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Glucotrol (Glipizide)

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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.

Other names for this medication:

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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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The contribution of extrapancreatic effects of sulfonylureas to the blood glucose-decreasing activity was reevaluated in vivo and in vitro with several conventional sulfonylureas and with the new one glimepiride. In vivo, in dogs, after single approximately equipotent blood glucose-decreasing doses, the sulfonylureas were tested for a ranking in the ratios of mean plasma insulin-increasing and blood glucose-decreasing activity. Studies were also performed in hyperglycemic hyperinsulinemic KK-Ay mice under once daily treatment for 8 weeks. In vitro, glimepiride and glibenclamide were tested for the ranking of their extrapancreatic activity with respect to the stimulation of glucose transport and glucose metabolizing processes in normal and insulin-resistant fat cells as well as in the isolated diaphragm. Furthermore, in vitro studies were performed, especially with glimepiride, in order to characterize the molecular mechanism for the extrapancreatic activity. The dog studies revealed a marked ranking in the ratios of plasma insulin-increasing and blood glucose-decreasing activity between the different sulfonylureas (glimepiride < glipizide < gliclazide < glibenclamide). In the hyperglycemic hyperinsulinemic KK-Ay mice, glimepiride reduced blood glucose by 40%, plasma insulin by 50% and HBA1c by 33%, whereas glibenclamide and gliclazide had no effect on these parameters. In vitro, glimepiride and glibenclamide had extrapancreatic effects within the lower microM range, with glimepiride exhibiting 2-3-fold lower ED50 values than glibenclamide. In the absence of insulin, both stimulated glucose transport--up to 60% of the maximum insulin response in the rat diaphragm and up to 35% in 3T3 adipocytes. Glycogenesis was stimulated in the rat diaphragm--up to 55% of the maximum insulin effect; lipogenesis in 3T3 adipocytes--up to 40%. The studies on the molecular mechanism of extrapancreatic activity with rat adipocytes and diaphragm suggest that these direct insulin-mimetic effects rely on the induction of GLUT4 translocation from internal stores to the plasma membrane and on the activation of the key metabolic enzymes, glycogen synthase and glycerol-3-phosphate acyltransferase. These processes occur within the same drug concentration range and with the same ranking between glimepiride and glibenclamide as observed for glucose utilization and transport. The direct effects of sulfonylureas may ultimately be regulated by a glycosyl-phosphatidylinositol-specific phospholipase C, shown to be activated by glimepiride in rat adipocytes. Lipolytic cleavage products thereby generated from glycolipidic structures may in turn stimulate specific protein phosphatases which activate key regulatory proteins/enzymes of glucose and lipid metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)

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In patients with type 2 diabetes, adding sitagliptin to metformin monotherapy improved glycaemic control over 2 years, similar to the glucose-lowering efficacy observed with adding glipizide, but with greater durability and generally better maintenance of beta-cell function. Sitagliptin was generally well tolerated with a lower risk of hypoglycaemia and weight loss compared with weight gain observed with glipizide.

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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 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.

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The effects of sulfonylureas on the production of plasminogen activator (PA) and antiactivator (PAI) were investigated using bovine aortic endothelial cells. All compounds studied stimulated PA release (1.3- to 5.2-fold), with glipizide being the most potent, followed by tolazamide, chlorpropamide, and tolbutamide, in that order, while glyburide was the least effective. Both tissue-type and urokinase-type PA production was enhanced. Studies using metabolic inhibitors indicated that both RNA and protein syntheses are required for the sulfonylurea-mediated stimulation of PA release. In addition to continuous release of the two PAs, there was also a continuous release of a single PAI, which did not show an increase after the sulfonylureas. These results suggest that, in addition to their beneficial effects in the treatment of diabetes mellitus, some sulfonylurea compounds may also have significant thrombolytic effects. These results also suggest that pharmacological enhancement of PA production by vascular endothelial cells may be a promising antithrombotic mechanism.

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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 effects of the potent ATP-sensitive K+ channel blocker glipizide were measured on the locomotor activity of rats after bilateral intracerebral administration into the dorsal pallidum. Glipizide (10 pmol) was found to reduce spontaneous locomotor activity measured during the night cycle of the rats, whereas the ATP-sensitive K+ channel activator (-)-cromakalim (5 fmol) enhanced spontaneous locomotor activity. Glipizide (0.5, 2.5 and 10 pmol) was also found to depress noticeably d-amphetamine-induced locomotor activity (1 mg/kg s.c.). These results are in agreement with the idea that ATP-dependent potassium channels within the dorsal pallidum are involved in controlling motor activity in the rat.

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153 men with NIDDM, aged 40 to 69 years, who had hemoglobin A1c (HbA1c) levels of greater than 6.55% while receiving sulfonylurea or insulin therapy.

