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Glucotrol

Glucotrol is a medication consists in a class of drugs called sulfonylureas. Glucotrol is used to treat type 2 diabetes. Glucotrol may be used along with diet, exercise and insulin therapy. Glucotrol works by controlling blood sugar levels in your organism.

Other names for this medication:

Similar Products:
Glucophage, Actos, Avandia, Amaryl, Diabinese, Amaryl, Glynase, DiaBeta, Tolinase, Glycron, Glynase PresTab, Micronase, Orinase, Tol-Tab

 

Also known as:  Glipizide.

Description

Glucotrol is a medication consists in a class of drugs called sulfonylureas.

Glucotrol is used to treat type 2 diabetes. Glucotrol may be used along with diet, exercise and insulin therapy.

Glucotrol is also known as Glipizide, Glytop SR.

Glucotrol works by controlling blood sugar levels in your organism.

Generic name of Glucotrol is Glipizide.

Brand names of Glucotrol are Glucotrol, Glucotrol XL.

Dosage

Take Glucotrol orally.

Do not chew, divide or crush the tablet. Swallow it whole.

Glucotrol is usually taken before breakfast if it is taken once a day, or before meals if it is taken several times each day.

Take each dose of Glucotrol with a full glass of water.

The dosage and the kind of tablets depend on the disease and its prescribed treatment.

While taking Glucotrol follow diet, medication and exercise routines closely.

If you want to achieve most effective results do not stop taking Glucotrol suddenly.

Overdose

If you overdose Glucotrol and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Glucotrol overdosage: hunger, nausea, anxiety, cold sweats, weakness, drowsiness, unconsciousness, coma.

Storage

Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Glucotrol are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Glucotrol if you are allergic to Glucotrol components.

Be careful with Glucotrol if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Glucotrol if you have kidney disease, liver disease, thyroid disease, type 1 diabetes, serious infection, illness, or injury.

Be careful with Glucotrol if you take aspirin or another salicylate such as magnesium/choline salicylate (Trilisate), salsalate (Disalcid, others), choline salicylate (Arthropan), magnesium salicylate (Magan) or bismuth subsalicylate (Pepto-Bismol); nonsteroidal anti-inflammatory drug (NSAID) such as ibuprofen (Motrin, Advil, Nuprin, others), ketoprofen (Orudis, Orudis KT, Oruvail), diclofenac (Voltaren, Cataflam), etodolac (Lodine), indomethacin (Indocin), nabumetone (Relafen), oxaprozin (Daypro), naproxen (Anaprox, Naprosyn, Aleve) and others; sulfa-based drug such as sulfamethoxazole-trimethoprim (Bactrim, Septra), sulfisoxazole (Gantrisin), or sulfasalazine (Azulfidine); monoamine oxidase inhibitor (MAOI) such as isocarboxazid (Marplan), tranylcypromine (Parnate) or phenelzine (Nardil); beta-blocker such as propranolol (Inderal), atenolol (Tenormin), acebutolol (Sectral), metoprolol (Lopressor) and others; diuretic (water pill) such as hydrochlorothiazide (HCTZ, Hydrodiuril), chlorothiazide (Diuril) and others; steroid medicine such as prednisone (Deltasone, Orasone, others), methylprednisolone (Medrol, others), prednisolone (Prelone, Pediapred, others) and others; phenothiazine such as chlorpromazine (Thorazine), fluphenazine (Prolixin, Permitil), prochlorperazine (Compazine), promethazine (Phenergan) and others; phenytoin (Dilantin); isoniazid (Nydrazid); prescription, over-the-counter, or herbal cough, cold, allergy or weight loss medications.

Avoid alcohol.

Do not stop taking Glucotrol suddenly.

glucotrol drug interactions

A new mechanism of action in the form of sodium-glucose co-transporter-(SGLT-)2 inhibitors will be available shortly for the treatment of type 2 diabetic patients.

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This study is a multicenter, randomized, double-blind, placebo-controlled clinical trial. A total of 304 type 2 diabetic patients with CAD, mean age = 63.3 years (range, 36-80 years), were enrolled. Participants were randomly assigned to receive either glipizide (30 mg daily) or metformin (1.5 g daily) for 3 years. The primary end points were times to the composite of recurrent cardiovascular events, including death from a cardiovascular cause, death from any cause, nonfatal myocardial infarction, nonfatal stroke, or arterial revascularization.

