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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.

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Also known as:  Glipizide.


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.


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.


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.


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.


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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Among 253 690 patients initiating treatment (98 665 with sulfonylurea therapy and 155 025 with metformin therapy), crude rates of the composite outcome were 18.2 per 1000 person-years in sulfonylurea users and 10.4 per 1000 person-years in metformin users (adjusted incidence rate difference, 2.2 [95% CI, 1.4 to 3.0] more CVD events with sulfonylureas per 1000 person-years; adjusted hazard ratio [aHR], 1.21 [CI, 1.13 to 1.30]). Results were consistent for both glyburide (aHR, 1.26 [CI, 1.16 to 1.37]) and glipizide (aHR, 1.15 [CI, 1.06 to 1.26]) in subgroups by CVD history, age, body mass index, and albuminuria; in a propensity score-matched cohort analysis; and in sensitivity analyses.

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This multicentre, double-blind, active-controlled study randomized 2639 patients aged 18-80 years to 104 weeks of treatment with metformin in addition to alogliptin 12.5 mg once daily (n = 880), alogliptin 25 mg once daily (n = 885) or glipizide 5 mg once daily, titrated to a maximum of 20 mg (n = 874). The primary endpoint was least square mean change from baseline in HbA1c level at 104 weeks.

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The discharge properties of dopaminergic neurons in substantia nigra are influenced by slow adaptive responses, which have not been fully identified. The present study describes, in a slice preparation from the rat, a complex afterhyperpolarization (AHP), elicited by action potential trains. The AHP could be subdivided into a fast component (AHP(f)), which was generated near action potential threshold, relaxed within approximately 1 s, and had highest amplitude when evoked by short-lasting (0.1 s) depolarizations, and a slow component (AHP(s)), which lasted several seconds, was evoked from subthreshold potentials, and required prolonged depolarizing stimuli (>0.1 s). A large proportion of the AHP(f) was sensitive to (i) 0.1 microM apamin, (ii) the Ca(2+) antagonists, Cd(2+) (0.2 mM) and Ni(2+) (0.3 mM), (iii) low (0.2 mM) extracellular Ca(2+) concentration, and (iv), Ca(2+) chelation with intracellular EGTA. The AHP(s) was resistant to the above treatments, and it was insensitive to 25 microM dantrolene or prolonged exposure to 1 microM thapsigargin. The reversal potential of the AHP(s) (-97 mV) was close to the K(+) equilibrium potential. It was significantly inhibited by 5 mM 4-aminopyridine, 5 microM haloperidol, 10 microM terfenadine, or high extracellular Mg(2+) (10 mM), but not by 30 mM tetraethylammonium chloride, 50 microM carbachol, 0.5 microM glipizide, 2 microM (-)sulpiride, 100 microM N-allyl-normetazocine, or 100 microM pentazocine. Haloperidol reduced the post-stimulus inhibitory period seen during spontaneous discharge, but had no detectable effect on spike frequency adaptation. It is concluded that the SK-type Ca(2+)-activated K(+) channels underlies a major component of the AHP(f), whereas the AHP(s) is Ca(2+)-independent and relies, in part, on a voltage-dependent K(+) current with properties resembling the ether-a-go-go-related gene K(+) channel. The latter component exerts a slow, spike-independent, inhibitory influence on repetitive discharge and contributes to the prolonged decrease in excitability following sustained depolarizing stimuli.

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The present study evaluates the presence of oxidative stress in the uncontrolled diabetic state. Glycemic control reduced the oxidative stress, but total normalization of the parameters of oxidative stress was not achieved, indicating continued oxidant injury despite optimal control of the diabetes. Vitamin E supplementation for 4 weeks in these patients further reduced the oxidative stress, suggesting that vitamin E supplementation might be helpful in reducing free-radical-induced oxidant injury.

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To evaluate the effect of these plants on in vitro and in vivo enzymatic starch digestion.

