c)与治疗前比较明显下降(P<0·05或P<0·01);空腹胰岛素(FINS)及HOMA模型IR指数(HOMA-IR)较治疗前也减低(P<0·05或P<0·01);血清脂联素水平、高密度脂蛋白(HDL-C)在12w治疗后显著升高,低密度脂蛋白(LDL-C)与治疗前比较明显降低(P<0·05或P<0·01),上述指标与安慰剂组比较差异均有显著意义(P<0·05或P<0·01)。但是总胆固醇(TC)、甘油三酯(TG)治疗前后无明显差异。结论国产吡格列酮可改善T2DM病人血糖及血脂代谢,降低IR并升高血清脂联素水平,有助于防治T2DM血管并发症。  相似文献   

3.
Pan C  Gao Y  Gao X  Li G  Luo B  Shi H  Tian H  Jia P  Lin H  Xing X  Zhao Y  Zhou L 《中华内科杂志》2002,41(6):388-392
目的 评价盐酸吡格列酮对 2型糖尿病患者合用磺脲类和双胍类药物时的降血糖作用 ,观察其安全性。方法 采用随机、双盲、安慰剂平行对照和多中心临床研究方法。对 2 83例应用磺脲类和双胍类治疗而血糖控制不佳 (7 0mmol/L≤空腹血糖 <13 0mmol/L)的 2型糖尿病患者随机分入吡格列酮 30mg组与安慰剂组治疗随访 6次共 12周。结果 于 12周时 ,试验组与对照组空腹血糖水平较基线值分别平均下降了 1 1mmol/L和 0 4mmol/L(P <0 0 0 1) ;餐后血糖分别下降了 1 5mmol/L和 0 3mmol/L(P <0 0 0 1) ;糖化血红蛋白 (HbA1c)分别下降了 0 7%和 0 4 % (P <0 0 1)。试验组空腹胰岛素下降幅度高于对照组 (P <0 0 5 ) ,其两组治疗前后的差值比较均分别具有显著性统计学差异。试验组HOMA IR显著降低 (P <0 0 1)。结论  12周的临床观察显示 ,对 2型糖尿病患者饮食、运动和口服降糖药 (磺脲类和双胍类 )治疗控制不佳者联合应用吡格列酮 (30mg/d) ,代谢控制可得到进一步的改善 ,胰岛素的敏感性增强 ,安全性和耐受性好。  相似文献   

4.
目的 探讨盐酸吡格列酮和盐酸二甲双胍对2型糖尿病患者高脂血症的疗效。方法 采取平行双盲随机对照法,两组病例随机分为盐酸二甲双胍治疗组和盐酸吡格列酮治疗组。治疗12周1个疗程。治疗前及治疗后分别检测血清脂质包括胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(IDL-C)、高密度脂蛋白胆固醇(HDL-C)、空腹血糖(FPG)、餐后2h血糖(2hPG)、肝功能、肾功能。结果 两种药均有降低甘油三酯、胆固醇、低密度脂蛋白胆固醇,升高高密度脂蛋白胆固醇作用。二甲双胍降低胆固醇的幅度低于吡格列酮,但两种药对甘油三酯、高密度脂蛋白胆固醇的影响幅度差异无显著性。结论 盐酸吡格列酮和盐酸二甲双胍两种药物对2型糖尿病的高脂血症疗效相当。  相似文献   

5.
2007年1月—2008年1月,我科使用吡格列酮联合胰岛素治疗60例初诊的2型糖尿病病人,对患者血糖、血脂、血压、肝肾功能、血常规及低血糖等方面进行了3个月追踪观察,现将观察结果报告如下。  相似文献   

6.
40例大剂量胰岛素治疗的2型糖尿病患者,加服盐酸吡格列酮15mg/d,进行为期16周的用药观察。结果:与治疗前比较:空腹及餐后血糖均明显下降(P〈0.05),糖化血红蛋白也下降0.9%(P〈0.05),胰岛素用量减少12U(P〈0.05)。结论:2种药物联合应用可使高血糖得到满意控制,同时可以改善胰岛B细胞功能,降低胰岛素抵抗,增加胰岛素敏感性,减少胰岛素用量,二者起协同作用。  相似文献   

