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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:

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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.

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A method for the separation of six selected antihyperglycemic (antidiabetic) drugs (tolbutamide, gliclazide, glimepiride, glibenclamide, repaglinide, and glipizide) was developed with use of micellar electrokinetic chromatography. Two non-ionic poly(ethylene glycol)-based surfactants Genapol X-080 and Triton X-114 (reduced) were studied as neutral pseudostationary phases. High alkaline pH 10.0 was used to obtain negative charges of separated antidiabetic drugs and non-ionic surfactants were employed for selectivity alteration. Both non-ionic surfactants provided good selectivity at concentration 0.2% (v/v) in sodium borate buffer and the separation of six drugs was obtained within 5min. An on-line preconcentration method based on reversed electrode polarity switching was employed for the determination of antihyperglycemic drugs in blood serum after acetonitrile protein precipitation. The limits of detection ranged from 20.8nmolL(-1) for tolbutamide to 6.5nmolL(-1) for glibenclamide, respectively.

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In this work, the effect of hydrogelation period in the design of glipizide-loaded biopolymer-based interpenetrating network (IPN) beads was investigated. Carboxymethyl locust bean gum and sodium alginate IPN beads were prepared by ionic crosslinking method using aqueous aluminium chloride salt solution as gelation medium. The longer exposure of the IPN beads in the gelation medium caused a considerable loss of the drug (∼ 8%), and also affected their surface morphology and drug release performance. Spherical shape of the IPN beads was observed under scanning electron microscope (SEM). The diameter of IPN beads increased with increasing gelation time. The IPNs cured for 0.5h exhibited slower drug release kinetics in HCl (pH 1.2) and phosphate buffer (pH 7.4) solution than those incubated for 1-2h. The drug release occurred at a faster rate in phosphate buffer solution and continued for a minimum period of 8h. The IPNs cured for the lowest period obeyed polymer chain-relaxation phenomenon as dominating mechanism for drug release. However, all the IPNs followed anomalous mechanism of drug transport. The drug release corroborated well with pH-dependent swelling behaviors of the IPNs. Thus, IPN beads cured for 0.5h were found most suitable for controlled delivery of BCS class II anti-diabetic drug glipizide.

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Fifteen patients (eight men, seven women) reported hypoglycaemia symptoms which were validated by their home glucose measurements (< 70 mg/dl). Heterozygosity and homozygosity for CYP2C9 variant alleles (*2 or *3) tended to be more frequent among patients who reported hypoglycaemic attacks (60 and 7%) than those who did not (39 and 3%). Similarly, the CYP2C8*1/*3 genotype tended to be more frequent in patients with (47%) than without (27%) hypoglycaemia, while no such trend was observed for CYP2C19 variants. However, only in the gliclazide group a significant association between CYP2C9 genotype and hypoglycaemic attacks was observed (P = 0.035). None of the other covariates showed any significant association with the risk of hypoglycaemic attacks.

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The objective of this study was to investigate the cost-effectiveness of saxagliptin (Onglyza(®)), a DPP-4 inhibitor, plus metformin compared with a sulphonylurea (SU) (Glipizide) plus metformin in Swedish patients not well controlled on metformin alone.

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These data provide evidence that ISIS 113715 exhibits no clinically relevant pharmacokinetic interactions on the disposition and clearance of the oral antidiabetic drugs. The results of these studies support further study of ISIS 113715 in combination with antidiabetic compounds.

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We studied 11 subjects without diabetes and 19 matched subjects with diabetes. The subjects with diabetes were randomly assigned to receive either 45 mg daily of pioglitazone (N = 8) or 10 mg daily of glipizide (N = 11) (median dose) for 12 weeks. Lipoprotein-associated phospholipase A2 (LpPLA2), vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1), and e-selectin were measured by established techniques before and after therapy with either agent. The subjects without diabetes were studied only once.

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We rejected the hypothesis that all human MODY-associated mutations in HNF1A / HNF4A induce changes in the pharmacokinetics of sulfonylureas in humans analogically to the Hnf1a(-/-) mouse model.

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Insulin in portal, hepatic and/or peripheral venous blood was determined in 16 patients admitted to a surgical ward for various diseases. Portal venous blood was obtained via a catheter introduced into the portal vein either through the umbilical vein remnant or transhepatically. Four subjects were given a peroral load of glucose, followed after 60 min by i.v. tolbutamide. In simultaneous blood samples, two of these subjects showed higher insulin concentrations in peripheral venous blood than in portal venous blood. Twelve subjects were given i.v. glipizide. In one subject blood samples were drawn from the portal vein, a hepatic vein and a peripheral vein and in six subjects from the portal vein and a hepatic vein. Two subjects showed higher insulin concentrations in peripheral venous blood than in portal venous blood. The mean peripheral insulin response (six subjects) was of the same magnitude as the mean hepatic insulin response (six subjects). It is suggested that these findings reflect a release of previously bound insulin from peripheral tissues.