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The role of insulin in the therapy of NIDDM is still under discussion. To clarify the problem we performed a randomized double-blind placebo controlled crossover study of insulin treatment for 4 weeks in diabetic patients (n = 18, age 52-74 years) who were unsatisfactorily controlled by oral antidiabetic agents. The patients continued to use these agents during the study. Special attention was given to informing the patients about the trial and, in particular, about self-monitoring the blood glucose by the use of a reflectance meter. Insulin treatment produced the following significant changes: decreases in blood glucose (at 7.00, 10.00, 16.00), mean daily blood glucose, HbA1, urinary glucose and low density lipoprotein (LDL) cholesterol and increased postglucose immunoreactive insulin (IRI) levels. Significant changes were also observed during the placebo periods: decreases in HbA1 urinary glucose and LDL cholesterol (but not in blood glucose). Therapy with insulin increased the body weight, whereas the placebo insulin had the opposite effect. The finding emphasizes the importance of using not only a run-in period but also a placebo design when the metabolic effects of antidiabetes therapy are to be evaluated. The study indicates that insulin therapy for patients with type 2 diabetes can be initiated at home.

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We identified a cohort of Medicare beneficiaries aged 66 years or older who took glyburide or glipizide for diabetes from a 5% national sample of Medicare Part D claims data in 2008 (n = 34,239). We tracked each participant's claims during 2008-2010 for a co-trimoxazole prescription and subsequent emergency room visits for hypoglycemia. Descriptive statistics and logistic regression modeling were used to evaluate hypoglycemia-related emergency room visits after coadministration of co-trimoxazole with sulfonylureas and its utilization patterns in older adults with diabetes.

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To compare the risk of serious hypoglycemia associated with the use of individual sulfonylureas in older people.

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Use of sulfonylureas compared with metformin for initial treatment of diabetes was associated with an increased hazard of CVD events or death.

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An 8-yr-old male golden lion tamarin ( Leontopithecus rosalia ) was diagnosed with diabetes mellitus based on hyperglycemia and persistent glycosuria. Initial treatment consisted of the oral antihyperglycemic medications glipizide and metformin that resulted in decreased blood glucose concentrations; however, marked glycosuria persisted. Insufficient improvement on oral antihyperglycemic therapy and poor feasibility of daily subcutaneous insulin therapy led to an investigation into an alternative therapy with extended-release exenatide, a glucagon-like peptide-1 (GLP-1) mimetic, at a dosage of 0.13 mg/kg subcutaneously once per month. Following treatment with exenatide, the persistent glycosuria resolved, the animal maintained normal blood glucose concentrations, and had lower serum fructosamine concentrations compared to pretreatment levels. Based on these findings, extended-release exenatide could be considered as a therapeutic option in nonhuman primates with diabetes mellitus that do not respond to oral antihyperglycemics and in which daily subcutaneous insulin is not feasible.

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Not all poorly controlled type 2 diabetic patients should automatically be treated with an oral agent and bedtime insulin. Two daily insulin injections is a valid choice, particularly if the patient has overall hyperglycaemia.

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A retrospective longitudinal (1984-1994) population-based study in two neighbour towns in southern Sweden. The mean prescribed daily dose was expressed as a fraction of the Defined Daily Dose (DDD) for each drug.

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Previous studies have described specific photoincorporation of radiolabeled sulfonylureas into a peptide with high molecular mass (140-175 kDa), which thus has been suggested to represent the sulfonylurea receptor. In the present study, a 125I-labeled 4-azidosalicyloyl analog of glibenclamide, 125I-N3-GA (N-[4-(2-(4-azido-2-hydroxy-5-125I- iodobenzamido)ethyl)benzenesulfonyl]-N'-cyclohexylurea), was used for photoaffinity labeling. This novel probe was specifically photoincorporated into a peptide with an apparent molecular mass of 160-175 kDa when samples from insulin-secreting HIT cells or cerebral cortex were boiled in a SDS-buffer prior to separation with SDS-polyacrylamide gel electrophoresis. However, omitting the heating step revealed specific labeling of an additional peptide with an apparent molecular mass of 38 kDa. The amount of radioactivity specifically photoincorporated into this peptide was 3-4-fold higher than that incorporated into the 160-175-kDa peptide. Both peptides displayed similar dissociation constants for binding of the sulfonylureas IN3-GA (N-[4-(2-(4-azido-2-hydroxy- 5-iodobenzamido)ethyl)benzenesulfonyl]-N'-cyclohexylurea), glibenclamide, glipizide, and tolbutamide. Analysis of photoaffinity labeling of solubilized fractions indicated an almost exclusive specific linkage to the 38-kDa peptide. The data support the view that the sulfonylurea receptor in insulin-secreting cells and cerebral cortex consists of a peptide with an apparent molecular mass of 38 kDa, which seems to Lipitor 40mg Prices be tightly coupled to a 160-175-kDa peptide.

