格列美脲治疗2型糖尿病有效性和安全性的临床观察

目的　评价新一代磺酰脲类药物格列美脲 (商品名亚莫利 ,Amaryl,安万特公司 )治疗2型糖尿病的有效性和安全性。方法　无磺酰脲类药物继发失效的 2型糖尿病患者 10 4例 ,以 2 :1的比例随机分入格列美脲组和格列苯脲组 ,观察时间为 16周 (8周剂量调整期 ,8周维持期 )。结果格列美脲降血糖的有效率为 88.7% ,格列苯脲组为 83.3% ,两组间差异无显著性。格列美脲组在降低空腹血糖、餐后 2小时血糖和HbA1c方面和格列苯脲同样有效。格列美脲对于餐后 2h血清胰岛素和C肽的升高作用低于格列苯脲 ,但空腹胰岛素及C肽水平两组相似。格列美脲组对肝肾功能和血压无不良影响 ,低血糖的发生率低于格列苯脲组 (18.2 %vs 33.3% ,P <0 .0 5 )。结论　格列美脲治疗 2型糖尿病安全有效。     

格列美脲与格列本脲分别与沙格列汀、二甲双胍联用治疗2型糖尿病的有效性及经济性评价

目的系统评价格列本脲联用沙格列汀、二甲双胍对比格列美脲联用沙格列汀、二甲双胍治疗2型糖尿病的疗效、安全性和经济费用。方法纳入威海市立医院内分泌科就诊的2型糖尿病患者140例,随机分为两组,A组应用格列本脲、沙格列汀及二甲双胍降糖治疗;B组应用格列美脲、沙格列汀及二甲双胍降糖治疗。A组与B组疗程均为12 w。观察2组空腹血糖、餐后2 h血糖、糖化血红蛋白、空腹C肽、餐后2 h C肽、空腹胰岛素原、餐后2 h胰岛素原、空腹胰岛素、餐后2 h胰岛素、体重、胰岛素抵抗指数等的变化及不良反应。结果 2组均具有良好的降空腹血糖、餐后2h血糖及糖化血红蛋白作用;经治疗2组空腹胰岛素、C肽水平均明显升高;而空腹胰岛素原和餐后2 h胰岛素原较前明显下降(均P<0.05)。低血糖反应发生率两组无明显差异(P>0.05),两组患者体重均无明显增加(P>0.05)。经济学成本A组明显低于B组(P<0.05)。结论格列美脲和格列本脲分别联用沙格列汀、二甲双胍治疗2型糖尿病疗效均良好,低血糖反应少,而格列本脲组经济学成本明显低于格列美脲组。     

格列美脲治疗2型糖尿病的临床疗效观察

目的为观察格列美脲治疗2型糖尿病的疗效,评价其有效性和安全性,按标准入选患者150例,其中格列美脲治疗组92例,格列苯脲组58例。方法选择2011年2月—2013年5月在该院收治的2型糖尿病患者,年龄30~37岁,平均年龄33.5岁,所有150例2型糖尿病患者分别给与格列美脲1 mg/d,早餐前顿服格列苯脲1.25 mg/d,根据空腹血糖水平,每1~2周调整用药剂量,12周后观察两组患者六项代谢指标的变化。结果两组治疗前后的空腹血糖(FBG)及糖化血红蛋白(Hb A1c)均明显下降;格列美脲组的治疗前后2h C-P明显下降;且两组的FC-P及体重指数(BMI)无明显变化。结论格列美脲和格列苯脲降血糖作用相似,但格列美脲可明显降低2h C-P水平,所以格列美脲是2型糖尿病患者的首选降糖药物。     

格列美脲与格列苯脲治疗2型糖尿病Meta分析

目的系统评价格列美脲与格列苯脲治疗2型糖尿病的疗效。方法计算机检索PubMed、Ov-id、中国知网(CNKI)、万方、维普、中国生物医学文献数据库(CBM)等数据库建库截至2010年12月的有关文献。按Cochrane系统评价的方法评价纳入研究质量,使用Review Manager 4.2软件进行Meta分析。结果本研究共纳入9个前瞻性随机对照试验(RCT)进行分析。研究结果显示,格列美脲在降低糖化血红蛋白、空腹及餐后血糖、胆固醇、甘油三酯方面与格列苯脲差异无统计学意义(P>0.05);在相同血糖水平下,格列美脲空腹及餐后胰岛素升高的程度明显低于格列苯脲(P<0.05),低血糖发生率低于格列苯脲(P<0.05),在降低体重指数方面优于格列苯脲(P<0.05)。结论与格列苯脲相比,格列美脲不仅可以降低血糖,还可以改善胰岛素抵抗及减轻体重,低血糖发生率低,是有效安全地治疗2型糖尿病的药物。     