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Epidemiological studies have implicated increased plasminogen-activated inhibitor 1 (PAI-1) as a marker or predictor of accelerated coronary atherosclerotic disease in type 2 diabetes. We sought to determine whether metabolic control, independent of its oral mode of implementation, affects PAI-1 in patients with marked hyperglycemia.

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We retrospectively examined data from 17,773 type 2 diabetic patients seen from March 2, 1998, to December 13, 2010, in 3 Veterans Administration medical centers. Severity was measured using patients' inpatient and outpatient comorbidities during the last year of visits. Severity-adjusted logistic regression was used to measure the odds ratio for mortality within the study period.

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Retrospective studies have identified oral sulfonylureas, age, and fasting as major risk factors for hypoglycemia in patients with type 2 diabetes. Sulfonylureas may be withheld from elderly patients out of concern for hypoglycemia.

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This study compares the human placental transport of glyburide, glipizide, chlorpropamide, and tolbutamide.

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The antioxidant activity was determined by the DPPH (2,2-diphenyl-1-picrylhydrazyl) radical scavenging activity where ascorbic acid was taken as positive control. The antioxidant property was later exploited and the methanolic extract of plant was tested for antihyperglycemic activity in glucose overloaded hyperglycemic mice. The extract was tested for its hypoglycemic activity at two-dose levels, 250 and 500 mg/kg respectively where Glipizide 5 mg/kg was taken as standard reference drug. All results are presented as mean ± SD (Standard Deviation). Significant differences between experimental groups were determined by Student's t-test.

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This case report outlines a very rare case of glipizide-induced severe proximal myopathy in a 61-year-old diabetic man. After taking 10 mg glipizide for 5 months, diabetes was well controlled but the patient presented with progressive proximal muscle weakness in all the four limbs. Clinical examination and relevant investigations suggested it to be a case of proximal myopathy and might be drug induced. De-challenge was done and was treated resulting in reversal of the diseased state. After 3 more months, controlled re-challenge was done and there was recurrence of proximal muscle weakness. There were no evidences of any other possible metabolic, infective, organic or other pathologic causes giving rise to that condition and Naranjo adverse drug reaction probability scale suggested that it was "probable" that glipizide was responsible for the development of myopathy in this patient.

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This randomized, double-blind, double-dummy, placebo-controlled, parallel-group, clinical study enrolled adult patients with type 2 diabetes mellitus who were already being treated with diet and a sulfonylurea. Patients were randomized to receive either GSR 10 mg PO QD or GIR 5 mg PO BID for 12 weeks. Because these 2 formulations differed in appearance, each patient also received placebo resembling the alternate formulation, to be received at the alternate frequency. Drugs dispensed but not used were returned to the investigators and counted to monitor compliance with the protocol. For efficacy assessment, fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA(1c)) were measured before and after treatment. Tolerability was measured by adverse events (AEs), which were evaluated by the attending physician during each clinical visit.

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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, 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.

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Forty-one patients with chemical diabetes had three oral glucose tolerance tests and underwent muscle biopsy three times over a period of three years. Twenty-three received glipizide and 18 placebo. Those taking placebo had an increase in the mean muscle capillary basement membrane width (p = 0.01), but those taking glipizide showed a decrease (p = 0.01) to values no different from those of nondiabetic subjects. Determinations of enzyme activities involved in the synthesis and degradation of glycoproteins revealed a three-year decrease (not significant) in muscle glucosyltransferase activity in the glipizide-treated patients, but a statistically significant difference (p less than 0.01) comparing the adjusted means of the two treatment groups. N-acetyl-beta-glucosaminidase activity was significantly increased in muscle from baseline values (p less than 0.01), with adjusted means also significantly different (p less than 0.01). The data suggest that changes in basement membrane and enzyme activities are correlated, and the latter may be a predictor to follow the development, progression, or regression of diabetic vasculopathy.

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Rat striatal synaptosomes and slices were used to investigate the responsiveness of different populations of nerve terminals to 3-nitropropionic acid (3-NP), a suicide inhibitor of the mitochondrial enzyme succinate dehydrogenase, and to elucidate the ionic mechanisms involved. 3-NP (0.3-3 mm) stimulated spontaneous gamma-aminobutyric acid (GABA), glutamate and [3H]-dopamine efflux but left unchanged acetylcholine efflux from synaptosomes. This effect was associated with a >70% inhibition of succinate dehydrogenase, as measured in the whole synaptosomal population. The facilitation was not dependent on extracellular Ca2+ but relied on voltage-dependent Na+ channel opening, because it was prevented by tetrodotoxin and riluzole. 3-NP also elevated spontaneous glutamate efflux from slices but in a tetrodotoxin-insensitive way. To investigate whether energy depletion could change the responsiveness of nerve endings to a depolarizing stimulus, synaptosomes were pretreated with 3-NP and challenged with pulses of KCl evoking 'quasi-physiological' neurotransmitter release. 3-NP potentiated the K+-evoked GABA, glutamate and [3H]-dopamine release but inhibited the K+-evoked acetylcholine release. The 3-NP induced potentiation of GABA release was Ca2+-dependent and prevented by tetrodotoxin and riluzole whereas the 3-NP-induced inhibition of acetylcholine release was tetrodotoxin- and riluzole-insensitive but reversed by glipizide, an ATP-dependent K+ channel inhibitor. We conclude that the responsiveness of striatal nerve endings to 3-NP relies on activation of different ionic conductances, and suggest that the selective survival of striatal cholinergic interneurons following chronic 3-NP treatment (as in models of Huntington's disease) may rely on the opening of ATP-dependent K+ channels, which counteracts the fall in membrane potential as a result of mitochondrial impairment.

