靶向抑制二肽基肽酶-Ⅳ基因的siRNA对糖尿病模型小鼠的降糖作用研究

目的:研究靶向抑制二肽基肽酶-Ⅳ(DPP-Ⅳ)基因的小干扰核糖核酸(siRNA)对糖尿病模型小鼠的降糖作用。方法:根据DPP-Ⅳ的refseq序列及siRNA设计原理设计3条靶向作用于DPP-Ⅳ基因不同位点的siRNA(siRNA-1、siRNA-2、siRNA-3);另取小鼠一次性腹腔注射链脲佐菌素150mg·kg-1建立糖尿病模型,成功后随机分为模型对照组、siRNA-1组、siRNA-2组、siRNA-3组,每组3只,除模型对照组外一次性尾静脉给予对应siRNA1nmol·mL-1,给药体积为小鼠体重的10%,给药后测定10d内的血糖含量,以及给药后第2天腹腔注射葡萄糖2.0g·kg-1后0、30、60、90、120min时的血糖含量,并计算耐糖曲线下面积(AUC)。结果:与模型对照组比较,siRNA-1、siRNA-2、siRNA-3组小鼠10d内均有不同程度的降糖作用,且第1天最明显(P<0.05);注射葡萄糖后,siRNA-1、siRNA-2、siRNA-3、模型对照组小鼠AUC0～120min分别为2280.3、2176.5、2773.5、4249.5mmol·L-1。结论:糖尿病模型小鼠给予靶向抑制DPP-Ⅳ的siRNA后可通过减少DPP-Ⅳ表达量、升高胰高血糖素样肽-1水平,从而缓解其高血糖症状。     

格列美脲治疗2型糖尿病安全性和有效性的多中心临床研究

目的 评价格列美脲对单纯饮食或用二甲双胍和/或阿卡波糖治疗控制不满意的2型糖尿病治疗的安全性、耐受性和有效性。方法 用多中心、开放性、非对照性临床研究,入选患者给予格列美脲1～4 mg,每日早餐前顿服,疗程16周。试验前后测定血糖、糖化血红蛋白、血脂和肝肾功能。结果129例患者人选,122例患者完成试验,格列美脲治疗16周空腹和餐后2h血糖平均分别下降1.3和1.8 mmol·L~(-1),糖化血红蛋白平均下降1.8％。治疗后空腹血浆胰岛素水平无变化,HOMA胰岛素抵抗指数明显下降,患者体重指数平均增加0.3 kg·m~(-2)。与格列美脲治疗有关的主要不良事件为低血糖反应和消化道症状,16例次与药物有关的低血糖反应均为轻度,进食后可自行缓解。对血脂和血压无不良影响。结论 格列美脲可以进一步降低单纯饮食控制或应用二甲双胍和/或阿卡波糖治疗的2型糖尿病患者的空腹和餐后2h时血糖以及糖化血红蛋白,且不增加空腹胰岛素水平,副作用小,耐受性好,使用较安全。     

帕罗西汀联合降糖药物治疗2型糖尿病疗效观察

目的 探讨帕罗西汀联合降糖药物治疗2型糖尿病的疗效及安全性.方法 收集2型糖尿病血糖控制差者,采用Zung的焦虑抑郁自评量表进行问卷调查,SDS,SAS标准分＞50的患者178例入组,随机分治疗组和观察组.治疗组同时口服帕罗西汀,观察组口服安慰剂.结果 24周后两组患者血糖、糖化血红蛋白( HbA1c)均较治疗前明显下降.观察组HbA1c下降29.1％,显著高于对照组的21.6％ (P＜ 0.05).空腹血糖≤7 mmol/L界定为空腹血糖达标,观察组89％达标,对照组16.6％,差异有显著性(P＜0.01).结论 2型糖尿病血糖控制欠佳患者,帕罗西汀联合降糖治疗,血糖控制更为理想.     