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A cohort of 33,243 sulfonylurea users chosen from 719 clinical practices in the United Kingdom were identified through the VAMP-Research database. Information on demographic characteristics, medical diagnoses and use of medical services was obtained through the computerized records. For a stratified sample of 500 patients, general practioners completed a structured questionnaire on the duration, treatment, and complications of diabetes mellitus, obesity, alcohol use, and smoking history. Patients with a diagnosis of hypoglycemia, as recorded in the database within a time-window of a sulfonylurea prescription, were identified. Incidence rates per person-year of sulfonylurea therapy were estimated.

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Glipizide is an effective antidiabetic agent, however, it suffers from relatively short biological half-life. To solve this encumbrance, it is a prospective candidate for fabricating glipizide extended release microcapsules. Microencapsulation of glipizde with a coat of alginate alone or in combination with chitosan or carbomer 934P was prepared employing ionotropic gelation process. The prepared microcapsules were evaluated in vitro by microscopical examination, determination of the particle size, yield and microencapsulation efficiency. The filled capsules were assessed for content uniformity and drug release characteristics. Stability study of the optimised formulas was carried out at three different temperatures over 12 weeks. In vivo bioavailability study and hypoglycemic activity of C9 microcapsules were done on albino rabbits. All formulas achieved high yield, microencapsulation efficiency and extended t 1/2. C9 and C19 microcapsules attained the most optimised results in all tests and complied with the dissolution requirements for extended release dosage forms. These two formulas were selected for stability studies. C9 exhibited longer shelf-life and hence was chosen for in vivo studies. C9 microcapsules showed an improvement in the drug bioavailability and significant hypoglycemic activity compared to immediate release tablets (Minidiab(®) 5 mg). The optimised microcapsule formulation developed was found to produce extended antidiabetic activity.

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Pharmacological modulation of pancreatic triacylglycerol lipase (PL) and α-amylase/α-glucosidase by A. capillus-veneris are evaluated.

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To evaluate the 2-year safety and efficacy of adding sitagliptin or glipizide to ongoing metformin in patients with type 2 diabetes.

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These results suggest that metabolic amplification of fuel-induced insulin secretion is not mediated by changes in the beta cell content of ATP and ADP, but might be due to export of citrate cycle intermediates to the beta cell cytosol.

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Cultured mouse pancreatic islets were prelabelled with 2-3H-adenosine in order to monitor the efflux pattern of radioactivity and insulin. The outflow of radioactivity decreased continuously when the islets were perifused with glucose (1.67 mmol/l). When raising the glucose concentration to 16.7 mmol/l, there was a prompt inhibition of the radioactive efflux concomitant with an increased rate of insulin release. These effects were reversed when the high glucose challenge was withdrawn. Similar radioactive efflux patterns were obtained after addition of alpha-ketoisocaproic acid, leucine or pyruvate to the perifusion medium, and also when the islets were challenged with high glucose concentrations in the absence of calcium. Both antimycin A and glipizide stimulated the efflux of radioactivity, although only the addition of glipizide was accompanied by a stimulation of the insulin release. Nucleotides constituted approximately 90% of the total effluent radioactivity. Decrease in the radioactive AMP and ADP efflux due to high glucose was furthermore found to be the cause of the observed inhibition of the total radioactive efflux. The changes in radioactive efflux induced by glucose probably reflect changes in the intracellular concentrations of AMP and ADP. It is concluded that no simple correlation exists between radioactive efflux and insulin release and that changes in the intracellular concentrations of nucleotides may be an early event in the stimulus-secretion coupling of glucose-induced insulin release.

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Children ingesting oral hypoglycemics should be admitted to a health care facility for 24 h observation. In this series a single tablet produced hypoglycemia.

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In a single-dose, four-period, four-treatment, Latin-square crossover study, the bioavailability of immediate-release glipizide 5mg (Glynase) [GL], extended-release glipizide 5mg (Glynase) XL [GLXL], Glucotrol XL [GTXL], and the new formulation developed in our laboratory [GLPF]) was compared. Plasma glipizide levels of the four formulations were determined at different time intervals, and pharmacokinetic parameters were analysed using a two-compartment body model.