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The aim of this study was to examine insulin and glucagon secretory patterns in successfully transplanted spontaneously diabetic BB/Wor dp rats. Diabetic, BB/Wor dp rats received abdominal, intratesticular islet grafts of MHC-compatible BB/Wor dr donor rats without immunosuppression. After a period of 74 +/- 15 days of normoglycemia, they were given the following challenges: 1) glucose, by mouth, 2) a single oral dose of glipizide, with glucose, and 3) arginine, by iv infusion. The pertinent results included the mean fasting plasma glucose levels of control, Sprague-Dawley (C), of transplanted BB/Wor dp (T), and nontransplanted, insulin treated, diabetic BB/Wor dp (D), and they were, respectively, 97 +/- 4 mg/dl, 110 +/- 3 mg/dl, and 350 +/- 40 mg/dl. Fasting plasma insulin levels in C and T rats were 21.9 +/- 3 microU/ml, and 20.4 +/- 2 microU/ml, respectively. Fasting plasma glucagon levels in C, T, and D, were 37.8 +/- 5.7 pg/ml, 43.4 +/- 4.6 pg/ml, and 47.4 +/- 4.9 pg/ml, respectively. During oral glucose tolerance test, the pattern of insulin secretion in the C and T rats was identical with a peak attained at 15 min. Glucose caused a 70% suppression of plasma glucagon levels in C rats (P less than 0.01); T rats suppressed 14%, but this was not statistically significant; D rats failed to suppress. Glipizide plus glucose caused an improved glucose tolerance in T rats without significantly affecting insulin levels. In the same rats, glipizide resulted in a significant suppression of glucagon compared with levels in the presence of glucose alone. Arginine caused a minimal release of insulin in T rats and a major glucagon secretory response in D rats. Pancreatic glucagon content was significantly (P less than 0.03) lower in C and T, compared with D rats. Furthermore, the transplanted testes of T contained substantial amounts of glucagon. In summary, these data suggest that grafted testes in spontaneously diabetic BB/Wor dp rats contain both beta and alpha-cells and that these cells have the capacity to respond to specific secretagogues independently.

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Double-blind, randomized, placebo-controlled, parallel trial.

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The observed differences with fluoxetine may be due to its pharmacological effects on thermoregulatory responses that influence tail blood flow, a hypothesis that remains to be tested. Based on these observations, we recommend the tail-bleeding technique for pharmacology or toxicology exposure and F% studies, particularly in early discovery work. Retro-orbital bleeding is controversial and is no longer considered a humane method. Cannula-bleeding, especially coupled with automated blood-collection techniques, has become the most efficient way for pharmaceutical industry to perform rat bioavailability studies.

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Type 2 diabetes mellitus is a common chronic disease that causes significant morbidity and mortality worldwide. The primary goal of treatment is to target glycemic control by maintaining the glycosylated hemoglobin level near 6-7% without predisposing patients to hypoglycemia. Diabetes results from a combination of increased hepatic glucose production, decreased insulin secretion from beta cells, and insulin resistance in the peripheral tissues. Currently available antidiabetic agents work by different mechanisms to lower blood glucose levels. Unfortunately, each of them has its tolerability and safety concerns that limit its use and dose titration. Sitagliptin is the first antidiabetic agent from the class of dipeptidyl peptidase-4 enzyme inhibitors. It increases the amount of circulating incretins, which stimulate insulin secretion and inhibit glucose production. Sitagliptin was approved by the US Food and Drug Administration (FDA) for use with diet and exercise to improve glycemic control in adult patients with type 2 diabetes. It can be used alone or in combination with metformin or a thiazolidinedione (pioglitazone or rosiglitazone) when treatment with either drug alone provides inadequate glucose control. The usual adult dose is 100 mg once daily. A dose of 25-50 mg once daily is recommended for patients with moderate-to-severe renal impairment. In randomized, placebo-controlled trials that lasted for up to 6 months, sitagliptin lowered glycosylated hemoglobin levels by 0.5-0.8%. In a 52-week clinical trial, sitagliptin was shown to be noninferior to glipizide as an add-on agent in patients inadequately controlled on metformin alone. Sitagliptin was well tolerated with the most common side effects being gastrointestinal complaints (up to 16%), including abdominal pain, nausea and diarrhea; hypoglycemia and body weight gain occurred at similar rates compared with placebo. Overall, sitagliptin provides a treatment option for patients with type 2 diabetes as a monotherapy, or as an adjunct to metformin or a thiazolidinedione when patients achieve inadequate glycemic control while on either of the agents. It is also an alternative therapy for those patients who have contraindications or intolerability to other antidiabetic agents.