格列本脲继发性失效患者应用格列美脲的疗效观察

对53例格列本脲继发性失效的2型糖尿病患者停用格列本脲，换用格列美脲治疗，结果：周后，FPG、2hPG和HbA1c降低（P〈0．05），FINS无明显变化（P〉0．05），PINS下降（P〈0．05），HOMA-IR明显降低（P〈0．05），BMI轻微下降但无统计学意义，TG、HDL—C较前改善（P〈0．05），血压无变化。结论格列美脲因其双重的降糖作用能有效控制口服格列本脲失效的2型T2DM患者的血糖，并对改善患者体重和血脂有益。     

格列美脲和格列苯脲治疗初诊2型糖尿患者时对心血管危险因素影响的对比研究

目的比较格列美脲和格列苯脲对初诊2型糖尿病患者糖、脂代谢及纤溶酶原活性等心血管危险因素的影响。方法比较格列美脲（n=333）和格列苯脲（n=232）治疗初诊2型糖尿病患者12周前后血糖、糖化血红蛋白、胰岛素抵抗改善情况．同时比较两组血脂及组织型纤溶酶原激活剂（tissue—type plasminogen activator,TPA）和纤溶酶原激活剂抑制物1（plasminogen activator inhibitor-1,PAI—1）的浓度。结果与治疗前相比,格列美脲和格列苯脲治疗后患者血糖均达到良好控制,格列美脲组治疗后低血糖发生率低于格列苯脲组,差异有统计学意义（0．3％vs.1．7％,P〈0．05）。格列美脲组治疗12周后,Homa-胰岛素抵抗比治疗前减少,差异有统计学意义（2．42％±0．91％vs.4．11％±0．85％,P〈0．01）;而在格列苯脲组,治疗前后Homa-胰岛素抵抗比较差异无统计学意义（P〉0．05）。格列美脲组治疗12周后,血清总胆固醇、三酰甘油、低密度脂蛋白胆固醇浓度比治疗前显著下降,而血清高密度脂蛋白胆固醇浓度升高,差异有统计学意义（P〈0．05）;而格列苯脲组治疗前后血脂浓度比较．差异无统计学意义（P〉0．05）。格列美脲治疗12周较治疗前明显升高t-PA,降低PAI-1,差异有统计学意义（P〈0．05）;而格列苯脲治疗前后t—PA、PAI-1比较,差异无统计学意义（P〉0．05）。结论对初诊2型糖尿病患者．格列美脲具有快速稳定控制血糖、改善脂质代谢和显著减轻胰岛素抵抗、改善纤溶活性的作用。     

格列美脲与格列吡嗪治疗2型糖尿病疗效比较

目的比较格列美脲与格列吡嗪治疗2型糖尿病的疗效。方法将42例2型糖尿病患者随机分为格列美脲组与格列吡嗪组。格列美脲组20例,格列吡嗪组22例,观察时间12周。治疗前后监测病人空腹血糖(FBG)、餐后2小时血糖(2hPBG)、空腹胰岛素(FINS)、餐后2小时胰岛素(2hPINS)、糖化血红蛋白(HbA1c)、体重指数(BMI)。结果两组治疗前后FBG、2hPBG、HbA1c均明显下降(P<0.05),但两组相比差异无统计学意义;两组治疗前后FINS差异无统计学意义;格列美脲组2hPINS和BMI升高低于格列吡嗪组,差异有统计学意义(P<0.05),低血糖发生率显著低于格列吡嗪组(P<0.05)。结论格列美脲降糖效果好,使用安全。     

