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Micronase

Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Other names for this medication:

Similar Products:
Glucophage, Actos, Glucotrol, Avandia

 

Also known as:  Glyburide.

Description

Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Generic Micronase is a sulfonylurea antidiabetic medicine. It works by causing the pancreas to release insulin, which helps to lower blood sugar.

Brand name of Generic Micronase is Micronase.

Dosage

Take Generic Micronase by mouth with food.

If you are taking 1 dose daily, take Generic Micronase with breakfast or the first main meal of the day unless your doctor tells you otherwise.

High amounts of dietary fiber may decrease Generic Micronase 's effectiveness, resulting in high blood sugar.

Generic Micronase works best if it is taken at the same time each day.

Continue to take Generic Micronase even if you feel well.

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

Overdose

If you overdose Generic Micronase and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children.

Side effects

The most common side effects associated with Micronase 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 Generic Micronase if you are allergic to Generic Micronase components.

Do not take Generic Micronase if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Micronase can ham your baby.

Do not take Generic Micronase if you have certain severe problems associated with diabetes (eg, diabetic ketoacidosis, diabetic coma).

Do not take Generic Micronase if you have moderate to severe burns or very high blood acid levels (acidosis) you are taking bosentan.

Do not take Generic Micronase if you are taking bosentan.

Be careful with Generic Micronase if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Generic Micronase if you have allergies to medicines, foods, or other substances.

Be careful with Generic Micronase if you have had a severe allergic reaction (eg, a severe rash, hives, itching, breathing difficulties, dizziness) to any other sulfonamide medicine, such as acetazolamide, celecoxib, certain diuretics (eg, hydrochlorothiazide), glipizide, probenecid, sulfamethoxazole, valdecoxib, or zonisamide.

Be careful with Generic Micronase if you have a history of liver, kidney, thyroid, or heart problems.

Be careful with Generic Micronase if you have stomach or bowel problems (eg, stomach or bowel blockage, stomach paralysis), drink alcohol, or have had poor nutrition.

Be careful with Generic Micronase if you have type 1 diabetes, very poor health, a high fever, a severe infection, severe diarrhea, or high blood acid levels, or have had a severe injury.

Be careful with Generic Micronase if you have a history of certain hormonal problems (eg, adrenal or pituitary problems, syndrome of inappropriate secretion of antidiuretic hormone [SIADH]), low blood sodium levels, anemia, or glucose-6-phosphate dehydrogenase (G6PD) deficiency.

Be careful with Generic Micronase if you will be having surgery.

Be careful with Generic Micronase if you are taking bosentan because liver problems may occur; the effectiveness of both medicines may be decreased; beta-blockers (eg, propranolol) because the risk of low blood sugar may be increased; they may also hide certain signs of low blood sugar and make it more difficult to notice; angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril), anticoagulants (eg, warfarin), azole antifungals (eg, miconazole, ketoconazole), chloramphenicol, clarithromycin, clofibrate, fenfluramine, insulin, monoamine oxidase inhibitors (MAOIs) (eg, phenelzine), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), phenylbutazone, probenecid, quinolone antibiotics (eg, ciprofloxacin), salicylates (eg, aspirin), or sulfonamides (eg, sulfamethoxazole) because the risk of low blood sugar may be increased; calcium channel blockers (eg, diltiazem), corticosteroids (eg, prednisone), decongestants (eg, pseudoephedrine), diazoxide, diuretics (eg, furosemide, hydrochlorothiazide), estrogens, hormonal contraceptives (eg, birth control pills), isoniazid, niacin, phenothiazines (eg, promethazine), phenytoin, rifamycins (eg, rifampin), sympathomimetics (eg, albuterol, epinephrine, terbutaline), or thyroid supplements (eg, levothyroxine) because they may decrease Generic Micronase 's effectiveness, resulting in high blood sugar; gemfibrozil because blood sugar may be increased or decreased; cyclosporine because the risk of its side effects may be increased by Generic Micronase.

Avoid alcohol.

Do not stop taking Generic Micronase suddenly.

micronase dosing

Repaglinide and glibenclamide show higher potency and efficacy in inhibiting the pancreatic than the cardiovascular K(ATP) channels, thus supporting their clinical use.

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15 patients (25-73 years old) presented with severe hypoglycaemia. All of them presented with neuroglycopenic symptoms (5-confusion, 6-drowsiness to loss of consciousness, 4-seizures and 1-coma) 12-36 h after ingestion of 'Power 1 Walnut'. Liquid chromatography-mass spectrometry (LC/MS) confirmed the presence of glibenclamide in the urine. None experienced a full-blown hypoglycaemia-associated autonomic response defined as sweating, sensation of warmth, anxiety, tremor, nausea, palpitations, tachycardia, and hunger. Only 4/16 patients had symptoms of a partial autonomic response, and 3/16 patients had tachycardia and/or hypertension.

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Modafinil is a well-known psychoactive drug used to treat narcolepsy, hypoglycemia, cerebral ischemia and Parkinson's disease. Previous studies showed that ATP-sensitive potassium channels (K(ATP)) play a key role in response to cerebral ischemia, hypoglycemia or metabolic inhibition. Modafinil (0.01-1 mM) dose-dependently decreased the GABA-activated currents (I(GABA)). Pretreatment with the K(ATP) channel blocker, glibenclamide (10 microM), significantly reduced the decrease of I(GABA) caused by modafinil. Thus, the inhibitory effect of modafinil on the I(GABA) is indirect by modulating K(ATP) channel activation, at least in part mediated by K(ATP) channel.