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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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Novel oral controlled release of glipizide was successfully achieved by incorporating glipizide solid dispersion into osmotic system.

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Saxagliptin + metformin was associated with fewer patients reporting hypoglycemia and fewer and less severe hypoglycemic events in those experiencing hypoglycemia compared with glipizide + metformin. registration number: NCT00575588.

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In patients with Type 2 diabetes, the appropriate intensity of glucose control is determined by age, life expectancy, and the presence of concomitant disease. Geriatric patients are especially susceptible to hypoglycaemia and therefore particular care should be taken in this group characterized by polypharmacy, renal or hepatic dysfunction, cardiovascular multimorbidity and malnutrition. As hypoglycaemia is a significant cause of morbidity and mortality, treatment regimens for diabetes should minimize the occurrence of hypoglycaemic episodes and be tailored to the patient's individual needs. The pharmacological options for treating Type 2 diabetes have increased considerably and the risk of hypoglycaemia of the currently available drugs varies considerably. Metformin, thiazolidinediones, and acarbose, oral antidiabetic drugs that decrease insulin resistance or postprandial glucose absorption, are associated with a low risk of hypoglycaemia. These drugs can also be used effectively in various combination regimens; however, by improving insulin sensitivity, combinations of metformin and thiolidinediones with sulphonylureas or meglitinides may considerably increase the risk of hypoglycaemia. On account of its complex pharmacoprofile glibenclamide is a problematic substance carrying a high risk of hypoglycaemia. There are limited preliminary data indicating that, under routine conditions, glimepiride may be associated with a lower risk of hypoglycaemia than glibenclamide and is no more likely to cause hypoglycaemia than other shorter-acting agents such as gliclazide and glipizide. Nateglinide and repaglinide as short-acting insulin secretagogues may be associated with a reduced risk of hypoglycaemia compared with glibenclamide, in particular when dosed flexibly. Repaglinide might be beneficial in individuals with renal impairment.

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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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We have examined the nonpancreatic actions of sulfonylureas on multiple aspects of insulin responsiveness in two target tissues for insulin, liver and fat. In vivo administration of tolazamide and glipizide reduced significantly the postabsorptive buy glucotrol serum glucose levels in rats without altering the levels of insulin. This was consistent with extrapancreatic sites of drug action. The number and affinity of hepatic insulin receptors was not different from those of control rats. Using a tissue culture system for rat adipose tissue, a 20-h treatment with sulfonylureas markedly potentiated insulin action in fat cells. The primary augmentation was at the level of insulin-stimulated glucose transport. Again, there was no alteration of the insulin receptors located on the adipose tissue. Furthermore, consistent with the lack of an influence on insulin-induced receptor loss after in vitro treatment with sulfonylureas, the in vivo administration of these agents did not alter the transglutaminase activity in rat hepatic tissue. The data demonstrate that sulfonylureas potentiate the responsiveness of the target tissues for insulin. Thus, these hypoglycemic agents probably act by correcting some of the cellular lesions associated with the insulin resistance in type II diabetes mellitus.

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The efficacy of diabetic medications among patients with multiple comorbidities is not tested in randomized clinical studies. It is buy glucotrol important to monitor the performance of these medications after marketing approvals.

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In vitro enzymatic starch digestion with aqueous extracts from plants at concentrations of 1, 5 buy glucotrol , 10, 12.5, 25, 50 and 100 mg/ml was assayed using α-amylase and α-amyloglucosidase. Acarbose was used as control and glucose liberation was determined by glucose oxidase method. Oral starch tolerance test (OSTT) and oral glucose tolerance test (OGTT) were determined for the plant extracts at concentrations 125, 250 and 500 mg/kg b.wt. on Sprague-Dawley rats. Blood glucose levels in rats treated with plant extracts and drugs (acarbose or metformin and glipizide) were measured at -30, 0, 45, 90 and 135 min.

glucotrol with alcohol 2016-06-28

The present work aims at the development of a low-cost controlled release buy glucotrol system of glipizide beads embedded in pectin to overcome the problem of frequent dosing of drug. The method of preparation has been optimised by experimental design to achieve satisfactory responses with respect to controlling variables. The controlling variables are X1, drug-polymer ratio; X2, surfactant concentration and X3, isooctane-acetone ratio. The most effective combination is X1(1:6), X2(1%), X3(50:50). Various parameters such as mucoadhesivity and swellability of beads, characterisation, dissolution, stability, ex vivo absorption and in vivo (Oral glucose tolerance test in rat) studies were performed with the optimised product. The optimised product was found quiet satisfactory that showed yield of 86.78%, drug entrapment efficiency (DEE) of 87.38% and drug release was extended up to 18 h. The present formulation of glipizide is a promising multiparticulate system of glipizide with significant hypoglycemic effect, and moreover it was prepared rapidly with ease.