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The influence of the hypoglycemic agent glipizide (0-100 microM) on the rate of gluconeogenesis from lactate, as well as on the levels of fructose 2,6-bisphosphate, has been investigated in hepatocytes isolated from genetically obese (fa/fa) Zucker rats and from their corresponding lean (Fa/-) littermates. As compared to lean rat hepatocytes, liver cells isolated from obese animals showed a lower rate of basal gluconeogenesis (0.9 +/- 0.2 vs 5.4 +/- 0.5 micromol of lactate converted to glucose/g cell x 30 min, n=4) and higher levels of fructose 2,6-bisphosphate (11.5 +/- 1.0 vs 5.9 +/- 0.4 nmol/g cell, n=8-9). In lean rat hepatocytes, the presence of glipizide in the incubation medium caused a dose-dependent inhibition of the rate of lactate conversion to glucose (maximal inhibition=46%; EC50 value=26 microM), and simultaneously raised the cellular content of fructose-2,6-bisphosphate (maximal increment=40%; EC50 value=10 microM). In contrast, in hepatocytes isolated from obese rats, the inhibition of gluconeogenesis and the increment in fructose-2,6-bisphosphate levels elicited by glipizide were significantly reduced (maximal effects of 22 and 13%, respectively). Similarly, the activation of glycogen phosphorylase and the increase in hexose 6-phosphate levels in response to glipizide were less marked in obese rat hepatocytes than in liver cells isolated from lean animals. These results demonstrate that the efficacy of sulfonylureas as inhibitors of hepatic gluconeogenesis is reduced in the genetically obese (fa/fa) Zucker rat.

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A placebo-controlled, double-blind, cross-over study.

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In this report we review the pharmacology of the hypoglycemic sulfonylurea drugs. The early work with sulfonylureas is briefly described. The pharmacokinetics of first-generation sulfonylureas, such as tolbutamide, chlorpropamide, acetohexamide and tolazamide, are described. The first-generation sulfonylureas are compared with second-generation sulfonylureas such as glyburide, glipizide and glibornuride. These latter drugs have a more nonpolar or lipophilic side chain, which results in a marked increase in their hypoglycemic potency. Because of the low serum concentration required for effective therapy, it is necessary to measure the serum concentration of second-generation sulfonylureas by gas-liquid chromatography or radioimmunoassay. The second-generation sulfonylureas do not produce facial flushing after ethanol ingestion (Antabuse effect) and are not uricosuric. Glyburide (but not glipizide or glibornuride) has been evaluated for its effect on water excretion. Glyburide not only does not increase water retention but in fact also increases free water clearance. The second-generation sulfonylureas bind to human serum albumin by nonionic forces in contrast with tolbutamide and chlorpropamide which bind by ionic forces. Thus, anionic drugs such as phenylbutazone, warfarin and salicylate do not displace glyburide from albumin as they displace tolbutamide and chlorpropamide. Therefore, it may be safer to administer the second-generation sulfonylureas than the more polar sulfonylureas when concurrent administration of other pharmacologic agents is likely. The sulfonylurea drugs lower plasma glucose concentrations in diabetic patients by stimulating insulin secretion and by potentiating the biologic effect of the insulin on such tissues as skeletal muscle, fat and liver. The mechanism of the latter so-called extra-pancreatic effect may be activated by increasing the deficient numbers of insulin receptors on muscle, fat or liver cells.

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The hypoglycemic effect of 2.5 mg glipizide and the potentiation of this effect by ethanol were studied in 10 normal-weight nondiabetic subjects. The reductions in blood glucose concentrations were similar in time of onset and extent (2 mM) whether glipizide was taken alone or in combination with ethanol. However, the return of blood glucose toward fasting level was delayed by ethanol. Beta-Cell secretory activity, evaluated from the concentrations of insulin and C-peptide, was unchanged by ethanol. The serum glipizide concentrations were reproducible within subjects, whereas there was a considerable interindividual variation. This heterogeneity in the rise in glipizide concentration was strongly correlated with blood glucose fall and insulin secretion. Thus, ethanol can prolong but does not augment the hypoglycemia induced by glipizide. The heterogeneity in glipizide concentration seems to be caused by an interindividual variation in kinetics.