盐酸二甲双胍联合格列苯尿治疗2型糖尿病疗效评价

目的观察盐酸二甲双胍（美迪康）对血糖、胰岛β细胞功能的影响。方法选择经诊断确诊为2型糖尿病患者152例,随机分为治疗组83例,对照组69例,治疗组服用盐酸二甲双胍加格列苯脲片,对照组单纯服用格列苯脲片,疗程12周。观察两组治疗前后空腹血糖、餐后2h血糖、糖化血红蛋白、空腹C肽、体重指数指标的变化。结果治疗后治疗组空腹血糖、餐后2 h血糖控制满意,糖化血红蛋白和体重指数下降,空腹C肽水平升高;对照组空腹血糖等各项检测指标有改善,但两组比较治疗组均优于对照组显著有统计学意义（P〈0.01）。结论盐酸二甲双胍片能抑制肝糖输出,增加胰岛素的敏感性,提高胰岛素的作用效能,是一种安全有效的降糖药物。     

再谈口服降糖药

糖尿病患者通过饮食治疗及适量运动血糖仍未得到控制时便需要服用降糖药。药物是重要的治疗方法,必须在饮食控制和运动治疗的基础上才能发挥应有的效果。药物的种类颇多,糖尿病患者不要擅自选购、使用药物,一定要遵守医嘱,通过科学的配伍,定时定量地服用,根据病情合理选择,以减少或避免不良反应的发生。口服降糖药的种类及特点促胰岛素分泌剂类药物磺脲类药物的特点:品种有优降糖(格列本脲)、美吡哒(格列吡嗪)、达美康(格列齐特)、糖适平(格列喹酮)、亚莫力(格列美脲)等。主要通过刺激胰岛β细胞产生胰岛素发挥降糖作用。对胰岛功能完全破坏…     

中西合璧消渴丸，标本兼治糖尿病

“消”除担忧一中西合璧，标本兼治 格列本脲：核心地位靠事实说话磺脲类降糖药物在糖尿病治疗领域的应用已经超过半个世纪了，至今仍以其有效、价廉等优势在2型糖尿病治疗中占据重要地位。其重要代表药格列本脲．在临床上仍然受到广泛的关注，很多著名的糖尿病研究都以格列本脲作为对照，     

Effects of glimepiride and glyburide on glucose counterregulation and recovery from hypoglycemia

Severe hypoglycemia, the most serious side effect of sulfonylurea therapy, has been reported to occur more frequently with glyburide than glimepiride. The present studies were undertaken to test the hypothesis that a differential effect on glucagon secretion may be involved. We performed hyperinsulinemic hypoglycemic (approximately 2.5 mmol/L) clamps in 16 healthy volunteers who received in randomized order placebo, glyburide (10 mg), and glimepiride (4 mg) just before beginning the insulin infusion and measured plasma glucagon, insulin, C-peptide, glucagon, epinephrine, cortisol, and growth hormone levels during the clamp and during a 3-hour recovery period after discontinuation of the insulin infusion. Neither sulfonylurea altered glucagon responses or those of other counterregulatory hormones (except cortisol) during the clamp. However, glyburide delayed plasma glucose recovery from hypoglycemia (plasma glucose at end of recovery period: control, 4.9 +/- 0.2 mmol/L; glyburide, 3.7 +/- 0.2 mmol/L; P = .0001; glimepiride, 4.5 +/- 0.2 mmol/L; P = .08). Despite lower plasma glucose levels, glyburide stimulated insulin secretion during this period (0.89 +/- 0.13 vs 1.47 +/- 0.15 pmol x kg(-1) x min(-1), control vs glyburide; P = .001), whereas glimepiride did not (P = .08). Short-term administration of glyburide or glimepiride did not alter glucagon responses during hypoglycemia. In contrast, during recovery from hypoglycemia, glyburide but not glimepiride inappropriately stimulates insulin secretion at low plasma glucose levels. This differential effect on insulin secretion may be an important factor in explaining why glyburide causes severe hypoglycemia more frequently than glimepiride.     