glucotrol and alcohol 2015-12-04

Insulin secretagogues display different tissue selectivity characteristics at therapeutic doses buy glucotrol . This may translate into different levels of cardiovascular risk.

glucotrol drug classifications 2016-01-23

Hypoglycemic sulfonylureas, such as tolbutamide, gliclazide and glipizide, provoked the translocation of Ca from an aqueous medium into or across an organic immiscible phase. The amount of Ca translocated into the organic phase was proportional to the square of the drug concentration, and appeared saturable at high Ca concentration. Non-hypoglycemic sulfonylureas and diazoxide had little or buy glucotrol no effect upon Ca translocation. The ionophoretic capacity of the hypoglycemic sulfonylureas was antagonized by suloctidil. Tolbutamide and gliclazide also provoked Na translocation into the organic phase, the amount of Na translocated being proportional to the drug concentration. Gliclazide-mediated Ca translocation was inhibited in a dose-related fashion by increasing concentrations of Na+ or H+. It is proposed that the ionophoretic capacity of hypoglycemic sulfonylureas may participate in their insulinotropic action.

glucotrol tablets 2017-10-09

The study demonstrated improved outcomes with saxagliptin at a cost that would likely be considered acceptable in the German setting. Furthermore, the findings of the sensitivity analysis suggest that the results are robust to various assumptions concerning input variables and modelling assumptions buy glucotrol .

buy glucotrol 2015-04-14

The electrochemical behavior of glipizide at the hanging mercury drop electrode (HMDE) was studied in B-R universal buffers of pH 1.7-11. The voltammograms exhibited a well-defined 4-electron irreversible cathodic peak which attributed to reduction of the two C=N of the pyrazine ring of glipizide molecule. Glipizide was found to has an interfacial adsorptive character onto the mercury electrode surface. A monolayer surface coverage of 1.02x10(-10)mol cm(-2) was estimated and hence each adsorbed glipizide molecule occupied an area of 1.63 nm(2) onto the mercury electrode surface. A simple and precise square-wave adsorptive cathodic stripping (SWAdCS) voltammetric procedure was described for quantification of bulk glipizide with a limit of detection of 1.5x10(-10)M and a limit of quantitation of 5x10(-10)M. The proposed procedure was successfully applied for quantitation of glipizide in its pharmaceutical formulation (Minidiab tablets buy glucotrol ) without interference from excipients.

glucotrol 5 mg 2017-05-17

Drug repurposing of non-cancer drugs represents an attractive approach to develop new cancer therapy. Using the TRAMP transgenic mouse model, glipizide, a widely used drug for type 2 diabetes mellitus, has been identified to buy glucotrol suppress prostate cancer (PC) growth and metastasis. Angiogenesis is intimately associated with various human cancer developments. Intriguingly, glipizide significantly reduces microvessel density in PC tumor tissues, while not inhibiting prostate cancer cell proliferation from the MTT assay and flow cytometry investigation. Moreover, glipizide inhibits the tubular structure formation of human umbilical vein endothelial cells by regulating the HMGIY/Angiopoietin-1 signaling pathway. Taken together, these results demonstrate that glipizide has the potential to be repurposed as an effective therapeutic for the treatment of PC by targeting tumor-induced angiogenesis.

glucotrol gel 2015-11-13

Sulfonylurea drugs including chlorpropamide, gliclazide, tolbutamide, glipizide, glibenclamide (glyburide) and glimepiride are the most widely used oral hypoglycaemic agents in people with type 2 diabetes. This review investigates the impact of genetic polymorphisms on the pharmacokinetics and pharmacodynamics of sulfonylurea drugs. CYP2C9 is the major enzyme involved in sulfonylurea drug metabolism. CYP2C9 variant allele carriers have significant lower apparent clearance of these medicines. CYP2C19 genotype is more influential for gliclazide pharmacokinetics when compared to CYP2C9. Sulfonylurea pharmacodynamics is affected by several genes. Sulfonylurea receptor 1 (SUR1, ABCC8 gene) and K+ inward rectifier Kir6.2 (KCNJ11) have been correlated to significant variation in sulfonylurea response. Diabetics with the SUR1 exon 33 G allele are more sensitive to gliclazide and the rs5210 variant of the KCNJ11 gene was associated with improved clinical efficacy of gliclazide. Carriers of Transcription factor 7-like 2 (TCF7L2) variants buy glucotrol are more likely to fail sulfonylurea therapy. On the other hand, patients with HNF-1alpha mutations had a significant greater response to gliclazide when compared to those with type 2 diabetes. The Arg972 polymorphism of insulin receptor substrate 1 (IRS1) may lead to secondary failure of sulfonylurea therapy. Calpain 10 gene (CAPN10) polymorphism has also been linked to sulfonylurea drug response. Despite the available evidence, larger population studies that investigate the pharmacokinetics and pharmacodynamics of sulfonylurea drugs are needed to investigate the influence of key SNPs amidst all potential contributing factors to variability in response to these which inturn will provide information to optimise sulfonylurea use in people with diabetes.