The Effect on Plasma Glucose,Insulin and Glucagon Levels of Treatment of Diabetic Rats with the Medicinal Plant Rhazya stricta and with Glibenclamide,Alone and in Combination

Because many diabetic patients in the United Arab Emirates use medicinal plants as a supplement to treatment with insulin or oral hypoglycaemic agents, the effect on plasma glucose, insulin and glucagon concentrations of simultaneous treatment of streptozotocin-diabetic rats with Rhazya stricta extract and glibenclamide has been examined. Treatment of control rats with the extract at oral doses of 0.5, 20 and 4.0 g kg^? did not significantly affect the concentration of glucose, insulin or glucagon for up to 4 h after administration of the extract. The same doses in diabetic rats reduced the glucose level 1 h (2 and 4 gkg^?) and 2h (4 gkg^?) after administration of the extract. This was accompanied by significant increases in insulin concentration 1, 2 and 4 h after administration of the extract at doses of 2 and 4 gkg^?. Glibenclamide (2.5, 5.0 and 10.0 mgkg^?) dose-dependently reduced glucose and glucagon levels, and increased that of insulin in normal and diabetic rats. Simultaneous treatment of normal and diabetic rats with the plant extract (0.5, 20 and 5.0 gkg^?) and glibenclamide (5.0 mg kg^?) significantly exacerbated the effects on glucose, insulin and glucagon induced by the extract or by glibenclamide when given separately. When the plant extract was given at doses of 0.5, 2 and 4 g kg^? per day for 6 consecutive days the glucose level was reduced by approximately 6, 8 and 30%, respectively. No significant effect was seen on the levels of cholesterol or protein. These results imply that co-administration of the extract with glibenclamide might adversely interfere with glycaemic control in diabetic patients.     

应用碘造影剂前后停用二甲双胍对糖尿病患者血糖水平的影响

目的探讨使用碘造影剂前后停用二甲双胍对糖尿病患者血糖水平的影响。方法研究对象选自2012年1月1日至12月31日在北京大学第一医院住院的糖尿病患者,入选标准为使用含二甲双胍方案治疗后血糖水平基本达标并维持平稳、应用碘造影剂前后48h内停用二甲双胍且有停药前后空腹、早餐后2h、午餐后2h、晚餐后2h和睡前血糖水平监测记录。停用二甲双胍期间调整降糖治疗方案者纳入调整组,未调整治疗方案者纳入未调整组。收集2组患者的病历资料进行回顾性分析。结果共收集到符合入选标准的患者80例,其中未调整组62例（87．5％）,调整组18例（22．5％）。二甲双胍停药时间为2—4d。未调整组停药后空腹、早餐后2h、午餐后2h、晚餐后2h和睡前血糖水平与停药前比较,均有不同程度的升高[（7．7±1．4）mmol／L比（7．0±1．2）mmol／L,（9．5±1．7）rnmol／L比（9．0±1．8）mmol／L,（10．9±2．3）mmol／L比（8．6±1．9）mmol,／L,（9．9±1．7）mmol／L比（8．6±1．7）mmol／L,（9．1±1．9）mmol／L比（8．5±1．6）mmo]／L],其中空腹、午餐后2h和晚餐后2h血糖水平与停药前比较差异有统计学意义（P=0．01,P=0．00,P=0．00）;调整组停用二甲双胍前后5个时间点血糖水平差异均无统计学意义[（7．9±1．2）mmol．／L比（8．1±1．8）mmol／L,（8．0±2．2）mmol／L比（8．5±2．4）mmo]／L,（9．2±2．9）mmol／L比（10．3±1．9）mmoL／L,（9．4±2．1）mmol／L比（9．1±2．4）mmol／L,（10．0±2．3）mmol／L比（9．3±2．2）mmol／L,均P〉0．05]。结论使用碘造影剂前后停用二甲双胍可导致停药期间未调整降糖治疗方案的糖尿病患者血糖水平出现有统计学意义的升高,调整降糖治疗方案有利于患者血糖水平控制更平稳。     

血糖波动对早期糖尿病肾病患者尿微量白蛋白及炎症因子水平的影响

目的 研究血糖波动对早期糖尿病肾病患者尿微量白蛋白及炎症因子水平的影响.方法 将2015年7月至2016年7月本院收治的88例早期糖尿病肾病患者,对患者的血糖采用动态血糖检测仪检测,分为血糖平稳者(MAGE＜5.0 mmol/L)45例、血糖波动者(MAGE≥5.0 mmol/L)43例,分析血糖波动对患者尿微白蛋白和炎症因子水平的影响.结果 血糖平稳者与血糖波动者的HbA1c、FA比较差异无统计学意义(P＞0.05);1,5-AG、UAE比较差异有统计学意义(P＜0.05).血糖平稳者与血糖波动者的炎症因子IGF-1、IL-6、TNF-α、hs-CRP比较差异有统计学意义(P＜0.05).结论 血糖波动的加剧可以加重机体的炎症,影响糖尿病肾病患者的病情.     