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The β-cell metabolism of glucose and of some other fuels (e.g. α-ketoisocaproate) generates signals triggering and acutely amplifying insulin secretion. As the pathway coupling metabolism with amplification is largely unknown, we aimed to narrow down the putative amplifying signals.

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Idiosyncratic toxicity to potentiated sulfonamides occurs in both humans and dogs, with considerable clinical similarities. The syndrome in dogs can consist of fever, arthropathy, blood dyscrasias (neutropenia, thrombocytopenia, or hemolytic anemia), hepatopathy consisting of cholestasis or necrosis, skin eruptions, uveitis, or keratoconjunctivitis sicca. Other manifestations seen less commonly include protein-losing nephropathy, meningitis, pancreatitis, pneumonitis, or facial nerve palsy. The pathogenesis of these reactions is not completely understood, but may be due to a T-cell-mediated response to proteins haptenated by oxidative sulfonamide metabolites. Our laboratory is working on tests to characterize dogs with possible idiosyncratic sulfonamide reactions, to include ELISA for anti-drug antibodies, immunoblotting for antibodies directed against liver proteins, flow cytometry for drug-dependent anti-platelet antibodies, and in vitro cytotoxicity assays. The management of idiosyncratic sulfonamide toxicity involves client education to identify clinical signs early and allow rapid drug discontinuation, supportive care to include possibly ascorbate and glutathione precursors, and avoidance of subsequent re-exposure. It is important to realize that only antimicrobial sulfonamides, such as sulfamethoxazole, sulfadiazine, and sulfadimethoxine, share this clinical syndrome. There is no evidence for cross-reactivity with drugs that have different underlying structures but share a sulfonamide moiety, such as acetazolamide, furosemide, glipizide, or hydrochlorthiazide.

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The main goal of the study of 153 male veterans was to determine whether a statistically and clinically significant difference in HbA1c could be achieved between a standard therapy and an intensively treated group of patients with type II diabetes. A second major goal was to assess the feasibility of collecting reliable high-quality endpoint data, including microvascular and macrovascular events. Retinopathy was defined as a key microvascular endpoint.

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Aim of the Study was to investigate herb-drug interaction (HDI) of Ridayarishta formulation through human hepatic cytochrome P450 (CYP450) enzyme inhibition assay.

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The observed increase in PWV is consistent with a decrease in the elastic properties of the aorta. The use of oral antidiabetic agents for the prevention of cardiovascular complications in non-diabetic African Americans with insulin resistance needs to be critically evaluated.

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Oral hypoglycemic (OH) agents have been available in the United States for the treatment of non-insulin-dependent diabetes mellitus (NIDDM) for almost 30 yr. During this time they have been subject to considerable controversy. In this article, we present pharmaceutical marketing research data that provide a review of several facets of OH use. The number of OH prescriptions dispensed peaked in 1973, decreased through 1980, and has been increasing since that year. In 1986, OH agents accounted for 21.5 million prescriptions: 1% of all prescriptions dispensed that year. Chlorpropamide is currently the most frequently ingested OH agent; it is used by 33% of the market. The two OH agents introduced in 1984, glyburide and glipizide, had acquired 41% of the OH market by the end of 1986. The rate of OH use per 1000 diabetes mellitus visits increases with patient's age. Patients aged 60 yr and older received OH prescriptions at a rate of 478 per 1000 diabetes mellitus visits in 1986. Data estimating both the number of patients diagnosed with diabetes and the number of diabetic patients taking OH agents indicate that the percentage receiving OH treatment has increased over the past 5 yr, with approximately 35% of all diabetic patients taking OH agents in 1986.

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The aim was to investigate the outcomes of individual sulfonylureas in patients with heart failure (HF).