glucotrol pill identifier 2017-10-12

The buy glucotrol Tennessee Medicaid Program.

glucotrol diabetic pills 2015-10-12

Two-year, randomized, double-blind, parallel-group clinical trial. buy glucotrol

glipizide glucotrol dosage 2016-10-13

The objective of the current study was to develop a method to blind commercially available Wellbutrin SR 150 mg sustained-release tablets for a clinical study. Overcoating was selected as the most appropriate blinding method. Hydroxypropyl methylcellulose (Opadry II) containing red iron oxide and titanium dioxide was applied to the Wellbutrin tablets at coating levels ranging from 0.5% to 4% weight gain. When compared against the uncoated product, no significant differences in drug release were noted over an 8-hr period. Matching placebo tablets, prepared using specially designed tablet tooling, were coated with the same cellulosic polymer that was used for the active. The coated active and placebo tablets were virtually indistinguishable. To test the applicability of this overcoating technique for blinding other controlled release products, the same procedure was used to coat Glucotrol XL 5 mg Augmentin 600 Suspension tablets and Theo-Dur 200 mg tablets. The debossing on the Theo-Dur tablets and the laser-drilled hole on the surface of the Glucotrol tablets prevented blinding. The Theo-Dur tablets were mechanically weak and not able to withstand the coating process. Dissolution testing revealed significantly higher amounts of drug were released from the blinded Glucotrol tablets compared to the unblinded product at the 12 hr time point. The findings from this study suggest that overcoating with pigmented hydroxypropyl methylcellulose may not be useful for blinding all controlled-release tablets.

glucotrol mg 2016-01-23

Herbal preparations of Ficus bengalensis had been considered as effective, economical and safe ethnomedicines Cymbalta Overdose Dosage for various ailments in Indian traditional system of medicine.

glucotrol medication 2016-07-09

In this small study, treatment with oral GSR (10 mg QD) was not significantly different from that of treatment with GIR (5 mg BID) with respect to short-term (12 weeks) FPG and HbA(1c) reductions in these ethnic Chinese adults with type Aciphex 5 Mg 2 diabetes mellitus receiving treatment with a sulfonylurea.

glucotrol maximum dose 2017-11-26

In anesthetized rats subjected to pressure-controlled hemorrhage, glipizide sodium salt improved mean arterial pressure in a dose-dependent manner. Compared with the vehicle-treated animals, mean arterial pressure increased from 41.6 +/- 4.6 to 63.1 +/- 3.1 mm Hg in the 20 mg/kg intravenous group and from 33 4 Mg Atarax .2 +/- 4.9 to 54.0 +/- 4.7 mm Hg in the 40 mg/kg intramuscular group 60 mins after a 40-mm Hg shock. Furthermore, the drug did not affect the hemorrhage-induced changes in blood glucose concentrations. However, the higher doses of glipizide sodium salt attenuated the increments in plasma concentrations of lactate, alanine aminotransferase, creatinine, and amylase. Moreover, the higher doses markedly improved short-term survival after pressure- and volume-controlled bleeding. Overall, the intramuscular injections of the drug exerted salutary effects that were comparable to the intravenous administration.

glucotrol reviews 2016-03-03

The interaction between sulfonylureas and membrane proteins from a hamster insulin-secreting tumor (HIT) cell line has been examined. Four HIT cell membrane proteins were covalently linked to an 125I-labeled glyburide analog by photolabeling. Three photolabeled polypeptides of M(r) 65,000, 55,000, and 30,000 were identified as low affinity Detrol Online "glyburide receptors." These proteins appear to be of similar abundance, when quantitated by photolabeling, with half-maximal displacements (Ki values) by glyburide, glipizide, and tolbutamide in the low micromolar range. The glyburide analog is more tightly bound to a M(r) 140,000 protein with dissociation constants, determined by filtration binding assays and by photolabeling, of 7 and 9.0 nM, respectively. The labeled analog was displaced from the M(r) 140,000 protein by glyburide, glipizide and tolbutamide with Ki values of 3.3 nM, 103 nM, and 25 microM, respectively, as estimated by photolabeling. Optimal conditions established for visualizing the M(r) 140,000 band on autoradiograms prepared after UV cross-linking and sodium dodecyl sulfate-polyacrylamide gel electrophoresis include irradiating the radioligand-receptor complex at 1.5 J/cm2 at 312 nm, followed by heating samples in pH 9.0 sodium dodecyl sulfate-gel sample buffer. With receptor sites partially occupied (5 nM radioligand), approximately 0.75% of the protein is photocoupled to the radioligand and visualized by autoradiography. Our results confirm that the M(r) 140,000 polypeptide contains the beta-cell high affinity glyburide binding site and show that the second generation sulfonylurea antidiabetic drugs have a selective increase in affinity for this receptor.