7.
本文用国产盐酸吡格列酮的Ⅱ期临床试验结果,来分析其对中国人2型糖尿病的疗效和安全性。  相似文献   

8.
目的探讨吡格列酮对2型糖尿病(T2DM)患者轻度认知功能障碍(MCI)的临床疗效。方法采用自身对照的方法,选取T2DM合并MCI患者56例,在常规降糖治疗的基础上给予盐酸吡格列酮15 mg/d口服治疗,疗程2年。于治疗前检测空腹胰岛素(FINs),C肽(FCP),空腹血糖(FPG),血压,血脂,血尿酸(UA),胰岛素样生长因子(IGF)-I,转化生长因子(TGF)-β1,以及动态血糖监测;同时给予蒙特利尔认知评价量表(MoCA)、MMSE以及P300评定;治疗1年和2年后再次抽血化验上述指标和心理评定。结果与治疗前比较,在吡格列酮治疗2年后糖化血红蛋白(Hb A1c)、FINs水平、HOMA-IR、P300潜伏期缩短,TGF-β1水平下降,IGF-I水平显著增加(P<0.05);Mo CA评分显著增加、MMSE评分显著增加、P300潜伏期和波幅显著降低(P<0.01)。结论吡格列酮治疗能够改善和延缓T2DM患者的认知功能减退,治疗需要时间长,可能与改善胰岛素抵抗有关。  相似文献   

9.
目的:观察吡格列酮对初诊2型糖尿病患者肠源性内毒素水平的影响,探讨其改善胰岛素抵抗的可能新机制。方法:97例初诊2型糖尿病患者按随机数字表法随机分为吡格列酮治疗组(49例)和二甲双胍治疗组(48例),治疗3个月后比较治疗前后血清肠源性内毒素及超敏C反应蛋白(hs-CRP)等相关生化指标的变化。以同期性别、年龄相匹配的健康体检者30名作为对照组。结果:①治疗前糖尿病组内毒素及hs-CRP水平均较正常对照组高(P<0.01);②吡格列酮治疗后空腹血糖(FPG)、血浆内毒素、hs-CRP及空腹胰岛素(FINS)水平均明显下降,差异有统计学意义(P0.05);④2型糖尿病患者血浆内毒素水平与三酰甘油、总胆固醇、FINS、hs-CRP及稳态模型评估的胰岛素抵抗指数(HOMA-IR)呈正相关(P<0.05),校正性别、年龄及体质量指数(BMI)等影响因素后,HOMA-IR是血浆内毒素的独立相关因素。结论:吡格列酮治疗能降低初诊2型糖尿病患者的肠源性内毒素水平,该作用可能是吡格列酮改善机体胰岛素抵抗状态的机制之一。  相似文献   

10.
选择350例应用盐酸吡格列酮治疗T2DM患者,观察12周,结果FPG,h2PG,HbAIc均低于治疗前,(P〈0.01);TC、TG、BMI下降,(P〈0.05);胰岛素敏感性指数明显升高(P〈0.01)。结论盐酸吡格列酮(瑞彤)可显著降低血糖,可做为基础用药。  相似文献   