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The aim of the present investigation was to develop controlled porosity osmotic system for poorly water-soluble drug based on drug in polymer-surfactant layer technology. A poorly water-soluble drug, glipizide (GZ), was selected as the model drug. The technology involved core of the pellets containing osmotic agent coated with drug dispersed in polymer and surfactant layer, finally coated with release-retardant layer with pore former. The optimized drug-layer-coated pellets were evaluated for solubility of GZ at different pH conditions and characterized for amorphous nature of the drug by differential scanning calorimetry and X-ray powder diffractometry. The optimized release-retardant layer pellets were evaluated for in vitro drug release at different pH, hydrodynamic, and osmolality conditions. The optimized drug layer showed improvement in solubility (10 times in pH 1.2, 11 times in pH 4.5, and 21 times in pH 6.8), whereas pellets coated with cellulose acetate (15.0%, w/w, weight gain) with pore former triethyl citrate (10.0%, w/w, of polymer) demonstrated zero-order drug release for 24 h at different pH conditions; moreover, retardation of drug release was observed with increment of osmolality. This system could be a platform technology for controlled delivery of poorly water-soluble drugs.

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During a median of 4.91 years of follow-up, 271 developed cancer. Glibenclamide, gliclazide and glipizide were ever used in 32.5% (n = 1983), 47.8% (n = 2920) and 13.5% (n = 823). After adjustment for covariates, use of gliclazide and glibenclamide was associated with reduced cancer risk in a dose-dependent manner. In addition, there were interactions between metformin and glibenclamide/glipizide use towards lower adjusted cancer risks.

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An analytical method based on isocratic reverse phase high-performance liquid chromatography was developed and validated for the separation and quantification of eight antidiabetic drugs: rosiglitazone, pioglitazone, glipizide, gliclazide, repaglinide, nateglinide, glibenclamide, and glimepiride for their application in human plasma assay. Metformin is used as internal standard. Analysis was done on Onyx monolithic C(18) column (100 × 4.6 mm, i.d., 5 μm) using a mixture of 0.05% formic acid in water and methanol in the ratio of 42 : 58 (v/v) fixed at a flow rate of 0.5 mL/min, and they were monitored at 234 nm. Separation was achieved in less than 20 min. The calibration curves were linear in the range of 50-2000 ng/mL. The method was validated for its recovery, intra- and interday precision, stability, specificity, and selectivity. Plasma samples were prepared using solid-phase extraction of analytes. Hence, the developed method was found to be suitable for the routine analysis of selected antidiabetic drugs in biological matrices.

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glucotrol pill identifier 2015-08-29

This study assessed the possible interactions of the cyclooxygenase inhibitor indobufen with one sulphonylurea, glipizide, and with two beta-adrenoceptor antagonists, one of which is extensively metabolised already in the first passage through the liver (propranolol) while the other essentially escapes biotransformation (atenolol). Indobufen was first given as a single 200 mg dose and then for a 5 day period in a dosage of 200 mg twice daily, to six healthy volunteers. Glipizide (5 mg), propranolol (80 mg) and atenolol (100 mg) were given as single doses before and during indobufen medication. The drug concentrations were measured by selective and sensitive h.p.l.c. methods. The findings suggest buy glucotrol that the lipophilic acid indobufen can inhibit the metabolic inactivation of another lipophilic acid, glipizide, but does not interfere with the disposal of the two basic drugs, propranolol and atenolol. The increased glipizide concentrations following indobufen were associated with an enhanced blood glucose reduction. Hence, this interaction may be clinically relevant.

glucotrol cost 2015-09-04

Activation of GPR40 is reported to enhance insulin secretion in the presence of glucose. We determined whether sulfonylureas could replace glucose for GPR40-mediated enhancement of insulin secretion and investigated underlying mechanisms using INS-1E cells. GW9508, a specific agonist of GPR40, significantly enhanced insulin secretion in the presence of high concentrations of glucose. In contrast, sulfonylureas increased insulin secretion in the absence of glucose. In the presence of sulfonylureas, activation of GPR40 significantly enhanced insulin secretion. The buy glucotrol L-type calcium channel (LTCC) activator S-(-)-Bay K8644 also concentration-dependently increased insulin secretion in the absence of glucose. In the presence of 10 micromol/L S-(-)-Bay K8644, GW9508 significantly increased insulin secretion. On the other hand, the LTCC blocker nifedipine significantly inhibited insulin secretion mediated by either glucose, glipizide or glucose plus GW9508. Thus, sulfonylureas could replace glucose to support GPR40-mediated enhancement of insulin secretion, whereas blockage of LTCC reduced both glucose and sulfonylurea-mediated insulin secretion.