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Based on its unique mechanism of action, sitagliptin will provide practitioners with an additional tool in the treatment of diabetes. Review of the literature to date implies sitagliptin may be effective as monotherapy in type 2 diabetes. In addition, existing evidence supports the use of sitagliptin as adjunct therapy to sulfonylureas and metformin. Another advantage of sitagliptin use is that it appears to be free from the adverse effects of weight gain and hypoglycemia that are associated with currently available treatments.

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Despite the substantial body of research investigating the use of liposomes, niosomes and other bilayer vesicles for drug delivery, the translation of these systems into licensed products remains limited. Indeed, recent shortages in the supply of liposomal products demonstrate the need for new scalable production methods for liposomes. Therefore, the aim of our research has been to consider the application of microfluidics in the manufacture of liposomes containing either or both a water soluble and a lipid soluble drug to promote co-delivery of drugs. For the first time, we demonstrate the entrapment of a hydrophilic and a lipophilic drug (metformin and glipizide respectively) both individually, and in combination, using a scalable microfluidics manufacturing system. In terms of the operating parameters, the choice of solvents, lipid concentration and aqueous:solvent ratio all impact on liposome size with vesicle diameter ranging from ∼90 to 300nm. In terms of drug loading, microfluidics production promoted high loading within ∼100nm vesicles for both the water soluble drug (20-25% of initial amount added) and the bilayer embedded drug (40-42% of initial amount added) with co-loading of the drugs making no impact on entrapment efficacy. However, co-loading of glipizide and metformin within the same liposome formulation did impact on the drug release profiles; in both instances the presence of both drugs in the one formulation promoted faster (up to 2 fold) release compared to liposomes containing a single drug alone. Overall, these results demonstrate the application of microfluidics to prepare liposomal systems incorporating either or both an aqueous soluble drug and a bilayer loaded drug.

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To determine whether the abnormal glucagon and amylin secretions in NIDDM are secondary to hyperglycemia and relative hypoinsulinemia.

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Glipizide GITS produced better cost outcomes than metformin and acarbose in a model of 3 years' treatment of type 2 diabetes mellitus. Glipizide GITS had pharmacoeconomic and quality of life advantages over diet alone in the short term, but more clinically relevant comparisons with other antidiabetic agents are needed. There are limitations to the present data, but the available pharmacoeconomic data have been favourable for glipizide GITS.

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To determine the pharmacokinetics and pharmacodynamics of glipizide given as a single, oral, 20-mg dose, versus three different divided-dose regimens totaling 20 mg each.

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A liquid chromatography-mass spectrometry approach was used to measure BCAA/AAAs in 30 insulin sensitive (IS) and 30 insulin resistant (IR) subjects before and after: (1) one dose of a sulfonylurea medication, glipizide, 5 mg orally; (2) two days of twice daily metformin 500 mg orally; and (3) a 75-g OGTT. Percent change in BCAA/AAAs was determined after each intervention.

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This is a brief summary of the extensive clinical experience with glipizide in the treatment of noninsulin-dependent diabetes mellitus. The data demonstrate that this agent, one of the newest oral hypoglycemics, is an effective and safe compound with unique properties. Among its other qualities, it has been shown (1) to stimulate insulin action through extrapancreatic effects that affect insulin-receptor binding and enhance tissue responsiveness to insulin; (2) to favorably influence the principal pathophysiologic abnormalities, defective secretory dynamics, and target-cell resistance to insulin observed in noninsulin-dependent diabetes; (3) to improve control of blood glucose, and when used in conjunction with insulin, to achieve glycemic control with reductions in insulin dosage; (4) to lower the level of plasma glucose and to maintain this effect despite a short half-life; (5) to stimulate insulin secretion following its oral administration; (6) to be more effective than tolbutamide in elderly patients with long-standing diabetes; and (7) to be well tolerated with few side effects. The occurrence of hypoglycemia with its use is uncommon and can be avoided by appropriate precautions and correct usage. These factors seem to recommend its use for the management of noninsulin-dependent diabetes mellitus.

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Thirty-four adults with non-insulin-dependent diabetes mellitus were randomly assigned to receive either oral glyburide or oral glipizide in a multicenter comparative trial. Fasting blood glucose and hemoglobin A1c (HbA1c) were assessed at the beginning of the titration phase, the beginning of maintenance therapy, and the end of maintenance therapy. Maintenance therapy lasted approximately 3 months. The initial mean total dose of glyburide (5.4 mg) was significantly lower than that of glipizide (10.6 mg) (P = 0.04) and remained significantly lower at the beginning of maintenance therapy (7.8 mg versus 15.3 mg; P < 0.01) and at the end of the trial (10 mg versus 16.8 mg; P = 0.05). Although significant differences were not detected for fasting blood glucose or HbA1c, patients received higher total doses of glipizide compared with glyburide at the middle and final evaluations to maintain the fasting blood glucose between 3.9 and 10 mmol/L and HbA1c at < 9%. No serious adverse reactions were observed in any patient. These results indicate that doses of glipizide required to maintain blood glucose between 3.9 and 10 mmol/L and HbA1c at < 9% increased over time. Seventy-five percent of patients receiving glyburide were controlled with once-daily dosing compared with 29.4% of those treated with glipizide. Both glyburide and glipizide provide safe and effective treatment for patients with non-insulin-dependent diabetes mellitus, but more patients will benefit from once-daily therapy with glyburide.