Relationship between Optimum Mini‐doses of Glucagon and Insulin Levels when Treating Mild Hypoglycaemia in Patients with Type 1 Diabetes – A Simulation Study

Hypoglycaemia remains the main limiting factor in type 1 diabetes management. We developed an insulin‐dependent glucagon dosing regimen for treatment of mild hypoglycaemia based on simulations. A validated glucose–insulin–glucagon model was used to describe seven virtual patients with insulin pump‐treated type 1 diabetes. In each simulation, one of ten different and individualized subcutaneous insulin boluses was administered to decrease plasma glucose (PG) from 7.0 to ≤3.9 mmol/l. Insulin levels were estimated as ratio of actual to baseline serum insulin concentration (se/ba‐insulin), insulin on board (IOB) or percentage of IOB to total daily insulin dose (IOB/TDD). Insulin bolus sizes were chosen to provide pre‐defined insulin levels when PG reached 3.9 mmol/l, where one of 17 subcutaneous glucagon boluses was administered. Optimum glucagon bolus to treat mild hypoglycaemia at varying insulin levels was the lowest dose that in most patients caused PG peak between 5.0 and 10.0 mmol/l and sustained PG ≥ 3.9 mmol/l for 2 hr after the bolus. PG response to glucagon declined with increasing insulin levels. The glucagon dose to optimally treat mild hypoglycaemia depended exponentially on insulin levels, regardless of how insulin was estimated. A 125‐μg glucagon dose was needed to optimally treat mild hypoglycaemia when insulin levels were equal to baseline levels. In contrast, glucagon doses >500 μg were needed when se/ba‐insulin >2.5, IOB >2.0 U or IOB/TDD >6%. Although the proposed model‐based glucagon regimen needs confirmation in clinical trials, this is the first attempt to develop an insulin‐dependent glucagon dosing regimen for treatment of insulin‐induced mild hypoglycaemia in patients with type 1 diabetes.     

对1例老年糖尿病足伴感染患者的药学监护

1例75a女性患者,因左足肿胀、皮肤破溃2月余,发热4d入院,入院后接受降糖、营养神经、改善微循环、抗感染、降压、调脂等综合治疗方案。药师参与了患者住院期间抗菌药物治疗方案的制定,药物不良事件的监护与处理等过程,为其提供了全程的药学服务。患者初始抗感染治疗时经验性选择头孢米诺联用莫西沙星,药敏结果回示后改为万古霉素静脉滴注,初次输液开始约20min后,患者出现面颈部发红、伴瘙痒,考虑为药物引起的红人综合征,次日滴速适当控制后未再出现类似症状。用药16d后,足部分泌物菌培养结果为阴性,遂停用万古霉素。患者用药期间,肌酐清除率由58mL·min-1下降至51mL·min-1,提示在应用万古霉素期间应密切监测其肾毒性等不良反应。患者于入院第5天清晨空腹血糖为2.9mmol·L-1,言语少,精神萎靡,但无饥饿、心慌、出汗等低血糖症状,当即嘱患者食糖块,卧床休息,20min后复查血糖升至5.8mmol·L-1,患者精神恢复,提示老年病人在应用胰岛素期间应密切监测血糖,以防发生症状不典型的低血糖事件。     

西格列汀治疗脆性糖尿病的有效性及安全性观察

目的 评价西格列汀在每日多次胰岛素注射(MDI)治疗血糖控制不良的脆性糖尿病中的有效性和安全性.方法 27例MDI治疗血糖控制不良的脆性糖尿病患者,在原方案基础上加用西格列汀100 mg· d-1,治疗12周,观察治疗前后患者的糖化血红蛋白(HbA1C)、1,5-脱水葡萄糖醇(1,5-AG)、血糖水平标准差(SDBG)、平均血糖波动幅度(MAGE)、体质量指数(BMI)和胰岛素剂量等指标的变化.结果 HbA1C从基线时的(8.4 ±1.2)%下降到12周时的(7.3 ±2.5)%(P<0.05),三餐前和三餐后2 h血糖均较基线下降,全天胰岛素剂量较基线减少(P<0.05).1,5-AG从基线时的(7.3 ±3.3)mg· L-1上升到12周时的(9.8 ±4.5)mg· L-1(P<0.05),SDBG和MAGE均较基线下降(P<0.05).BMI没有变化,低血糖事件减少.基线BMI与HbA1C变化值呈正相关.年龄与1,5-AG变化值呈正相关,与SDBG和MAGE变化值呈负相关.结论 西格列汀改善MDI治疗血糖控制不良的脆性糖尿病的血糖控制和血糖波动,减少低血糖事件,不增加体质量.     