glucotrol 20 mg 2017-12-26

Conditions for the extractive alkylation of eight sulphonylurea hypoglycemic drugs have been evaluated. Extractive methylation of the compounds was achieved within 90 min using tetrabutylammonium as counter-ion (0.1 M at pH = 6.9) with 5% methyl iodide in dichloro-methane as organic phase. Mass spectral analysis showed derivatives methylated at the sulphonamide nitrogen. A higher pH or use of tetrapentylammonium as counter-ion caused hydrolysis of the sulphonylureas. The derivatives showed buy glucotrol a high electron-capture response with minimum concentrations detectable in the range 1-4 x 10(-16) moles sec-1. Therapeutic plasma concentrations of glipzide and tolbutamide were determined by direct extractive methylation of the compounds from the plasma sample. The glipizide derivative was determined by electron-capture gas chromatography down to about 20 ng/ml in a 0.5-ml plasma sample. The relative standard deviation at the 0.2 microgram/ml level of glipizide was 6% (n = 6). The corresponding figure in the determination of tolbutamide at the 10 microgram/ml level was 3% (n = 10).

glucotrol maximum dosage 2017-08-07

The oral antidiabetics glibenclamide and glipizide, and the diuretics bendroflumethiazide and furosemide, all sulphonamide derived drugs, were buy glucotrol investigated in vitro for phototoxic properties. Irradiation with broad-band UV induced phototoxic inhibition of colony forming ability in cell cultures. During irradiation, the substances lost one absorption maximum in the UVA region, demonstrated by UV spectroscopy. These findings correlate well with the UV applied, the action spectrum being in the UVA region. Photoproducts detected during and after irradiation showed a decomposition of the substances due to ionization and fragmentation. Incubation of these preirradiated drugs with the cell cultures revealed no phototoxic effects.

glucotrol xl generic 2016-02-18

Despite extensive clinical experience with second-generation oral hypoglycemic agents, the relative dosing equivalence of glyburide and glipizide remains controversial. A prospective survey was conducted to determine the feasibility and cost of converting noninsulin-dependent diabetic patients from glipizide to glyburide. A total of 211 patients previously stabilized on glipizide were converted to glyburide and returned to their respective clinics at least once during the following six months. The mean daily dose (+/- SD) of glipizide before conversion was 18.7 +/- 12.32 mg; the mean daily dose of glyburide after seven months buy glucotrol was 9.9 +/- 6.52 mg (P less than 0.001, paired t test). Glyburide was well tolerated. The conversion program appeared to be successful and resulted in a 47% reduction in the mean daily dose after conversion from glipizide to glyburide, which, in turn, conferred a 43% savings in the projected yearly expenditures for second-generation oral hypoglycemics.

glucotrol drug class 2017-12-03

G-proteins are important mediators of hormonal inhibition of insulin secretion. To characterize the pertussis toxin-sensitive substrates present in HIT cell membranes, we performed immunoblots with specific antisera and found evidence for the presence of Gi alpha 1, Gi alpha 2, Gi alpha 3, and three forms of Go alpha. We observed that pertussis toxin-sensitive substrates mediate all of the effects of SRIF, and a major portion of the effects of EPI, on insulin buy glucotrol secretion from rat islets during static incubations. These results agree with our previously reported studies examining phasic glucose-induced insulin secretion from HIT cells. To ascertain whether inhibition of adenylate cyclase, presumably involving coupling of the catalytic subunit to Gi, may be a common mechanism for both hormones, we studied the effects of 8-bromo-cyclic AMP and found that this agent partially prevented the inhibitory effects of both hormones. We also observed that the inhibitory effects of SRIF and EPI on insulin were nonadditive, that both hormones were additive to nickel chloride during inhibition of insulin release, and that they noncompetitively inhibited glipizide-induced insulin secretion through pertussis toxin-sensitive mechanisms. Together, these results suggest that both hormones exert their effects on insulin secretion at multiple G-protein-regulated sites including adenylate cyclase and sites distal to the glipizide-binding site on the KATP channel.