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In this experiment, we examined the influence of the posterior hypothalamic adenosine A(2A) receptors on the central cardiovascular regulation of blood pressure (BP) and heart rate (HR). Posterior hypothalamic injection of drugs was performed in anesthetized, artificially ventilated male Sprague-Dawley rats. Injection of CGS-21680HCl (CGS; 20 nmol), an adenosine A(2A) receptor agonist, elicited a decrease of arterial BP and HR, while injection of 8-(3-Chlorostyryl)caffeine (CSC; 10 nmol), an adenosine A(2A) receptor antagonist, blocked the depressor and bradycardiac effects of CGS (20 nmol). To examine the mechanisms of cardiovascular regulation of adenosine A(2A) receptors in the posterior hypothalamus, we applied the adenylate cyclase and guanylate cyclase inhibitors, to the posterior hypothalamus. Pretreatment with MDL-12,330 (MDL; 10 nmol), an adenylate cylase inhibitor, attenuated the depressor and bradycardiac effects of CGS. However, pretreatment with, LY-83,583 (LY; 5 nmol), a soluble guanylate cyclase inhibitor, did not alter the effects of CGS. Additionally, we examined the modification of the cardiovascular effects of adenosine A(2A) receptors through the ATP-sensitive K+ channel in the posterior hypothalamus. Posterior hypothalamic administration of glipizide (20 nmol) significantly attenuated the cardiovascular depressor actions elicited by CGS. These results suggest that adenosine A(2A) receptors in the posterior hypothalamus play an inhibitory role in central cardiovascular regulation, and that adenylate cyclase, but not guanylate cyclase, mediates the depressor and bradycardiac actions of adenosine A(2A) receptors. Furthermore, ATP-sensitive K+ channels mediate the posterior hypothalamic cardiovascular regulation of adenosine A(2A) receptors.

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Glibenclamide, glipizide and phentolamine, three drugs which have been reported to block ATP-dependent potassium channels, increased the coronary perfusion pressure in guinea-pig isolated hearts perfused at constant flow. Blockers of other types of potassium channels, 4-aminopyridine and UK-66,914, did not significantly increase perfusion pressure. Exposing hearts to a single concentration of 3 microM glibenclamide caused a greater degree of vasoconstriction than when this was preceded by lower concentrations. The 3 microM glibenclamide-induced vasoconstriction was reduced by prazosin (1 microM), mepyramine (0.1 microM) and ranitidine (10 microM) but not by a combination of mepyramine and ranitidine or by ritanserin (0.01 microM). These results suggest that a component of the vasoconstriction induced by glibenclamide may result indirectly from the release of vasoactive mediators.

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HbA1c decreased on average by 1.8, 1.0 and 1.5 percentage points in the IO, IS, and IM groups, respectively (p always <0.025). Body weight increased, most in the IO patients (+6.2 kg), least in the IM patients (+3.4 kg). Analysing all treatment groups combined, a similar HbA1c reduction was observed in patients with overall hyperglycaemia (low fasting plasma glucose/HbA1c ratio) and in patients with fasting hyperglycaemia (high fasting plasma glucose/HbA1c ratio). Within the overall hyperglycaemia group, the IS and IM patients had smaller decreases in HbA1c (-1.5 and -1.3 percentage points, respectively) than the IO patients (-2.7 percentage points). On the other hand, within the fasting hyperglycaemia group HbA1c reductions were -1.2, -0.8 and -1.5 percentage points, in the IO, IS, and IM groups, respectively.