乌拉坦诱导的高血糖反应(英文)

目的:观察麻醉剂量的乌拉坦对空腹大鼠、葡萄糖负荷大鼠,肾上腺素或四氧嘧啶诱发高血糖大鼠血糖水平的影响,并探讨其对外源性胰岛素降血糖作用的影响。方法:葡萄糖氧化酶法测定血糖含量。结果:麻醉剂量1.5g·kg~(-1)乌拉坦(sc,ip各半)显著升高空腹大鼠和葡萄糖负荷大鼠的血糖水平,但对肾上腺素(胰岛功能正常)或四氧嘧啶(胰岛功能受损)诱发的高血糖大鼠的血糖水平无明显影响。在四氧嘧啶诱发的高血糖大鼠,乌拉坦显著对抗外源性胰岛素的降血糖作用。结论:乌拉坦升高血糖的作用除与已知的释放肾上腺素有关外,抑制胰岛素的降血糖作用也是其升高血糖的机制之一。     

静脉滴注人免疫球蛋白致婴儿血糖升高3例

3例婴儿(例1男,2日龄;例2女4,1日龄;例3男,1日龄)为增强免疫功能分别静脉滴注人免疫球蛋白2.5、2.5及1.25 g。用药后2 h血糖分别升至11.0、9.6、8.0 mmol/L。随后3例患儿血糖均于24 h内恢复正常。例1再次接受静脉滴注人免疫球蛋白2.5 g后,再次出现血糖升高,达10.1 mmol/L,未予处理,10 h后血糖降至5.0 mmol/L。     

Slow acting protein extract from fruit pulp of Momordica charantia with insulin secretagogue and insulinomimetic activities

The protein from Thai bitter gourd (Momordica charantia) fruit pulp was extracted and studied for its hypoglycemic effect. Subcutaneous administration of the protein extract (5, 10 mg/kg) significantly and markedly decreased plasma glucose concentrations in both normal and streptozotocin-induced diabetic rats in a dose-dependent manner. The onset of the protein extract-induced antihyperglycemia/hypoglycemia was observed at 4 and 6 h in diabetic and normal rats, respectively. This protein extract also raised plasma insulin concentrations by 2 fold 4 h following subcutaneous administration. In perfused rat pancreas, the protein extract (10 mug/ml) increased insulin secretion, but not glucagon secretion. The increase in insulin secretion was apparent within 5 min of administration and was persistent during 30 min of administration. Furthermore, the protein extract enhanced glucose uptake into C(2)C(12) myocytes and 3T3-L1 adipocytes. Time course experiments performed in rat adipocytes revealed that M. charantia protein extract significantly increased glucose uptake after 4 and 6 h of incubation. Thus, the M. charantia protein extract, a slow acting chemical, exerted both insulin secretagogue and insulinomimetic activities to lower blood glucose concentrations in vivo.     

Beta-blockers and glucose control

Literature on the effects of beta-blockers on blood glucose is reviewed. Data are presented regarding the adrenergic influences on glucose regulation and the effects of beta-blockade during hypo- and hyperglycemia in normal and diabetic individuals. beta-adrenergic stimulation enhances insulin and glucagon secretion, as well as glycogenolysis, gluconeogenesis, and lipolysis. alpha-adrenergic stimulation inhibits insulin secretion and may inhibit glucagon secretion and enhance liver glycogenolysis. In nondiabetics, beta-blockers represent minimal risk of affecting glucose control. In insulin-dependent diabetics, beta-blockers can prolong, enhance, or alter the symptoms of hypoglycemia, while hyperglycemia appears to be the major risk in noninsulin-dependent diabetics. beta-blockers can potentially increase blood glucose concentrations and antagonize the action of oral hypoglycemic drugs.     

Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin-diabetic rats: role of glucagon in the hyperglycaemic response.

