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Two review authors read all abstracts and full-text articles/records, assessed quality and extracted outcome data independently. One review author extracted data which were checked by a second review author. We resolved discrepancies by consensus or the involvement of a third review author. For meta-analyses we used a random-effects model with investigation of risk ratios (RRs) for dichotomous outcomes and mean differences (MDs) for continuous outcomes, using 95% confidence intervals (CIs) for effect estimates. We carried out trial sequential analyses (TSAs) for all outcomes that could be meta-analysed. We assessed the overall quality of the evidence by using the GRADE instrument.
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To examine the options for add-on therapy in patients with type 2 diabetes whose disease is no longer adequately controlled by lifestyle interventions and oral antidiabetic drug (OAD)monotherapy.
The addition of telmisartan to vildagliptin demonstrated the best control over blood pressure, glycemia and diabetic nephropathy markers, renal structural changes and improvement of renal function as opposed to monotherapy with either drug, possibly because of the dual inhibitory effect on the renin-angiotensin system.
The genetically polymorphic cytochrome P450 (CYP) enzyme CYP2C9 metabolizes most sulphonylurea oral hypoglycaemic agents. The aim of this study was to test the hypothesis that individuals with genotypes predicting low CYP2C9 activity may be at a higher risk of severe drug-associated hypoglycaemia.
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In the rat liver microsome system, glimepiride showed a slight inhibition of losartan at concentrations of 1-10 μmol/l, whereas losartan exhibited no inhibitory effect on glimepiride. In vivo, glimepiride did not modify the plasma concentration of losartan and its metabolite E-3174. The alteration of an increased AUC and Cmax was observed in the pharmacokinetic parameters of glimepiride and hydroxy glimepiride.
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The objective of this study was to prepare solid self-nanoemulsifying drug delivery system (S-SNEDDS) for the improved oral delivery of glimepiride and to evaluate its therapeutic efficacy in albino rabbits.
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We performed a 3-year observation study of type 2 diabetic patients treated with glibenclamide or glimepiride and found that the annual progression of the maximum carotid intima-media thickness was significantly attenuated in the subjects treated with glimepiride (n=20) as compared with those treated with glibenclamide (n=20) (-0.044±0.171 mm/year vs. 0.077±0.203 mm/year, p=0.0474).
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In isolated pancreatic islets of mice, the relationships between free glimepiride concentration and membrane binding or inhibition of ATP-sensitive K+ channels were examined. Microsomal membrane binding and K+ channel inhibition were half-maximal at 0.7 and 0.3 nmol/l glimepiride, respectively. The corresponding concentrations for glibenclamide were 0.4 and 0.6 nmol/l. Administration of glimepiride (10 nmol/l) or glibenclamide (10 nmol/l) to isolated mouse islets perifused with albumin-containing media induced a slow increase in insulin secretion. The kinetics of the secretory responses to glimepiride and glibenclamide were identical. Determination of albumin binding revealed that the free glimepiride and glibenclamide concentrations applied in our investigation were in the range of therapeutic serum concentrations of the free drugs. It is concluded that the effects of glimepiride and glibenclamide are very similar in mouse beta-cells.
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The studies were performed on healthy male Wistar rats with a body mass of 220+/-30 g, fed with LSM-type standard chow, and given water ad libitum. Transient or prolonged hyperglycemia was induced by intraperitoneal administration of streptozotocin. Blood samples were taken from the right heart ventricle to heparinized test tubes and centrifuged for 10 minutes at 700 i. g. Plasma was collected and the glucose level was determined. From each animal 1 g of skeletal muscle and 1 g of liver were collected as well, placed in liquid nitrogen and stored until determination of the affinity and number of receptors.
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The effects of intensive glucose control on cardiovascular events in patients with long-standing type 2 diabetes mellitus remain uncertain.
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Pharmaceuticals are emerging contaminants in the natural environment. Most studies of the environmental fate of these chemicals focus on their behavior in wastewater treatment processes and in sewage sludge. Little is known about their behavior in soils. In this study adsorption and biodegradation of four antidiabetic pharmaceuticals - glimepiride, glibenclamide, gliclazide and metformin - were examined in three natural soils. The sorption of sulfonylurea derivatives was high (higher than sulfonylurea herbicides for example), whereas metformin showed high mobility. Desorption rates were highest for metformin. Sorption isotherms in two of three soils fitted best to the Freundlich model. Despite their high affinity to for soil surfaces, biodegradation studies revealed that transformation of the drugs occurred. Biodegradation results were described by pseudo-first order kinetics with half-life values from 5 to over 120 d (under aerobic conditions) and indicate that none of the tested drugs can be classified as quickly biodegradable. Biodegradation under anoxic conditions was much slower; often degrading by less than 50% during time of the experiment.
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To compare the use of sitagliptin and glimepiride as early add-on drugs along with metformin in young patients with DM to achieve optimum glycemic targets.
To review the clinical pharmacology data regarding the sulfonylurea glimepiride, and to summarize the clinical trials of glimepiride efficacy and safety alone and in combination with insulin for the treatment of type 2 diabetes mellitus.