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glucotrol dosage administration 2016-05-19

Of the 57 patients (37 men, 20 women) enrolled in the study, 41 completed it. All were Han Chinese of Taiwanese origin, and had the following characteristics: age range, 33 to 69 years; mean (SE) height, 161.99 (9.42) cm; and mean (SE) body mass index, 25.21 (3.43) kg/m2. An intent-to-treat analysis found that the mean (SE) changes from baseline in FPG (-30.00 [10.67] vs -25.96 [11.15] mg/dL) and in buy glucotrol HbA(1c) (-0.08% [0.24%] vs +0.14% [0.22%]) during the 12-week period of the study were not significantly different between the 2 formulations. For patients in the per-protocol analysis, mean (SE) changes from baseline in FPG (-30.00 [10.67] vs -16.52 [7.79] mg/dL) and HbA(1c) (-0.08% [0.24%] vs +0.11% [0.25%]) were also not significantly different. The most frequently reported AEs were urinary abnormality (22.2%) and tachycardia (6.7%) for the GSR group and GIR group, respectively. No serious drug-related AEs were observed in either group.

glucotrol medication 2017-07-29

APPROACH has fully enrolled a high-risk patient population and will compare the glucose-independent effects of rosiglitazone and glipizide on the progression of coronary atherosclerosis, as well as provide additional data on the cardiovascular safety of rosiglitazone in patients buy glucotrol with type 2 diabetes and coronary artery disease.

glucotrol with alcohol 2015-05-03

All individuals are challenged with buy glucotrol 5 mg glipizide × 1; twice daily 500 mg metformin × 2 days; and 75-g oral glucose tolerance test following metformin. Genetic variants associated with glycemic traits and blood glucose, insulin, and other hormones at baseline and following each intervention are measured.

glucotrol drug class 2015-11-02

Glycemic control was markedly impaired at baseline (mean HbA(1c) 10.4 +/- 0.2% glipizide GITS; 10.0 +/- 0 buy glucotrol .2% metformin) but improved comparably with each agent as monotherapy and in combination (P < 0.0001 vs. baseline), as assessed with meal tolerance studies, fructosamine values, and HGO. Body weight and abdominal fat distribution did not change significantly in either group. PAI-1 concentrations were extraordinarily high (5- to 10-fold more than normal) at baseline (202 +/- 12 ng/ml glipizide GITS; 201 +/- 13 ng/ml metformin) but declined comparably, and significantly, after treatment with either agent as monotherapy and decreased further with combination therapy.

glucotrol 10 mg 2015-06-14

To study buy glucotrol the effects of CYP2C9 and CYP2C19 genetic polymorphisms on the pharmacokinetics and pharmacodynamics of glipizide.

glucotrol 5 mg 2016-10-24

The fasting plasma glucose in the I + G arm was buy glucotrol 6.8 (121.8 mg/dl) vs. 8.7 mmol/L (156.0 mg/dl) in the I + P arm, P < 0.001. Mean plasma glucose over 24 hours was 9.8 (176.9 mg/dl) for I + G vs. 11.3 mmol/L (203.8 mg/dl) for I + P, P < 0.001. Glycated hemoglobin was significantly different (9.8 I + G vs. 11.4% I + P, P < 0.008). The total daily insulin dose required was significantly lower with I + G (69.1 vs. 87.3 U, P < 0.0005). However, there were no significant differences in free insulin levels.

glucotrol tab 2015-10-20

The oral hypoglycemic drugs carbutamide, chlorpropamide, glibenclamide, glubornuride, gliclazide, glipizide, gliquidone, glisoxepide, glymidine, tolazamide and tolbutamide, and the diuretics acetazolamide, bemetizide, bendroflumethiazide, benzthiazide, benzylhydrochlorothiazide, bumetanide, butizide, chlorazanile, chlorothiazide, chlortalidone, clopamide, cyclopenthiazide, cyclothiazide, diazoxide, etozoline, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, mefruside, metolazone, piretanide, polythiazide, trichlormethiazide, and xipamide were investigated for photohemolytic properties in vitro. Irradiation with a SOL 3 apparatus (solar simulating irradiation) revealed hemolysis in the presence of five oral hypoglycemic agents and in the presence of 19 out of the 25 tested diuretics. Photohemolysis was induced in the presence of three substances, respectively, after exposure to UVA or visible light. UVB buy glucotrol alone did not induce phototoxic hemolysis in the presence of the tested drugs. Compared to clinical reports on photosensitivity reactions, the photohemolysis model seems a good predictive model in recognizing potential photosensitizing sulfonamides.