Increase in overall mortality risk in patients with type 2 diabetes receiving glipizide, glyburide or glimepiride monotherapy versus metformin: a retrospective analysis

Aims: It remains uncertain if differences in mortality risk exist among the sulfonylureas, especially in patients with documented coronary artery disease (CAD). The purpose of this study was to assess the overall mortality risk of the individual sulfonylureas versus metformin in a large cohort of patients with type 2 diabetes. Methods: A retrospective cohort study was conducted using an academic health centre enterprise‐wide electronic health record (EHR) system to identify 23 915 patients with type 2 diabetes who initiated monotherapy with metformin (N = 12774), glipizide (N = 4325), glyburide (N = 4279) or glimepiride (N = 2537), ≥18 years of age, with and without a history of CAD, and not on insulin or a non‐insulin injectable at baseline. The patients were followed for mortality by documentation in the EHR and Social Security Death Index. Multivariable Cox models with propensity analysis were used to compare cohorts. Results: An increase in overall mortality risk was observed in the entire cohort with glipizide (HR 1.64; 95% CI 1.39–1.94), glyburide (HR 1.59; 95% CI 1.35–1.88), and glimepiride (HR 1.68; 95% CI 1.37–2.06) versus metformin; however, in those patients with documented CAD, a statistically significant increase in overall mortality risk was only found with glipizide (HR 1.41; 95% CI 1.07–1.87) and glyburide (HR 1.38; 95% CI 1.04–1.83) versus metformin. Conclusions: Glipizide, glyburide and glimepiride are associated with an increased risk of overall mortality versus metformin. Our results suggest that if a sulfonylurea is required to obtain glycaemic control, glimepiride may be the preferred sulfonylurea in those with underlying CAD.     

Comparison of metabolic effects of pioglitazone, metformin, and glimepiride over 1 year in Japanese patients with newly diagnosed Type 2 diabetes.

AIMS: To compare the metabolic effects of pioglitazone, metformin, and glimepiride in the treatment of Japanese patients with newly diagnosed Type 2 diabetes. METHODS: A total of 114 patients with Type 2 diabetes who had never used oral hypoglycaemic drugs were studied for 12 months. Patients were randomly assigned to pioglitazone (30-45 mg/day, n = 38), metformin (750 mg/day, n = 39), or glimepiride (1.0-2.0 mg/day, n = 37). The effect of treatment on fasting plasma glucose (FPG), glycated haemoglobin (HbA(1c)), 1,5-anhydroglucitol (1,5AG), total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, free fatty acids (FFA), and fasting plasma insulin levels was monitored monthly. Body weight and safety data were also collected. RESULTS: Eight patients withdrew from the study (three in the pioglitazone group, two in the metformin group, and three in the glimepiride group). The rate of reduction of HbA(1c) was fastest in patients receiving glimepiride and slowest in patients receiving pioglitazone. Although there were no significant differences among the three groups in HbA(1c) levels at the end of the study, patients taking pioglitazone had relatively lower FPG and 1,5AG levels than patients taking the other two drugs. These results suggest that pioglitazone acts predominantly on nocturnal metabolism rather than at mealtimes. FFA were reduced significantly in those taking pioglitazone (542.2 microEq/l vs. 237.3 microEq/l; P < 0.01) before a decrease in HbA(1c) was apparent. The change in FFA levels correlated with the change in HbA(1c) (r = 0.409, P < 0.01). There were no significant differences in other lipid parameters among the groups. CONCLUSIONS: Pioglitazone, metformin, and glimepiride are equally effective in reducing blood glucose in patients with newly diagnosed Type 2 diabetes. However, their specific characteristics, such as the rapid action on blood glucose levels of glimepiride and the favourable action on FPG and FFA of pioglitazone, should be considered when choosing an appropriate agent.     

A comparison of glycemic effects of glimepiride, repaglinide, and insulin glargine in type 2 diabetes mellitus during Ramadan fasting