11.
AIM: The effects of pioglitazone hydrochloride monotherapy on abnormal lipid control were evaluated in Japanese patients with type 2 diabetes mellitus, comparing with glibenclamide monotherapy. METHODS: Patients were randomly assigned to receive, once daily, pioglitazone hydrochloride, at 15 mg or 30 mg (n=46), or glibenclamide, at 1.25 mg or 2.5 mg (n=46). The 24-week study included patients with type 2 diabetes having high levels of triglyceride (TG). RESULTS: Pioglitazone hydrochloride produced beneficial effects on dyslipidemia in patients with type 2 diabetes, compared with the baseline and the glibenclamide group, as demonstrated by increases in high-density lipoprotein cholesterol (HDL-C) levels and low-density lipoprotein cholesterol (LDL) particle size, a fall in TG levels, and an increased ratio of visceral to subcutaneous fat volumes (V/S). Pioglitazone hydrochloride reduced fasting serum insulin levels, with low fasting plasma glucose (FPG) and glycohemoglobin levels, compared to the baseline, suggesting an improvement of insulin resistance. CONCLUSION: As expected, glibenclamide reduced FPG levels through increased insulin secretion. Pioglitazone hydrochloride and glibenclamide were well tolerated. Pioglitazone hydrochloride improved dyslipidemia related to insulin resistance, whereas glibenclamide enhanced insulin secretion, with only a minor effect on lipid control, in Japanese patients with type 2 diabetes.  相似文献   

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13.
Atherosclerosis is one of the major causes of morbidity and mortality in patients with type 2 diabetes mellitus. Pioglitazone has been reported to have antiatherogenic effects. The aim of this study was to investigate whether pioglitazone affects pulsatility index (PI) of the cerebral arteries and the carotid intima-media thickness in type 2 diabetic patients. A total of 40 type 2 diabetic patients were included in this study. They were divided into 2 groups: the pioglitazone-treated group (pioglitazone 15 mg/d with gliclazide 80-320 mg/d for 12 weeks) and the gliclazide-treated group (gliclazide 80-320 mg/d for 12 weeks). Transcranial Doppler ultrasonography was performed for each cerebral artery, and PI was calculated as (systolic velocity-diastolic velocity)/mean velocity. The pioglitazone treatment significantly increased high-density lipoprotein cholesterol and decreased triglyceride levels and insulin resistance. This study revealed that the change in mean intima-media thickness was not significant in both groups, but the change in PI was significantly decreased with pioglitazone compared to gliclazide. In conclusion, pioglitazone decreased PI and improved cerebrovascular resistance in type 2 diabetic patients.  相似文献   

14.
Fetuin-A (α2-Heremans-Schmid glycoprotein), a circulating glycoprotein, can inhibit insulin signaling both in vivo and in vitro. Recently, we and another independent group have shown that fetuin-A is positively associated with insulin resistance in humans. Furthermore, it has been reported that higher fetuin-A levels are associated with metabolic syndrome and atherogenic lipid profiles. These data suggest that fetuin-A might be a regulator of insulin resistance and/or metabolic syndrome. However, it is not clear how fetuin-A levels are regulated. To address this, we investigated the effects of representative insulin-sensitizing therapies such as pioglitazone, metformin, and aerobic exercise on fetuin-A levels. Twenty-seven patients with type 2 diabetes mellitus were divided into pioglitazone-treated (Pio), metformin-treated (Met), and exercise-treated (Ex) groups. Ten patients in the Pio group and 9 patients in the Met group took 15 or 30 mg/d pioglitazone or 500 or 750 mg/d metformin, respectively, for 6 months. Eight patients in the Ex group underwent a 3-month aerobic exercise program. Serum fetuin-A levels were measured before and after each intervention. Intervention significantly decreased hemoglobin A1c in all groups. After treatment, serum fetuin-A levels significantly decreased in the Pio group (291.2 ± 57.7 to 253.1 ± 43.9 μg/mL, P = .006), whereas there were no changes in serum fetuin-A after intervention in either the Met or the Ex groups. We hypothesize that pioglitazone could partially ameliorate insulin resistance via modulating fetuin-A levels.  相似文献   