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Ridayarishta formulation alone and cocktail with amlodipine besilate, atenolol, atorvastatin, metformin, glipizide, glimepiride had Effexor Common Dosage negligible or insignificant effect on CYP450 inhibition. It may be concluded that consumption of Ridayarishta along with selective cardio protective, antihypertensive and anti-diabetic conventional medicine is safe with negligible or without any significant CYP450 (CYP1A2, 2C19, 2D6 and 3A4) inhibition mediated HDI.

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Indirect evidence suggests that sulfonylureas, in addition to stimulating insulin release, exert additional effects Feldene Gel Piroxicam at extrapancreatic levels which are of value in the management of type 2 diabetes. In order to characterize in vivo some of these effects, insulin sensitivity was studied in 9 type 1 diabetics with no residual insulin secretory activity, during treatment with chlorpropamide (250 mg b.i.d. for 8 days) and with glipizide (5 mg t.i.d. for 8 days). Employing the glucose clamp technique with the aid of an artificial pancreas (Biostator), glucose disposal during insulin infusion (0.1 U/kg in 60 min) was calculated by the amount of glucose required to keep the blood glucose at preinfusion levels. Chlorpropamide and glipizide administration was accompanied by a significant increase of the amount of glucose required to clamp blood glucose levels, while serum (free) insulin levels were superimposable during the different clamping studies. In the absence of endogenous insulin release, these data strongly suggest that the two sulfonylureas employed enhance in vivo the peripheral sensitivity to insulin. Further studies are required to indicate a preferential site of action (liver, muscle, adipose tissue) of sulfonylureas.

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Three cases of apparently drug-induced Grinspan's syndrome involving the triad of oral lichen planus, diabetes mellitus, and Nexium 40 Mg Treatment hypertension are reported. Because drug therapy for diabetes mellitus and hypertension is capable of producing lichenoid reactions of the oral mucosa, the question arises as to whether Grinspan's syndrome is an iatrogenically induced syndrome.

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Sulfonylureas are powerful hypoglycemic drugs that have been used for decades to treat diabetic patients. This paper describes a 86Rb+ flux technique that permits one to study easily the properties of ATP-modulated K+ channels in RINm5F insulinoma cells. Sulfonylureas inhibit this type of K+ channel under conditions of intracellular ATP depletion. The most potent sulfonylureas (glibenclamide Depakote Normal Dose Range , glipizide, and gliquidone) are acting in the nanomolar range of concentration. Inhibition of the single ATP-modulated K+ channels by low concentrations of sulfonylureas was also observed using the patch-clamp technique. The sulfonylurea receptor has been biochemically identified with [3H]glibenclamide. For 10 different sulfonylureas (or sulfonylurea analogs) there was an excellent correlation between efficacy of blockade of ATP-modulated K+ channels and efficacy of binding to the sulfonylurea receptors using the 3H-ligand.

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Evidence concerning the efficacy and safety of glucose-lowering agents for treating pre-existing and new-onset diabetes in kidney transplant recipients is limited. Existing studies examine more intensive versus less intensive insulin therapy, and the use of DPP4 inhibitors and pioglitazone. The safety and efficacy of more intensive compared to less intensive insulin therapy is very uncertain and the safety and efficacy of DPP4 inhibitors and pioglitazone is uncertain, due to data being limited and of poor quality. Additional RCTs are required to clarify the safety and efficacy of current glucose-lowering agents for kidney Requip 2mg Tablet Side Effects transplant recipients with diabetes.