Although diabetics may be exempted from Ramadan fasting, many patients still insist on this worship. Aim of the present study is to compare the effects of glimepiride, repaglinide, and insulin glargine in type 2 diabetics during Ramadan fasting on the glucose metabolism. Patients, who were willing to fast, were treated with glimepiride (n=21), repaglinide (n=18), and insulin glargine (n=10). Sixteen non-fasting control type 2 diabetics matched for age, sex, and body mass index were also included. Fasting blood glucose (FBG), post-prandial blood glucose (PBG), HbA1c, and fructosamine as well as lipid metabolism were evaluated in pre-Ramadan, post-Ramadan, and 1-month post-Ramadan time points. There was no significant change from pre-Ramadan in FBG, PBG, and HbA1c variables in fasting diabetics at post-Ramadan and 1-month post-Ramadan. However, PBG was found higher in non-fasting control diabetics at post-Ramadan and 1-month post-Ramadan (p<0.05 and p<0.001, respectively). In fructosamine levels, a significant increase was noted both in fasting group and non-fasting group at 1-month post-Ramadan (p<0.01 for all). However, no significant difference was found in the comparison of the changes in fructosamine levels between fasting group and non-fasting group. Risk of hypoglycemia did not significantly differ between fasting and non-fasting diabetics. There was no significant difference between three drug therapies regarding glucose metabolism and rate of hypoglycemia. No adverse effects on plasma lipids were noted in fasting diabetics. In this fasting sample of patients with type 2 diabetes, glimepiride, repaglinide, and insulin glargine did not produce significant changes in glucose and lipid parameters.     

Impact of rosiglitazone on beta-cell function, insulin resistance, and adiponectin concentrations: results from a double-blind oral combination study with glimepiride

Addition of rosiglitazone to sulfonylurea has been shown to improve glycemic control in patients with type 2 diabetes previously treated with sulfonylurea monotherapy alone. This investigation was performed to assess the specific impact of rosiglitazone on insulin resistance, beta-cell function, cardiovascular risk markers, and adiponectin secretion in this treatment concept. One hundred two patients from a double-blind, 3-arm comparator trial (group 0, glimepiride + placebo, n = 30; group 4, glimepiride + 4 mg rosiglitazone, n = 31; group 8, glimepiride + 8 mg rosiglitazone, n = 41; 48 women, 54 men; age [mean +/- SD], 62.8 +/- 9.1 years; body mass index, 28.7 +/- 4.5 kg/m2; diabetes duration, 6.4 +/- 4.8 years; HbA1c, 8.1% +/- 1.5%) were analyzed after 0 and 16 weeks of treatment. Observation parameters were HbA1c, glucose, homeostasis model assessment for insulin resistance score, insulin, intact proinsulin, and adiponectin. Insulin resistance was defined by elevated intact proinsulin values or homeostasis model assessment for insulin resistance score of more than 2. All parameters were comparable in the 3 groups at baseline. Substantial and significant dose-dependent improvements were observed after addition of rosiglitazone for fasting glucose (group 0, -9 +/- 48 mg/dL; group 4, -38 +/- 47 mg/dL; group 8, -46 +/- 53 mg/dL), HbA1c (-0.1% +/- 0.7%, -1.1% +/- 1.2%, -1.3% +/- 1.2%), insulin (1.4 +/- 6.2, -1.2 +/- 5.3, -3.7 +/- 9.9 microU/mL), intact proinsulin (1.6 +/- 7.1, -2.0 +/- 4.6, -3.1 +/- 6.1 pmol/L), and high-sensitivity C-reactive protein (0.2 +/- 2.6, -1.7 +/- 3.5, -2.1 +/- 3.5 mg/L). After adjustment for changes in body weight, significant increases in adiponectin were detected with rosiglitazone, whereas glimepiride alone did not induce a comparable effect (-0.5 +/- 5.8, 8.8 +/- 22.9, 14.3 +/- 19.9 mg/L). The number of insulin-resistant patients decreased in both rosiglitazone treatment groups, whereas no change was seen with glimepiride alone. Next to the reported effects on glucose control, rosiglitazone provided an additional beneficial effect on insulin resistance, beta-cell function, and cardiovascular risk markers. In conclusion, our short-term investigation of rosiglitazone action provides further experimental support for the rationale of combining rosiglitazone with sulfonylurea drugs in patients with type 2 diabetes.     

Glyburide prevents isoflurane’s reducing effects on hydroxyl radical formation in the postischemic reperfused rat heart

BACKGROUND:

The role of K_ATP channels in isoflurane’s reducing effects on oxygen free radical formation are not well known.

OBJECTIVES:

To investigate whether glyburide, an ATP-regulated potassium (K_ATP) channel blocker, abolishes isoflurane-induced cardioprotective effects and whether it affects hydroxyl radical formation in the postischemic reperfused heart.