glucotrol drug interactions 2017-02-11

Danazol is a steroid analogue with anabolic and androgenic effects and is indicated for the treatment of endometriosis, fibrocystic diseases of the breast, and hereditary angioedema. Lovastatin has been prescribed to lower total cholesterol and low-density lipoprotein cholesterol, reducing cardiovascular-related morbidity and mortality in patients with hypercholesterolemia. As monotherapies, both danazol and Motilium 10mg Tablets lovastatin have been reported to induce myopathy and pancreatitis.

glucotrol overdose 2016-01-10

The ATP-sensitive K+ channel, an octameric complex of two structurally unrelated types of subunits, SUR1 and Kir6.2, plays Antabuse Online Paypal a central role in the physiological regulation of insulin secretion. The sulfonylurea glibenclamide, which trigger insulin secretion by blocking the ATP-sensitive K+ channel, interacts with both high and low affinity binding sites present on beta-cells. The high affinity binding site has been localized on SUR1 but the molecular nature of the low affinity site is still uncertain. In this study, we analyzed the pharmacology of glibenclamide in a transformed COS-7 cell line expressing the rat Kir6.2 cDNA and compared with that of the MIN6 beta cell line expressing natively both the Kir6.2 and the SUR1 subunits. Binding studies and Scatchard analysis revealed the presence of a single class of low affinity binding sites for glibenclamide on the COS/Kir6.2 cells with characteristics similar to that observed for the low affinity site of the MIN6 beta cells.

glucotrol generic names 2017-02-11

Cytochrome P450 (CYP) 2C9 and CYP2C19 genetic mutant could influence the plasma concentration of glipizide in human subjects, which refers to glipizide safety and adverse effects in clinic practice. A further study to investigate the relationship of the concentrations between glipizide and its metabolites in human with different CYP mutants was valuable. We firstly develop a validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for simultaneous quantification of glipizide and its hydroxylated metabolites in human urine. After simple protein precipitation with methanol including 4'-OH-tolbutamide and gliclazide (both are internal standards), the analytes were chromatographed on a reversed-phased column with a mobile phase of 0.1% formic acid in acetonitrile and 0.1% formic acid in water by a gradient elution. The ion transitions of the precursor to the product ion were principally protonated ions [M+H](+) at m/z 446.4→m Anafranil Drug Interactions /z 321.1 for glipizide, m/z 462.2→m/z 321.1 for the four hydroxylated forms of glipizide, m/z 287.2→m/z 188.0 for 4'-OH-tolbutamide, and m/z 324.1→m/z 127.1 for gliclazide. The method was linear over a concentration range of 0.02-20.0ng/mL. The intraday and inter-day variances were less than 9.9%, and accuracy was within ±6.8%. The method was successfully applied to the urinary phenotyping study in volunteers after a single oral administration of 5-mg glipizide tablet, and two new hydroxycyclohexyl metabolites of glipizide (OH-gp), 4-cis-OH-gp and 3-trans-OH-gp, were found in this study.

glucotrol xl dosing 2017-08-19

Nested case-control study Risperdal 80 Mg .

glucotrol glipizide dose 2016-04-29

Ten Type 2 diabetics were examined during long-term treatment, at two dosage levels, with chlorpropamide once daily and glipizide t.i.d. Drug concentrations were measured by gas chromatography and high-pressure liquid chromatography, respectively, plasma insulin (IRI) by radio-immunoassay, and blood glucose enzymatically. Both drugs gave continuous sulfonylurea exposure, even at the lower dosage, and the mean plasma concentrations were almost doubled after the increase in dose. Neither the IRI nor the glucose response to meals showed any therapeutic improvement following the increase in chlorpropamide dosage. The lower dosage of glipizide produced better glucose utilization than chlorpropamide. On the other hand, the increased dose of glipizide led to impairment Clomid Ovulation Pills instead of further improvement. As this was associated with enhanced rather than reduced IRI levels, the impairment might have been due to increased peripheral insulin resistance. Thus, glipizide offers a therapeutic advantage over chlorpropamide, but its effectiveness may be restricted not only by limitations set by the disease, but also by counter-regulatory mechanisms that develop during continuous exposure to sulfonylureas at high levels.