glucotrol generic names 2016-02-08

Thirty-four adults with non-insulin-dependent diabetes mellitus were randomly assigned to receive either oral glyburide or oral glipizide in a multicenter comparative trial. Fasting blood glucose and hemoglobin A1c (HbA1c) were assessed at the beginning of the titration phase, the beginning of maintenance therapy, and the end of maintenance therapy. Maintenance therapy lasted approximately 3 months. The initial mean total dose of glyburide (5.4 mg) was significantly lower than that of glipizide (10.6 mg) (P = 0.04) and remained significantly lower at the beginning of maintenance therapy (7.8 mg versus 15.3 mg; P < 0.01) and at the end of the trial (10 mg versus 16.8 mg; P = 0.05). Although significant differences were not detected for fasting blood glucose or HbA1c, patients received higher total doses of glipizide compared with glyburide at the middle and final evaluations to maintain the buy glucotrol fasting blood glucose between 3.9 and 10 mmol/L and HbA1c at < 9%. No serious adverse reactions were observed in any patient. These results indicate that doses of glipizide required to maintain blood glucose between 3.9 and 10 mmol/L and HbA1c at < 9% increased over time. Seventy-five percent of patients receiving glyburide were controlled with once-daily dosing compared with 29.4% of those treated with glipizide. Both glyburide and glipizide provide safe and effective treatment for patients with non-insulin-dependent diabetes mellitus, but more patients will benefit from once-daily therapy with glyburide.

glucotrol glipizide dose 2017-01-23

Glipizide GITS produced better cost outcomes than buy glucotrol metformin and acarbose in a model of 3 years' treatment of type 2 diabetes mellitus. Glipizide GITS had pharmacoeconomic and quality of life advantages over diet alone in the short term, but more clinically relevant comparisons with other antidiabetic agents are needed. There are limitations to the present data, but the available pharmacoeconomic data have been favourable for glipizide GITS.

glucotrol alcohol 2016-08-02

The influence of different sulfonylureas on the rate of acid and pepsinogen secretion was studied in isolated rabbit gastric glands. Neither tolbutamide (10-500 microM), chlorpropamide (10-500 microM), glibenclamide (1-50 microM) nor glipizide (1-50 microM) exerted a secretory effect. In contrast, gliquidone caused a marked and dose-dependent stimulation of acid production in gastric glands incubated under basal conditions and buy glucotrol potentiated the stimulatory effect of both histamine and carbachol. Gliquidone also increased the rate of pepsinogen release in gastric glands incubated either under basal conditions or in the presence of cholecystokinin-octapeptide or isoproterenol. The secretory effects of gliquidone were associated with a significant increase in the glandular content of cyclic AMP, caused by a competitive inhibition of low-Km cyclic AMP phosphodiesterase. Our results indicate that, among the assayed sulfonylureas, only gliquidone, in the micromolar range, stimulates acid and pepsinogen secretion through a cyclic AMP-dependent mechanism.

glucotrol renal dosing 2015-08-19

Any hospitalization or emergency department visit owing to buy glucotrol hypoglycemia within 14 days of antimicrobial exposure.

glucotrol xl dose 2017-12-02

Patients receiving antidiabetic and antihypertensive drugs concomitantly during the 4-week study buy glucotrol period were included.

glucotrol xl tablets 2015-08-10

To evaluate the effect of treatment for tonifying qi, nourishing yin, activating blood circulation and removing stasis on insulin resistance (IR) in patients of type 2 diabetes mellitus (T2DM) complicated buy glucotrol with hypertension.

glucotrol maximum dose 2016-10-18

The oral ethanol loading test (0.5 g per kg b.m. given as 40% solution) was carried out in 5 groups, each of 10 patients with non-insulin-dependent (type 2) diabetes before and after 10 days of treatment with one of the following sulphonylurea derivatives: tolbutamide 0.5 t.i.d., chlorpropamide 0.5 once daily morning, glibornuride 0.025 t.i.d, glibenclamide 0.005 t.i.d. and glipizide 0.005 t.i.d. The response to alcohol (facial flush, heart rate, blood pressure) were compared, and blood concentration of ethanol, acetaldehyde, pyruvate, lactate, carbonates as well as blood pH, pO2 and pCO2 were determined in fasting state and during 6 hours after alcohol ingestion. In all patients the family history of diabetes and the presence and degree of vascular complications were registered. Evident flushing phenomenon was observed in 6 patients treated with chlorpropamide, in 3 treated with tolbutamide, in 2 treated with glibenclamide, in one receiving glibornuride and in none treated with glipizide. All drugs caused a greater rise of blood ethanol and acetaldehyde levels in relation to the control tests, but the difference reached statistical significance only in the group receiving chlorpropamide. Moreover, patients (pooled) with positive thermographic response had also significantly higher blood levels of ethanol and acetaldehyde during the second test. The ratio of acetaldehyde to ethanol concentration in blood (mumol:mmol) was not significantly changed in any group indicating parallel impairment of both steps of ethanol metabolism. All studied drugs intensified to a similar degree the alcohol-induced hypoglycaemia, but had no significant effect on the decrease of blood pyruvate level neither on the increase of blood lactate level. They didn't change the post-alcohol decrease of blood bicarbonate and pH, and didn't modify the behaviour of partial gas pressure. There was also no difference between pooled groups of patients with positive and negative thermographic reaction with respect to family history of diabetes and frequency and intensity of vascular complications. It is concluded that in buy glucotrol patients with non-insulin-dependent (type 2) diabetes the second generation sulphonylurea derivatives are associated with lower risk of alcohol intolerance in case of its incidental ingestion in small amounts. The hypothesis of association of positive thermographic reaction to alcohol during treatment with sulphonylurea derivatives with more frequent occurrence of diabetes in family members and lower tendency to vascular complications was not confirmed.