1. Lithium salts, used in the treatment of affective disorders, may have adverse effects on glucose tolerance in man, and suppress glucose-stimulated insulin secretion in rats. 2. To study the interaction of these effects with pre-existing diabetes mellitus, plasma glucose and insulin responses to lithium chloride were measured in male Wistar rats made diabetic with intraperitoneal streptozotocin, and in normal controls. 3. In both normal and diabetic anaesthetized rats, intravenous lithium (4 mEq kg-1) caused a rise in plasma glucose. In absolute terms, the rise was greater in diabetic (5.2 mmol l-1) than in normal rats (2.3 mmol l-1). 4. Plasma insulin concentrations were reduced by lithium in normal rats, but the low insulin concentrations measured in the diabetic rats were not significantly changed. 5. After intravenous glucose (0.5 g kg-1), lithium-treated diabetic rats showed a second rise in plasma glucose at 60-90 min without any insulin response, while normal rats showed typically reduced insulin responses and initial glucose disappearance rates. 6. Intravenous glucose reduced plasma glucagon concentrations to a greater extent in normal than in diabetic rats, but lithium induced an equal rise in plasma glucagon in both groups, with a time-course similar to that of the hyperglycaemic effect. 7. The hyperglycaemic action of lithium is greater in the hypoinsulinaemic diabetic rats and appears to involve a stimulation of glucagon secretion in both normal and diabetic animals.     

Intramuscular or intravenous glucagon for sulphonylurea hypoglycaemia?

Summary Because of the differing opinions on the value of glucagon and the best way of administering it in severe hypoglycaemia induced by sulphonylurea drugs, experiments were conducted on normal subjects, and in diabetic patients before and during treatment with chlorpropamide. In all subjects glucagon raised blood sugar concentrations, and produced a greater and more prolonged increase in blood glucose concentrations when given intramuscularly than when given intravenously. Hypoglycaemia did not occur in any subject.     

保肾降糖胶囊对糖尿病大鼠降糖及肾保护作用研究

目的：探讨保肾降糖胶囊对糖尿病大鼠肾脏的保护作用及其机制。方法：将SD大鼠分为6组,测定第1、8周血清肌酐及血清胰岛素、胰高血糖素、糖化血红蛋白等生化指标和尿液各项指标;取肾上腺皮质测定SOD、GSH-Px、MDA、NO2-/NO3-和NOS,评价保肾降糖胶囊的降糖作用及对糖尿病肾病的保护作用。结果：给药保肾降糖胶囊60d后,高剂量组和中剂量组大鼠的血糖值明显降低,血清肌酐清除率显著增加,尿微量清蛋白排泄率明显降低,血清胰岛素明显升高,胰高血糖素、糖化血红蛋白、尿微量清蛋白均显著降低;肾上腺皮质中的T-SOD、GSH-Px、NO^2-/NO^3-、NOS含量增加,MDA含量显著降低。结论：保肾降糖胶囊可降低糖尿病大鼠的血糖,明显减轻糖尿病大鼠蛋白尿,改善肾小球滤过率。通过提高抗氧化酶活性、清除ROS、增加NOS活性从而延缓肾小球硬化进程,减轻糖尿病肾病并发症。     

高分子化学材料负载短效胰岛素对糖尿病大鼠的降血糖作用

目的研究高分子化学材料制备水凝胶负载短效胰岛素对糖尿病大鼠的降糖作用。方法大鼠以65mg·kg^-1剂量腹腔注射链脲佐菌素制备糖尿病大鼠模型,随机分为模型组、常规组(常规胰岛素注射)、水凝胶组(水凝胶负载短效胰岛素注射),另设正常对照组,每组10只。监测各组大鼠药物干预后24 h内血糖的变化;高糖灌胃后血糖的变化;观察药物干预后肝肾功能水平变化。结果 24h内模型组大鼠血糖无明显变化,常规组与水凝胶组的血糖均于3h时显著下降至最低点后上升,但水凝胶组的血糖上升至12 h后再次下降,并于24 h内维持在原水平的49.3%~55.6%,显著低于同时间常规组的血糖(P<0.05)。高糖灌胃后常规组大鼠血糖于0.5 h下降,于1.5~2.5 h维持于原水平的59.8%~66.4%,显著低于同时间段模型组血糖(P<0.05),水凝胶组血糖值自0.5h持续显著下降(P<0.05),2.5~3.5h时血糖值均较同时间常规组血糖值明显降低(P<0.05),实验过程中无明显低血糖。同时,水凝胶组大鼠的谷丙转氨酶及谷草转氨酶显著低于模型组,其中谷草转氨酶明显低于常规组,但高于正常对照组(P<0.05)。结论高分子化学材料水凝胶负载短效胰岛素后使其不仅降糖效果优于常规胰岛素,并且作用时间明显延长,可进一步应用于胰岛素新剂型的开发。     