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Eighty cases of metabolic syndrome were randomly divided into an electroacupuncture combined with western medicine group (observation group) and a simple western medicine group (control group), 40 cases in each Nexium Medicine Uses group. The observation group was treated with electroacupuncture at Back shu points, Zusanli (ST 36),Zhongwan (CV 12),Sanyinjiao (SP 6) etc. as main combined with oral administration of Simvastatin, Glipizide XL, and Felodipine sustained-release tablets for lipid-lowering, glucose-lowering and antihypertensive treatment; the control group was treated with oral administration of western medicine only (the medicine was the same with observation group). The Body Mass Index (BMI) and the blood lipid of the patients were detected respectively before and after treatment.

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This 52-week, double-blind, multicenter, active-controlled, noninferiority trial randomized patients with type 2 diabetes (baseline mean HbA1c, 7.7 %), who were receiving metformin monotherapy, to add-on dapagliflozin (n = 406) or glipizide (n = 408) up-titrated over 18 weeks, based on glycemic response and Generic Viagra Costa Rica tolerability, to ≤ 10 or ≤ 20 mg/day, respectively.

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The intracellular recording and whole-cell recording technique were used to record the NFA-induced response on the acutely-isolated Diamox Dosing Pseudotumor SMA preparation.

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To describe an unusual treatment strategy for certain patients with both acromegaly Claritin Reviews and insulin-requiring diabetes.

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A 62-year Nizoral Oral Tablet Side Effects old woman with obesity, high blood pressure and type 2 diabetes mellitus (DM2) was referred to a Vascular Risk Unit of the Internal Medicine Department due to elevated HbA1C (8.1%) in spite of having taken metformin (850 mg/12h) and glipizide (10 mg/12 h) regularly. She tries to exercise daily (walking 30 min) and has lost weight (from 5 to 12 kg) several times, but always regains what she has lost. Furthermore, she monitors her glucose levels in fasting every two weeks and generally has between 120 and 160 mg/dL. Her high blood pressure is being treated with enalapril/HCTZ and she also takes aspirin 100mg/day and simvastatin 20 mg/day. It is seen in her family background that one brother died suddenly at 50 years of age. Her physical examination shows a BMI of 32.4 Kg/m(2), and she has no edemas in the lower limbs. Her BP is 154/82 mmHg and creatinine 0.9 mg/dL. She has no microalbuminuria and her liver function is normal. What treatment do you think would be the more appropriate? 1 - Add glitazones. 2 - Add incretin mimetics (GLP 1/ DPP-4). 3 - Slow acting insulin.

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Glucokinase activators increase insulin release from pancreatic beta-cells and hepatic glucose utilization by modifying the activity of glucokinase, a key enzyme in glucose-sensing and glycemic regulation. Sulfonylureas are antihyperglycemic agents that stimulate insulin secretion via a glucose-independent mechanism that is vulnerable to secondary failure through beta-cell desensitization. The present study determined whether glucokinase activator treatment retains its glucose-lowering efficacy in male, adult Trileptal Missed Dose , non-diabetic Sprague-Dawley rats desensitized to sulfonylurea treatment and whether glucose-lowering during chronic glucokinase activator treatment is subject to secondary failure. Animals were given food containing either glimepiride (a sulfonylurea), Compound B (3-[(1S)-2-hydroxy-1-methylethoxy]-5-[4-(methylsulfonyl)phenoxy]-N-1,3-thiazol-2-ylbenzamide, an experimental glucokinase activator), or no drug for up to 5 weeks. Food containing 0.04% of either drug produced acute (within 4-8 h) and significant (P<0.05) reductions in blood glucose to approximately 50% of control levels. Chronic treatment with either 0.01% or 0.04% glimepiride resulted in complete failure of glucose-lowering efficacy within 3 days whereas the efficacy of Compound B was sustained throughout the entire study. Glipizide, also a sulfonylurea, had no glucose-lowering effect when given by gavage (3mg/kg) to glimepiride-desensitized animals whereas Compound B retained full glucose-lowering efficacy in glimepiride-desensitized animals. Oral glucose tolerance was significantly impaired, compared with controls, in animals treated with glimepiride for two weeks but was enhanced to a small extent in animals treated with Compound B. Compound B also significantly increased pancreatic insulin content, compared with controls. These findings suggest that Compound B has sustained glucose-lowering effects in a rat model of sulfonylurea failure.