glucotrol dosage 2016-01-30

Using this method, repeat analysis of samples can be avoided. This is useful for the bioanalysis of toxicokinetic studies with wide dose ranges and studies Azulfidine Dosage where the sample volume is limited.

glucotrol pill identifier 2016-01-01

Insulin secretory physiology has been characterized in tumor cell lines derived by primary culture of insulinomas that developed in transgenic mice expressing the large T-antigen of SV40 in pancreatic islet beta-cells. Cells in one of these lines, beta TC-3, contain large amounts of insulin (3100 +/- 294 ng/100 micrograms cellular protein). Constitutive release of insulin over 2 h in static incubation was low at 31.9 ng/100 micrograms protein and was increased 2-fold by glucose (16.7 mM) and 8-fold by depolarizing concentrations of potassium (45 mM). Isobutylmethylxanthine (IBMX; 0.5 mM) and forskolin (5 and 50 microM), which elevated cellular levels of cAMP, were ineffective as secretagogues, but dramatically potentiated glucose and potassium effects on insulin release (6.5- and 4-fold, respectively). A variety of other known insulin secretagogues stimulated insulin release in a manner analogous to their effects in normal islets. The sulfonylurea glipizide (1 microM) and the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (1 microM) stimulated insulin release 3.4- and 13.7-fold, respectively. The cholinergic agonist carbachol (2 microM) was ineffective alone, but potentiated glucose-induced insulin release 2.8-fold. Comparable stimulation of insulin release by glucose (16.7 mM) and glucose (16.7 mM) plus IBMX (0.5 mM) was noted Desyrel Medicine with several other beta TC lines, which were derived independently from separate transgenic mice. Glucose- and glucose- plus IBMX (0.5 mM)-induced insulin release occurred progressively from 0.15-16.7 mM, indicating that insulin release from beta TC-3 cells occurred at much lower levels than that from normal islets. However, as in the normal islet, the glucose concentration dependency for insulin release was highly correlated (r = 0.93) with the glucose concentration dependency for glucose utilization (measured by 3H2O formation from [5-3H]glucose). This suggests that glucose induces insulin release from beta TC-3 cells by a mechanism similar to that in the normal islet. The high insulin content, the multifold stimulation of insulin release by a variety of secretagogues, their convenient propagation in culture, and the renewable source of these cell lines make the beta TC cells a convenient model for studies of beta-cell function.

glucotrol xl generic 2015-12-16

G. graveolens and V Cordarone Brand Name . iphionoides can be considered as potential candidates for therapeutic modulation of impaired fasting glycemia, impaired glucose tolerance, and type 2 diabetes.

glucotrol diabetes medicine 2015-08-07

The objective of this study was to investigate the changes in plasma post-heparin lipoprotein lipase activity, as it relates to the total amount of weight loss and the changes in plasma lipoproteins, during acute weight reduction and after weight maintenance in type II diabetic patients. Twenty-eight severely obese (mean weight = 106 +/- 21.7 kg, BMI = 36.4 +/- 6.0 kg/m2), diabetic patients lost, on the average, 13.3 kg on a 500 kcal (2100 kJ) diet in eight weeks. Weight loss was maintained throughout the study, which lasted 24 weeks. At the baseline, post-heparin lipoprotein lipase activity did not correlate with degree of obesity, but correlated inversely with fasting plasma glucose (r = -0.64, P less than 0.0001) and triglyceride (r = -0.63, P less than 0.0001). Both during acute caloric restriction and after weight maintenance suppression in post-heparin lipoprotein lipase activity correlated directly with the amount of weight reduction (r = 0.37, P less than 0.05 during weight loss and r = 0.42, P less than 0.03 during weight maintenance). At the end of the study patients were divided into tertiles according to the amount of weight loss achieved and baseline characteristics of the highest and lowest weight loss groups were compared. Before weight loss, despite having similar weights, the highest weight loss group had higher lipoprotein lipase activity (211 +/- 32 mU/ml vs 166 +/- 35 mU/ml, P less than 0.05) and lower plasma triglyceride (1.64 +/- 0.62 mmol/l vs 2.81 +/- 1.28 mmol/l, P less than 0.05) as compared to the lowest Triphala Powder Dosage weight loss group.(ABSTRACT TRUNCATED AT 250 WORDS)