ANIMALS AND METHODS:

Thirty-nine male Wistar rats were divided into four groups: group C (control, n=10), group I (isoflurane, n=9), group G (glyburide, n=10) and group GI (glyburide and isoflurane, n=10). The hearts were perfused as a Neely’s working heart model. Afterwards, global heart ischemia was induced for 15 min followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent and heart was measured with high performance liquid chromatography.

RESULTS:

Isoflurane alone and glyburide alone produced significant decreases in the duration of ventricular fibrillation during reperfusion (group C 452±345, group I 247±60, group G 261±135 s; P<0.05). In the presence of glyburide, isoflurane did not further decrease the duration of arrhythmia (group GI 230±48 s). Isoflurane reduced hydroxyl radical formation significantly in the coronary effluent during ischemia and reperfusion, but this was prevented by glyburide.

CONCLUSION:

The results suggest that isoflurane reduces hydroxyl radical formation, at least in part, through activation of K_ATP channels.     

Efficacy and safety of treatment with sitagliptin or glimepiride in patients with type 2 diabetes inadequately controlled on metformin monotherapy: a randomized, double-blind, non-inferiority trial

Aim: To evaluate the efficacy and safety of adding sitagliptin or glimepiride to the treatment regimen of patients with type 2 diabetes mellitus and inadequate glycaemic control on metformin monotherapy. Methods: Patients with type 2 diabetes and an HbA_1c of 6.5–9.0% while on a stable dose of metformin (≥1500 mg/day) combined with diet and exercise for at least 12 weeks were randomized in a double‐blind manner to receive either sitagliptin 100 mg daily (N = 516) or glimepiride (starting dose 1 mg/day and up‐titrated, based upon patient's self‐monitoring of blood glucose results, to a maximum dose of up to 6 mg/day) (N = 519) for 30 weeks. The primary analysis assessed whether sitagliptin is non‐inferior to glimepiride in reducing HbA_1c at week 30 (based on the criterion of having an upper bound of the 95% CI less than the prespecified non‐inferiority bound of 0.4%). Results: The mean baseline HbA_1c was 7.5% in both the sitagliptin group (n = 443) and the glimepiride group (n = 436). After 30 weeks, the least squares (LS) mean change in HbA_1c from baseline was ?0.47% with sitagliptin and ?0.54% with glimepiride, with a between‐group difference (95% CI) of 0.07% (?0.03, 0.16). This result met the prespecified criterion for declaring non‐inferiority. The percentages of patients with an HbA_1c < 7.0% at week 30 were 52 and 60% in the sitagliptin and glimepiride groups, respectively. The LS mean change in fasting plasma glucose from baseline (95% CI) was ?0.8 mmol/l (?1.0, ?0.6) with sitagliptin and ?1.0 mmol/l (?1.2, ?0.8) with glimepiride, for a between‐group difference (95% CI) of 0.2 mmol/l (?0.1, 0.4). The percentages of patients for whom hypoglycaemia was reported were 7% in the sitagliptin group and 22% in the glimepiride group (percentage‐point difference = ?15, p < 0.001). Relative to baseline, sitagliptin was associated with a mean weight loss (?0.8 kg), whereas glimepiride was associated with a mean weight gain (1.2 kg), yielding a between‐group difference of ?2.0 kg (p < 0.001). Conclusions: In patients with type 2 diabetes and inadequate glycaemic control on metformin monotherapy, the addition of sitagliptin or glimepiride led to similar improvement in glycaemic control after 30 weeks. Sitagliptin was generally well tolerated. Compared to treatment with glimepiride, treatment with sitagliptin was associated with a lower risk of hypoglycaemia and with weight loss versus weight gain ( ClinicalTrials.gov : NCT00701090).     