glucotrol 5 mg 2017-07-20

To examine whether sulphonylureas influence hyperglycaemia-induced glucose disposal and suppression of hepatic glucose production (HGP) in type 2 diabetes mellitus, a 150-min hyperglycaemic (plasma glucose 14 mmol/l) clamp with concomitant somatostatin infusion was used in eight type 2 diabetic patients before and after 6 weeks of glipizide (GZ) therapy. During the clamp a small replacement dose of insulin buy glucotrol was given (0.15 mU/kg per min). Isotopically determined glucose-induced glucose uptake was similar before and after GZ administration which led to improved glycaemic control (basal plasma glucose 12.2 +/- 1.3 vs 8.9 +/- 0.7 mmol/l; P < 0.01). Glucose-induced suppression of HGP was, however, more pronounced during GZ treatment (0.96 +/- 0.14 vs 1.44 +/- 0.20 mg/kg per min; P < 0.02). Following GZ treatment hyperglycaemia failed to stimulate glycogen synthase activity. Moreover, GZ resulted in a significant increase in the immunoreactive abundance of the insulin-regulatable glucose transport protein (GLUT 4) (P < 0.02). In conclusion, these results suggest that GZ therapy in type 2 diabetic patients enhances hepatic sensitivity to hyperglycaemia, while glucose-induced glucose uptake remains unaffected. In addition, GZ tends to normalize the activity of glycogen synthase and increases the content of GLUT 4 protein in skeletal muscle.

glucotrol generic names 2017-11-18

Wolfram syndrome 1 is a very rare monogenic disease buy glucotrol resulting in a complex of disorders including diabetes mellitus. Up to now, insulin has been used to treat these patients. Some of the monogenic forms of diabetes respond preferentially to sulphonylurea preparations. The aim of the current study was to elucidate whether exenatide, a GLP-1 receptor agonist, and glipizide, a sulphonylurea, are effective in a mouse model of Wolfram syndrome 1. Wolframin-deficient mice were used to test the effect of insulin secretagogues. Wolframin-deficient mice had nearly normal fasting glucose levels but developed hyperglycaemia after glucose challenge. Exenatide in a dose of 10 μg/kg lowered the blood glucose level in both wild-type and wolframin-deficient mice when administered during a nonfasted state and during the intraperitoneal glucose tolerance test. Glipizide (0.6 or 2 mg/kg) was not able to reduce the glucose level in wolframin-deficient animals. In contrast to other groups, wolframin-deficient mice had a lower insulin-to-glucose ratio during the intraperitoneal glucose tolerance test, indicating impaired insulin secretion. Exenatide increased the insulin-to-glucose ratio irrespective of genotype, demonstrating the ability to correct the impaired insulin secretion caused by wolframin deficiency. We conclude that GLP-1 agonists may have potential in the treatment of Wolfram syndrome-related diabetes.

glucotrol xl dose 2016-09-05

The effect of combined insulin-glibenclamide therapy on glucose control was evaluated in a double-blind placebo controlled study of 20 patients with non-insulin-dependent diabetes mellitus (NIDDM) and second failure to oral antidiabetic therapy with glibenclamide or glipizide. After an observation period of 1-3 months, insulin treatment was initiated which resulted in rapid improvement of the glycemic control within 6 weeks. Thereafter glibenclamide or placebo was added to insulin for a further 12 weeks. Glibenclamide improved the glycemic control as expressed by a diminution of blood glucose and HbA1c. This was observed in spite of the fact that the daily insulin dose was reduced by approximately 30% in the glibenclamide-treated group of patients. It is concluded that buy glucotrol in NIDDM patients with second failure to glibenclamide ot glipizide therapy, the responsiveness to glibenclamide may be at least partially restored by a short period of insulin treatment. It is suggested that therapy with insulin and glibenclamide is an appropriate treatment regimen for NIDDM patients with second failure to sulfonylurea therapy.