大豆异黄酮对糖尿病大鼠肾脏的保护作用及其机制

目的探讨大豆异黄酮(SI)对糖尿病大鼠肾脏保护作用及其机制。方法建立链脲佐菌素诱导的糖尿病大鼠模型,将模型大鼠随机分为糖尿病组(DM组)、大豆异黄酮低[40 mg/(kg·d),SI1组]、中[120mg/(kg·d),SI2组]、高[360 mg/(kg·d),SI3组]及正常对照组(NC组)。8周末检测大鼠血糖、24 h尿蛋白、肾指数、总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、血清肌酐(SCr)、血尿素氮(BUN)水平;Western blot检测肾组织nephrin表达。结果 SI3组尿蛋白(0.88±0.15)mg·d-1、肾指数(4.16±0.36)mg·g-1与DM组尿蛋白(1.26±0.45)mg·d-1、肾指数(6.13±0.76)mg·g-1比较明显降低(P<0.05);SI2组TC(2.07±0.52)mmol·L-1、TG(0.99±0.07)mmol·L-1、LDL-C(0.75±0.03)mmol·L-1和BUN(13.37±5.393)mmol·L-1与DM组TC(2.75±0.47)mmol·L-1、TG(1.36±0.35)mmol·L-1、LDL-C(0.83±0.01)mmol·L-1、BUN(24.32±6.31)mmol·L-1比较亦有明显降低(P<0.05);Western blot结果显示DM组nephrin蛋白表达较NC组显著降低(P<0.05),但SI使nephrin蛋白表达增加(P<0.05),且呈剂量依赖性。结论 SI保护糖尿病大鼠肾脏的机制可能部分与增加nephrin表达有关。     

短程强化血糖控制对初诊2型糖尿病患者胰岛β细胞功能的影响

目的探讨单纯口服降糖药（OHA）、单纯胰岛素强化治疗（Ins）对短病程、未用过降糖药的2型糖尿病（T2DM）患者减轻胰岛素抵抗、改善胰岛功能的效应差异。方法60例病程≤1年、未用过降糖药的T2DM患者随机分为2组,即OHA组、Ins组。每组有效病例30人,进行强化降糖治疗,以末梢空腹血糖≤6．5mmol／L和餐后2h血糖≤8．0mmol／L为血糖控制目标,使血糖在5—10d达标,并维持达标4周。比较2组治疗前后的静脉葡萄糖耐量试验（IVGTT）胰岛素第一时相分泌、胰岛素抵抗指数（Homa A）和胰岛素分泌指数（Homa B）的变化。结果2组治疗后IVGTT曲线下面积和HomaB均明显升高,HomaA明显下降。2组间治疗前后变化的差异不显著。结论2种强化降糖治疗方案均可以使短病程、未用过降糖药的T2DM患者胰岛素抵抗以及胰岛β细胞功能得到同样程度的改善。     

短程强化血糖控制对初诊2型糖尿病患者胰岛β细胞功能的影响

目的探讨单纯口服降糖药（OHA）、单纯胰岛素强化治疗（Ins）对短病程、未用过降糖药的2型糖尿病（T2DM）患者减轻胰岛素抵抗、改善胰岛功能的效应差异。方法60例病程≤1年、未用过降糖药的T2DM患者随机分为2组,即OHA组、Ins组。每组有效病例30人,进行强化降糖治疗,以末梢空腹血糖≤6．5mmol／L和餐后2h血糖≤8．0mmol／L为血糖控制目标,使血糖在5～10d达标,并维持达标4周。比较2组治疗前后的静脉葡萄糖耐量试验（IVGTT）胰岛素第一时相分泌、胰岛素抵抗指数（HomaA）和胰岛素分泌指数（HomaB）的变化。结果2组治疗后IVGTT曲线下面积和HomaB均明显升高,HomaA明显下降。2组问治疗前后变化的差异不显著。结论2种强化降糖治疗方案均可以使短病程、未用过降糖药的T2DM患者胰岛素抵抗以及胰岛β细胞功能得到同样程度的改善。