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Albiglutide, as part of triple therapy, provided effective glucose-lowering and was generally well tolerated.
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This review provides a comprehensive summary of available data on the pharmacology, pharmacokinetics, efficacy, and safety profile of glimepiride in the treatment of type 2 diabetes. It also examines the use of glimepiride to achieve and maintain good glycemic control in patients with type 2 diabetes in current clinical practice.
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5847 patients received linagliptin (5 mg: 5687, 10 mg: 160) and 3612 comparator (glimepiride: 775, voglibose: 162, placebo: 2675); cumulative exposure, 4421.3 and 3254.7 patient-years, respectively. 4P-MACE incidence rates: 13.4 per 1000 patient-years, linagliptin (60 events), 18.9, total comparators (62 events); overall hazard ratio (HR), 0.78 (95% confidence interval [CI], 0.55-1.12). HR for adjudicated hospitalization for CHF (n = 21): 1.04 (0.43-2.47). For placebo-controlled trials, 4P-MACE incidence rates: 14.9 per 1000 patient-years, linagliptin (43 events), 16.4, total comparators (29 events); overall HR, 1.09 (95% CI, 0.68-1.75). Occurrence of investigator-reported events suggestive of CHF was low for linagliptin- (26 events, 0.5%; serious: 16 events, 0.3%) and placebo-treated (8 events, 0.2%; serious: 6 events, 0.2%) patients.
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This crossover study randomised T2D patients (n = 42) with glycated haemoglobin (HbA1c) ≤7.5%, no diagnosed macro- or microvascular disease and on stable metformin background to linagliptin 5 mg qd, glimepiride 1-4 mg qd or placebo for 28 days. Fasting and postprandial macrovascular endothelial function, measured using brachial flow-mediated vasodilation, and microvascular function, measured using laser-Doppler on the dorsal thenar site of the right hand, were analysed after 28 days.
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Plasma glucose level at 30, 60, 120, and 180 min was significantly improved by mitiglinide. Whereas, glimepiride showed a significant improve plasma glucose at 0, 180 min. Peak IRI shifted from 120 to 30 min by mitiglinide treatment. The pattern of insulin secretion was not changed by glimepiride treatment. Whereas mitiglinide did not affect the PI/I ratio, glimepiride tended to increase the PI/I ratio. Moreover, although mitiglinide did not affect PI/I ratio as a whole, marked reduction was noted in some patients treated by mitiglinide. PI/I ratio was reduced significantly in the responder group. The responder subgroup exhibited less insulin resistance and higher insulinogenic index at baseline than non-responders. Moreover, the triglyceride level of responders was significantly lower than that of non-responders.
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The blood glucose profile of our patients during Ramadan is characterized by important glycaemic excursions.
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Canagliflozin is an SGLT2 inhibitor, which has been the subject of two recent clinical trials, which are evaluated.
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Liraglutide (monotherapy or added to metformin) significantly reduced fat mass and fat percentage vs. glimepiride in patients with T2D.
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Hemoglobin A(1c) values, blood glucose levels, insulin dose, and body weight.
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The method was proved to be simple, rapid, precise, accurate, and cost effective.
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Almost 20% of patients were exposed to a potential drug-drug interaction with a CYP2C9 inhibitor during sulphonylurea treatment. More than 75% of the potential interactions occurred with trimethoprim, metronidazole and fluconazole. When all sulphonylureas were pooled and adjusted for age, gender, ward and sulphonylurea dose, mean and maximum fasting plasma glucose concentrations as well as maximum values of glycosylated haemoglobin were significantly lower during the interaction periods compared with control periods, whereas mean and minimum activities of alanine amino transferase and gamma-glutamyl transferase were higher. The minimum fasting plasma glucose values were more often below the target range in patients with potential interactions. The sulphonylurea dose did not differ significantly between patients who were or were not concomitantly treated with a potentially interacting drug.
Linagliptin is not associated with increased CV risk versus pooled active comparators or placebo in patients with T2DM.
HbA1c was reduced significantly from 8.6 ± 1.6% to 6.9 ± 0.9% (p < 0.001); 60.9% of the subjects achieved HbA1c <7% at study endpoint. The reduction in FPG and 2hPPG were 2.3 mmol/L and 4.4 mmol/L (p < 0.001) respectively. Insulin resistance was improved significantly with HOMA-IR decreasing from 2.5 ± 2.3 to 2.2 ± 1.9 (p = 0.009). The incidence of confirmed hypoglycemia (BG ≤ 3.9 mmol/L) was 3.1%.
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Thirty-six subjects (17 men and 19 women) aged 67.8 +/- 11.3 years with an average insulin dose of 0.46 +/- 0.17 U/kg bodyweight, a duration of insulin therapy of 6.1 +/- 8.2 years and an average hemoglobin A1c (HbA1c) of 6.8 +/- 1.3% were switched from insulin injection therapy to pioglitazone, glimepiride and voglibose combination therapy.
A malnourished 58-year-old man with diabetes developed hypoglycemia after receiving levofloxacin in conjunction with glipizide.