Efficacy of glimepiride in Japanese type 2 diabetic subjects

We investigated the efficacy of glimepiride, a third-generation sulfonylurea (SU), in Japanese type 2 diabetic patients in whom glycemic control had been inadequate with a conventional SU, gliclazide or glibenclamide. A total of 172 Japanese type 2 diabetic patients (HbA1C > or = 7.0%), maintained on a conventional SU, were randomly assigned to the 3rd SU group (SU treatments switched to glimepiride) or the 2nd SU group (treatments not changed). The conventional SU was switched to the indicated doses of glimepiride (gliclazide 40 mg = glimepiride 1 mg, glibenclamide 2.5 mg = glimepiride 2 mg). After 6 months, glycemic control (HbA1C and fasting plasma glucose) had not changed significantly in either the 2nd or the 3rd SU group. The homeostasis assessment model of insulin resistance (HOMA-IR) in the 3rd SU group was decreased by more than 10% (p = 0.015), whereas no change was observed in the 2nd SU group. The triglyceride level was decreased by approximately 10% in the 3rd SU group, not a significant change (p = 0.080). Patients who had been treated with only SU, or treated with SU for a short time (less than 5 years), and who were also obese (BMI > or = 25) or had a high HOMA-IR (HOMA-IR > or = 3), showed significantly reduced insulin resistance. According to logistic regression analysis, high BMI ( > or = 25) was the only variable predicting that glimepiride would more effectively improve HbA1C than conventional SU treatment. In conclusion, switching conventional SUs to glimepiride reduced insulin resistance without improving glycemic control. A notable finding of this study is that glimepiride was more beneficial in obese than in non-obese Japanese type 2 diabetic patients.     

Liraglutide versus glimepiride monotherapy for type 2 diabetes (LEAD-3 Mono): a randomised, 52-week, phase III, double-blind, parallel-treatment trial

BACKGROUND: New treatments for type 2 diabetes mellitus are needed to retain insulin-glucose coupling and lower the risk of weight gain and hypoglycaemia. We aimed to investigate the safety and efficacy of liraglutide as monotherapy for this disorder. METHODS: In a double-blind, double-dummy, active-control, parallel-group study, 746 patients with early type 2 diabetes were randomly assigned to once daily liraglutide (1.2 mg [n=251] or 1.8 mg [n=247]) or glimepiride 8 mg (n=248) for 52 weeks. The primary outcome was change in proportion of glycosylated haemoglobin (HbA(1c)). Analysis was done by intention-to-treat. This trial is registered with ClinicalTrials.gov, number NTC00294723. FINDINGS: At 52 weeks, HbA(1c) decreased by 0.51% (SD 1.20%) with glimepiride, compared with 0.84% (1.23%) with liraglutide 1.2 mg (difference -0.33%; 95% CI -0.53 to -0.13, p=0.0014) and 1.14% (1.24%) with liraglutide 1.8 mg (-0.62; -0.83 to -0.42, p<0.0001). Five patients in the liraglutide 1.2 mg, and one in 1.8 mg groups discontinued treatment because of vomiting, whereas none in the glimepiride group did so. INTERPRETATION: Liraglutide is safe and effective as initial pharmacological therapy for type 2 diabetes mellitus and leads to greater reductions in HbA(1c), weight, hypoglycaemia, and blood pressure than does glimepiride.     

Effect of gemigliptin on glycaemic variability in patients with type 2 diabetes (STABLE study)

The aim of this study was to evaluate the effect of gemigliptin vs sitagliptin or glimepiride as initial combination therapy with metformin on glycaemic variability and to assess the correlation between glycaemic variability reduction and the dipeptidyl peptidase‐4 (DPP‐4) inhibition in patients with type 2 diabetes. This multicentre, randomized, active‐controlled, open‐label exploratory study included 69 patients with HbA1c > 7.5%. Subjects were randomized to receive gemigliptin 50 mg (n = 24), sitagliptin 100 mg (n = 23) or glimepiride 2 mg (n = 22) for 12 weeks. After 12 weeks, the change in mean amplitude of glycaemic excursion (MAGE) compared with baseline was significantly lower in the DPP‐4 inhibitor groups compared with that in patients who received glimepiride. Furthermore, the standard deviation (SD) of glucose was significantly lower in patients who received gemigliptin than that in patients who received sitagliptin or glimepiride. The DPP‐4 inhibition was significantly correlated with changes in MAGE and SD of glucose. In conclusion, gemigliptin and sitagliptin were more effective than glimepiride in reducing glycaemic variability as initial combination therapy with metformin in patients with type 2 diabetes, and the DPP‐4 inhibition was associated with a reduction in glycaemic variability.