15.
Kubo K 《Endocrine journal》2002,49(3):323-328
The objective of this study was to clarify the influence of pioglitazone (Pio) on proinsulin (PI) in patients with type 2 diabetes mellitus. The subjects were 55 patients with type 2 diabetes. Among them, 18, 18, and 19 patients were respectively treated with Pio alone (group P), gliclazide (Gli) alone (group G), or Pio plus Gli (group PG) for 12 weeks. Fasting blood samples were obtained before and after treatment and were used to measure fasting plasma glucose (FPG), HbA1C, immunoreactive insulin (IRI), and PI. The levels of FPG, HbA1C, and IRI showed a significant decrease after treatment with Pio in groups P and PG. Treatment with Pio also caused PI to decrease significantly (group P: from 24.7 +/- 12.9 (mean +/- SD) to 14.0 +/- 6.2 pmol/L, p < 0.01, group PG: from 24.3 +/- 11.3 to 14.4 +/- 6.5 pmol/L, p < 0.01). In group G, treatment with Gli caused FPG and HbA1C to decrease significantly, but PI showed no change (21.5 +/- 12.3 to 21.6 +/- 10.4 pmol/L, p = n.s.). In patients with type 2 diabetes, treatment with Pio achieved an improvement of glycemic control and reduced the load on the pancreatic beta cells.  相似文献   

16.
目的探讨老年2型糖尿病并发症相关指标的临床意义。方法对住院老年2型糖尿病160例病人随机分组,监测其生化指标(FBG、HbA1C、TC、TG、HDL-C)并作统计学处理。结果相关生化指标测值的比较,糖尿病并发症与无并发症组病例差异有显著性(P〈0.05)。结论对老年2型糖尿病除控制血糖外,更应重视对高血压、血脂异常的治疗,以减少各种并发症的发生。  相似文献   

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OBJECTIVE: This prospective study evaluates the effect of insulin sensitizers, pioglitazone (PGZ) and metformin (MET) on plasma adiponectin and leptin levels in subjects newly diagnosed with type 2 diabetes mellitus (T2DM). DESIGN: Double blind, randomized, active control, dose escalation study of 12 weeks treatment duration. PATIENTS: Thirty apparently healthy, treatment-naive T2DM patients diagnosed within the past 6 months. MEASUREMENTS: Plasma adiponectin and leptin levels were estimated by enzyme-linked immunosorbent assay (ELISA), and insulin resistance by the homeostasis model of assessment (HOMA-IR). RESULTS: Baseline plasma levels of adiponectin were lower in diabetic (n = 30) subjects than matched controls (n = 10, 6.6 +/- 1.1 vs 10.4 +/- 4.2 microg/ml, P = 0.021). The 12-week treatment with PGZ significantly increased adiponectin concentrations (6.6 +/- 1.1-17.9 +/- 7.4 microg/ml, P < 0.001) with no alteration in the MET treated group (6.8 +/- 1.5-6.7 +/- 2.8 microg/ml, P = 0.9). A significant decrease in plasma leptin levels was observed in the MET treated group (32.0 +/- 28.9-21.4 +/- 23.3 ng/ml, P = 0.024) but not in the PGZ treated group (23.9 +/- 24.1-22.4 +/- 25.4 ng/ml, P = 0.69). The alterations in plasma adiponectin and leptin levels were not associated with any change in body mass index (BMI). PGZ therapy improved insulin sensitivity to a greater degree (P = 0.007 and P = 0.001 for fasting plasma insulin (FPI) and HOMA-IR, respectively) than MET (P = 0.75 and P = 0.02 for FPI and HOMA-IR, respectively) but this improvement was not significantly different from that of MET at the end of 12 weeks (P = 0.146 and P = 0.09 for FPI and HOMA-IR, respectively). However, improvement in insulin sensitivity with PGZ was not commensurate with the increase in adiponectin. Better control of postbreakfast plasma glucose (PBPG) as well as decrease in serum triglycerides (TGs) were also seen with PGZ (PBPG, P < 0.001; TGs, P = 0.013). The rest of the parameters were comparable. Adverse reactions reported were minor and did not result in treatment discontinuation. CONCLUSIONS: Pioglitazone therapy appears to be better in achieving glycaemic control and increasing plasma adiponectin and insulin sensitivity in newly detected type 2 diabetics.  相似文献   

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