glucotrol online 2016-01-31

Repaglinide (Prandin), NovoNorm, GlucoNorm, an oral insulin secretagogue, was the first meglitinide analogue to become available for use in patients with type 2 diabetes mellitus. The drug lowers postprandial glucose excursions by targeting early-phase insulin release, an effect thought to be important in reducing long-term cardiovascular complications of diabetes. Repaglinide provided similar overall glycaemic control to that achieved with glibenclamide (glyburide), as assessed by glycosylated haemoglobin (HbA(1c)) and fasting blood glucose levels, and was generally well tolerated in well designed clinical trials. Its rapid onset and relatively short duration of action allow for flexible meal schedules. Two modelled US cost-effectiveness analyses projected lifetime costs and outcomes for a hypothetical cohort of patients with type 2 diabetes. Both analyses projected long-term complications using data on HbA(1c) level changes from short-term clinical trials. Repaglinide plus rosiglitazone was dominant over rosiglitazone in one analysis, and repaglinide plus metformin was dominant over nateglinide plus metformin in the other. A similar Canadian analysis showed a favourable incremental cost-effectiveness ratio (Desyrel Generic Name metabolised by the cytochrome P450 (CYP) 3A4 enzyme system and therefore has the potential to interact with other CYP3A4 substrates when administered concurrently. A number of studies in healthy volunteers have shown no clinically significant pharmacokinetic drug interactions when repaglinide was administered concomitantly with digoxin, theophylline, warfarin, cimetidine, ketoconazole, rifampicin (rifampin), ethinylestradiol, simvastatin or nifedipine. However, a clinically significant increase in systemic exposure to repaglinide occurs when clarithromycin and repaglinide are administered concurrently, which may necessitate a reduction in repaglinide dosage. Moreover, a potentially hazardous interaction occurs when gemfibrozil (alone or with itraconazole) is used concomitantly with repaglinide. In view of the marked increase in systemic exposure to repaglinide, the combination of repaglinide and gemfibrozil should be avoided if possible. Pharmacoeconomic Analyses of RepaglinideTwo US cost analyses have been conducted with repaglinide in patients with type 2 diabetes (both published in full). One was a retrospective analysis of pharmacy and medical claims data from a large managed care organisation in which costs were adjusted for age, gender and comorbidities. Total adjusted (year 2000) cost per patient over a 9-month period was numerically lower for those treated with a combination of repaglinide plus metformin (dollars US 8924) than for patients who received metformin only (dollars US 9448), metformin plus glibenclamide (dollars US 9576) or repaglinide only (dollars US 11910), although there were no statistically significant differences between treatment groups. The other study, a literature-based decision-tree analysis, projected the proportion of patients achieving a target HbA(1c) level (<7%) and the associated direct medical costs over a 3-year period from the time of diagnosis. Among six different treatment regimens evaluated, costs ranged from dollars US 6106 with glipizide gastrointestinal therapeutic system (GITS) to dollars US 9298 with repaglinide monotherapy (2001/2002 values). Probabilistic sensitivity analysis indicated that first-line therapy with glipizide GITS or metformin would be associated with lower total medical costs than rosiglitazone or repaglinide monotherapy. Three cost-effectiveness analyses, all of which are modelled studies published as abstracts and/or posters, have been conducted with repaglinide in patients with type 2 diabetes. (ABSTRACT TRUNCATED)

glucotrol xl dosage 2016-04-05

Somatostatin inhibition of growth hormone (GH) secretion from adenohypophysis cells in culture was antagonized by Atarax Reviews the antidiabetic sulfonylurea glipizide (K0.5 = 10 +/- 5 nM). Although all cells that hyperpolarize with somatostatin have ATP-sensitive K+ channels, the antagonistic actions of the hormone and of the antidiabetic drug are due to effects on different types of K+ channels. Diazoxide, an opener of ATP-sensitive K+ channels, abolished the increase of intracellular Ca2+ provoked by growth hormone releasing factor (GRF) and induced inhibition of GRF stimulated GH secretion (K0.5 = 138 microM). This inhibition by diazoxide was largely suppressed by glipizide which blocked the ATP-sensitive K+ channels opened by diazoxide. In summary, hormonal activation of GH secretion is inhibited by openers of ATP-sensitive K+ channels, while hormonal inhibition of GH secretion is suppressed by blockers of ATP-sensitive K+ channels.