generic glucotrol xl 2016-07-24

The sulfonylurea class of compounds has demonstrated its effectiveness in treating non-insulin-dependent diabetes mellitus, although the exact mechanisms of action are still not fully defined. Clinical studies have suggested the action may be at least in part due to alterations of insulin's effect on liver. We have examined the effects of glyburide and glipizide on insulin metabolism in isolated hepatocytes and perfused livers. Our studies show that both drugs increase insulin binding to hepatocyte, but only glyburide-treated animals exhibit a concomitant increase in degradation. Studies with recycling perfused liver agreed with these results, with glyburide treatment causing a significantly more rapid clearance than control or glipizide treatment. Single-pass perfusion studies showed significantly less insulin retained by glipizide-treated animals as compared to control- and glyburide-treated animals. Further, hepatocytes from glipizide-treated animals required higher concentrations of insulin to achieve the same stimulation of amino acid transport (as Artane Medication Class measured by aminoisobutyric acid uptake) as in control- and glyburide-treated animals, suggesting that the altered processing affects insulin's action. Taken together, these studies demonstrate alterations in liver insulin metabolism that may explain clinical differences identified in these two drugs.

glucotrol renal dosing 2015-09-04

Peripheral blood glucose, plasma insulin and C-peptide levels were investigated after giving a standardized breakfast (500 kcal, 60 g carbohydrates) to 10 nonobese Type 2 diabetic patients previously treated by diet alone. Each patient received at random, at 1 week intervals, either 5 mg glipizide (meal + glipizide) or a placebo (meal alone) 30 min before breakfast. Basal values of blood glucose, plasma insulin and C-peptide were similar on both occasions. After meal + glipizide, the Valtrex Prophylactic Dose blood glucose increase was sharply limited whereas the rise in plasma insulin was steeper and reached twice as high a level. In contrast, the rise in plasma C-peptide was similar in both conditions. Consequently, the areas under the curves (0-300 min) showed a marked reduction in blood glucose after meal + glipizide (2289 +/- 149 versus 3101 +/- 169 mmol X min/1; 2p less than 0.001), associated with a significant increase in plasma insulin (14219 +/- 3261 versus 7591 +/- 1173 microU X min/ml; 2p less than 0.025) but no significant change in plasma C-peptide (342 +/- 45 versus 326 +/- 34 pmol X min/ml; N.S.). The insulin/C-peptide molar ratio was thus significantly increased after meal + glipizide (0.41 +/- 0.06 versus 0.23 +/- 0.04 at the 60th min; 2p less than 0.02). The dissociation between the responses of insulin and C-peptide suggests that a single dose of 5 mg glipizide in Type 2 diabetic subjects may enhance availability of peripheral insulin by extrapancreatic mechanism(s). This phenomenon may result in a higher circulating level of the hormone and therefore represent a further mode of action of sulphonylureas.(ABSTRACT TRUNCATED AT 250 WORDS)

buy glucotrol online 2016-12-05

In the 141 (99.3% male, 53.9% CrCl less than 50 mL per minute, mean age = 74.0 years) patients meeting inclusion criteria between 2008-2010, the average change in A1c (+ 0.34) Calan Pill was nonequivalent after conversion from glyburide to glipizide (7.08% vs. 7.42%, respectively). Hypoglycemia occurred more frequently during treatment with glyburide than glipizide (31.2% vs. 12.8%, respectively, P less than 0.001). Mean dose conversion ratios were consistent with VHA recommendations (1 mg per day glyburide = 1.26- 1.55 mg per day glipizide).

glucotrol tab 2016-03-08

Pioglitazone, a peroxisome proliferator-activated receptor agonist and glipizide, an insulin secretagogue, 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.

glucotrol drug 2015-06-23

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.

glucotrol xl reviews 2016-12-07

To evaluate the long-term durability of the efficacy of alogliptin compared with glipizide in combination with metformin in people with type 2 diabetes inadequately controlled on stable-dose metformin.

glucotrol brand name 2016-12-28

An outpatient clinic at the Helsinki University Hospital, Finland.

glucotrol alcohol 2015-06-17

To determine whether glipizide, a sulfonylurea, can prevent diabetes in the diabetic-prone BB rat model, rats were studied from 35 to 240 days of age. Treated animals received oral glipizide (10 or 100 mg/kg/day) from 35 to 200 days of age, and control rats received oral placebo. From 80 to 135 days of age at both drug doses, glipizide decreased the incidence of diabetes, thus delaying disease onset (P < 0.02). At the higher dose of glipizide, a diabetes preventive effect was observed (P < 0.025). There were no significant differences in body weights between the treated and control groups. At 240 days, i.e. 40 days after stopping glipizide and placebo treatments, diabetes incidence remained stable in the two groups; thus the effect of glipizide persisted after discontinuation of the drug. Serum glucose and insulin levels measured at 90 and 200 days did not reveal differences between the glipizide treated and control groups. To determine whether the sulfonylurea affected autoimmune events, the prevalence and severity of islet inflammation were examined. In glipizide-treated BB rats at 240 days, only 44% of rats had islet inflammation compared to 86% in the control group (P < 0.01). At both 90 and 240 days the severity of islet inflammation was decreased in the glipizide treatment groups compared with the control groups (P < 0.01). These data indicate that glipizide (a) prevents diabetes in the diabetic-prone BB rat strain, (b) decreases the prevalence and severity of islet inflammation even after drug withdrawal and (c) may dampen autoimmune events leading to diabetes onset.