glucotrol drug interactions 2016-03-12

The present study was designed to evaluate the long-term effects of a short course of insulin therapy on glycaemic control in type 2 diabetic patients after failure with oral therapy. Twenty type 2 diabetic patients poorly controlled with maximal doses of sulfonylurea were given intensified insulin treatment for 12-14 days adjusted so as to achieve near normoglycaemia. They were then restarted on their previous oral medication to which one bedtime injection of NPH insulin was added if the mean diurnal glucose profile exceeded 10 mM (n = 8). At the follow up evaluation (n = 18), 6 +/- 1 months later, fasting glucose (12.3 +/- 1.1 to 8.3 +/- 0.6 mM) and HbA1c (10.2 +/- 0.5 to 8.5 +/- 0.5%) levels were significantly improved buy glucotrol in the patients receiving a combined therapy. In the group maintained on sulfonylurea alone, fasting glucose (13.2 +/- 0.7 to 6.9 +/- 0.7 mM) and HbA1c (9.6 +/- 0.6 to 6.9 +/- 0.6%) were also significantly improved in 5 patients who had lost weight (-6 +/- 1 kg) whereas none of these parameters were significantly different from the preinsulin value in the 6 patients whose weight remained unchanged. In conclusion, the current results do not provide any evidence that short-term insulin therapy is able to reinduce the efficacy of a previously ineffective sulfonylurea treatment, on a long term basis.

glucotrol xl medication 2015-01-24

Pioglitazone, a peroxisome proliferator-activated receptor agonist and glipizide, an insulin secretagogue buy glucotrol , are commonly used to treat type 2 diabetes. Our study was designed to examine the effects of pioglitazone versus glipizide on body water, body composition, and hemodynamic parameters in the presence of comparable glycemic control between groups.

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Cats were randomly assigned to 2 treatment groups (5 mg of glipizide, PO or transdermally) and a control group. Blood samples were collected 0, 10, 20, buy glucotrol 30, 45, 60, 90, and 120 minutes and 4, 6, 10, 14, 18, and 24 hours after administration to determine concentrations of insulin, glucose, and glipizide.

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181 African American subjects with insulin resistance and normal glucose tolerance test were randomised to receive glipizide buy glucotrol 5 mg/day (n = 25), metformin 500 mg/day (n = 59), or placebo (n = 97) for 24 months. Insulin sensitivity, glucose tolerance, lipid profile, left ventricular mass (echocardiography), aortic distensibility (echocardiography, blood pressure), aortic pulse wave velocity (PWV, carotid to femoral artery, Doppler) were measured at baseline and at 12 and 24 months after randomisation.

glucotrol alcohol 2015-08-16

This study showed that the addition of 2.5 mg glipizide GITS to metformin significantly improved glucose control in patients buy glucotrol with type 2 diabetes inadequately controlled by metformin monotherapy.

glucotrol user reviews 2016-04-28

Twenty-three nonobese KK mice with abnormal tolerance to glucose, hyperinsulinemia with insulin resistance and human diabetic-like nephropathy were treated with either saline (12 mice) or glipizide, an oral hypoglycemic compound, 1 mg/kg, (11 mice) from 120 to 360 days of age. These mice develop significant increases in mesangial volume and matrix by 40 days of age. Oral glucose tolerance (OGTT), glucosyltransferase and N-acetyl-beta-glucosaminidase (enzymes involved in synthesis and degradation Salbutamol Ventolin Syrup of kidney glycoproteins, respectively) in the kidney and serum, 24-hr proteinuria, and light microscopy studies of the kidney were performed. Glipizide-treated mice improved their OGTT. There was no difference in body weight; however, a 16% decrease (P less than 0.05) in kidney weight was observed in glipizide-treated mice. Both enzymes were significantly increased in the kidneys of mice treated with glipizide. No difference in serum enzymes was found between the two groups of mice. About 58% of the saline-treated mice had moderate glomerulosclerosis. By contrast, only 27% of glipizide-treated mice had moderate glomerulosclerosis. Also, a significant decrease in proteinuria was found in glipizide-treated mice. These data suggest that glipizide improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals.

glucotrol with alcohol 2015-09-04

Medication errors remain an important cause of patient morbidity and mortality. Although all medications have the potential to induce unwanted adverse effects, data on the actual incidence and overall severity of preventable adverse drug reactions remains unknown. An Institute of Medicine report (Institute of Medicine. Preventing medication errors: Quality chasm series. Washington DC, National Academies Press. 2007-06-15) estimated that 1.5 million preventable adverse drug events occur annually in the US and that from 44,000 to 98,000 individuals die in hospitals annually from preventable medication errors. The types of medication errors of clinical relevance leading to moderate to severe outcomes are unfortunately numerous. Such errors would include wrong drug, wrong dose / wrong dose interval and represent the more serious form of a medication error. Institutionalized patients and those patients cared for in long-term care facilities appear to be at heightened risk for a medication error Imdur Bid Dosing . These patients often receive multiple medications and suffer from variable degrees of cognitive impairment which complicates or negates patient-caregiver communication, one of the most important means to prevent medication errors. Moreover, the increasing financial constraints placed upon treatment facilities encourage the use of generic, rather than name brand medications by their pharmacy provider. While the use of bioequivalent generic medications is completely appropriate and can be very cost-effective, generic drug manufacturers are less often manufacturing their generic medications to look like the name brand drug. Rather, more and more generic medications are plain appearing with no resemblance whatsoever to the name brand product. This difference in drug appearance between the generic and the brand name product as well as differences in drug appearance between different generic drug manufacturers for the same medication represents another, important means by which patients may experience moderate to serious consequences from a medication error. We report such an experience where a patient in a long-term care facility received multi-day, excessive dosing of glipizide rather than her anti-spasticity medication, baclofen.

glucotrol drug classification 2017-06-30

The aim was to investigate the Nizoral Generic Shampoo outcomes of individual sulfonylureas in patients with heart failure (HF).

glucotrol xl dosage 2015-10-20

Occurrence of hypoglycemia (defined as plasma glucose level <3.33 mmol/L [60 mg/dL]) and hormonal parameters during the final 9 hours of Altace With Alcohol the 23-hour fast in patients who had taken sulfonylureas vs placebo.

glucotrol usual dosage 2017-12-26

To identify the incidence of and risk factors associated with hypoglycemia in Sustiva Dosing hospitalized patients taking sulfonylureas.

glucotrol glipizide dose 2017-06-18

1. The effects of several K+ channel blockers (sulphonylureas, 4-aminopyridine and tetraethylammonium) on the antinociception induced by clonidine, baclofen and U50,488H were evaluated by use of a tail flick test in mice. 2. Clonidine (0.125-2 mg kg-1, s.c.) induced a dose-dependent antinociceptive effect. The ATP-dependent K+ (KATP) channel blocker gliquidone (4-8 micrograms/mouse, Zocor Dosage Elderly i.c.v.) produced a dose-dependent displacement to the right of the clonidine dose-response line, but neither 4-aminopyridine (4-AP) (25-250 ng/mouse, i.c.v.) nor tetraethylammonium (TEA) (10-20 micrograms/mouse, i.c.v.) significantly modified clonidine-induced antinociception. 3. The order of potency of sulphonylureas in antagonizing clonidine-induced antinociception was gliquidone > glipizide > glibenclamide > tolbutamide, which is the same order of potency as these drugs block KATP channels in neurones of the CNS. 4. Baclofen (2-16 mg kg-1, s.c.) also induced a dose-dependent antinociceptive effect. Both 4-AP (2.5-25 ng/mouse, i.c.v.) and TEA (10-20 micrograms/mouse, i.c.v.) dose-dependently antagonized baclofen antinociception, producing a displacement to the right of the baclofen dose-response line. However, gliquidone (8-16 micrograms/mouse, i.c.v.) did not significantly modify the baclofen effect. 5. None of the K+ channel blockers tested (gliquidone, 8-16 micrograms/mouse; 4-AP, 25-250 ng/mouse and TEA, 10-20 micrograms/mouse, i.c.v.), significantly modified the antinociception induced by U50,488H (8 mg kg-1, s.c.). 6. These results suggest that the opening of K+ channels is involved in the antinociceptive effect of alpha 2 and GABAB, but not kappa-opioid, receptor agonists. The K+ channels opened by alpha2-adrenoceptor agonists seem to be ATP-dependent channels, whereas those opened by GABAB receptor agonists are not.