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A 43-year-old lady with long standing non-insulin dependent diabetes mellitus on glibenclamide presented with cholestatic liver disease. Initially she was thought to have developed primary biliary cirrhosis (PBC). When she made a spontaneous recovery following the withdrawal of glibenclamide, it became obvious that the patient had been suffering from drug-induced chronic cholestasis (DICC). The subtle differences between PBC and DICC are highlighted.

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The electromechanical effects of calcitonin gene-related peptide (CGRP) on intact and endothelium-denuded rabbit ophthalmic arteries were studied. CGRP inhibited norepinephrine (NE)-induced contractions. In intact arteries after washout of CGRP the contractile sensitivity to NE was increased. Conversely, in endothelium-denuded arteries, the relaxation induced by CGRP was prolonged, and after washout of CGRP the contractile sensitivity to NE was diminished. In intact arteries NE contractions were enhanced by NG-monomethyl-L-arginine (L-NMMA), an inhibitor of endothelium-derived relaxing factor (EDRF) synthesis, and in the presence of L-NMMA, CGRP-induced relaxations resembled those seen in endothelium-denuded arteries. This result suggests that there is an increased EDRF synthesis in intact arteries during NE stimulation and that CGRP may inhibit either the synthesis or the activity of EDRF. High concentrations of CGRP hyperpolarized the smooth muscle membrane both in intact and endothelium-denuded arteries. Hyperpolarizations were blocked by glibenclamide, indicating that they are mediated by activation of ATP-sensitive K+ channels. However, glibenclamide had little effect on the CGRP-induced relaxation. These results suggest that in normal physiological conditions CGRP-induced relaxation of the rabbit ophthalmic artery is mediated mainly by mechanisms other than hyperpolarization.

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Repaglinide is a newly developed oral blood glucose-lowering agent that exerts its effect by stimulating insulin secretion. This multicenter study was designed to compare the efficacy and safety of this drug with glyburide in a 1-year randomized double-blind study of outpatients with type 2 diabetes.

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Glimepiride (Hoe 490) is a new sulfonylurea. After oral administration of Hoe 490 to rabbits, blood glucose was lowered 3.5 times more than after glibenclamide (HB 419) and after intravenous administration, 2.5 times more. This superiority in efficacy was demonstrated by onset, maximum and duration of action. In rats, intravenous and oral Hoe 490 has a much shorter effect on blood glucose than HB 419, but the initial effect of Hoe 490 orally was up to 6 times and i.v. up to 2 times stronger than that of HB 419. In dogs, oral and intravenous Hoe 490 had a considerably longer blood glucose-lowering effect than HB 419. However, the effect of intravenous Hoe 490 was only half as intense as that of HB 419 in the first hours after treatment and the effect of oral Hoe 490 was initially stronger and thereafter temporarily distinctly weaker than that of HB 419. The more rapid decrease in blood glucose in the dog after oral administration of Hoe 490 was accompanied by a correspondingly earlier and higher plasma insulin increase. In accordance with the less intense initial blood glucose decrease in the dog after intravenous Hoe 490 there was a weaker and slower rise and faster drop of plasma insulin. The long action of oral and intravenous Hoe 490 in the dog can, however, not be sufficiently explained by the plasma insulin values. In the isolated rat pancreas perfused with glucose-free medium, HB 419 released glucagon beside insulin and somatostatin. The threshold concentration for the glucagon secretion was lower as those for the insulin and somatostatin release.(ABSTRACT TRUNCATED AT 250 WORDS)

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Microglial cell plays a crucial role in the development and establishment of chronic neuropathic pain after spinal cord injuries. As neuropathic pain is refractory to many treatments and some drugs only present partial efficacy, it is essential to study new targets and mechanisms to ameliorate pain signs. For this reason we have used glibenclamide (GB), a blocker of KATP channels that are over expressed in microglia under activation conditions. GB has already been used to trigger the early scavenger activity of microglia, so we administer it to promote a better removal of dead cells and myelin debris and support the microglia neuroprotective phenotype. Our results indicate that a single dose of GB (1 μg) injected after spinal cord injury is sufficient to promote long-lasting functional improvements in locomotion and coordination. Nevertheless, the Randall-Selitto test measurements indicate that these improvements are accompanied by enhanced mechanical hyperalgesia. In vitro results indicate that GB may influence microglial phagocytosis and therefore this action may be at the basis of the results obtained in vivo.

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The effect of glibenclamide and glimepiride, two orally active antidiabetic sulphonylurea derivatives, on the development of myocardial infarction has been compared. Permanent coronary artery ligation was induced in rats and the development of infarction was evaluated by a computer-assisted method after nitroblue-terazolium staining. Seven-day coronary ligation produced enlargement of the left ventricular cavity, scar thinning and thickening of the non-infarcted myocardium. Glibenclamide treatment (5 mg/kg b.i.d. intraperitoneally) decreased the infarct volume (29.1 +/- 3.5% vs. 39.1 +/- 3.2% in controls), that occurred primarily as a result of more significant thinning of the scar tissue (1.6 +/- 0.04 mm vs. 2.0 +/- 0.13 mm in controls). Glibenclamide also inhibited the thickening of the non-infarcted ventricular septum (2.1 +/- 0.10 mm vs. 2.9 +/- 0.10 mm in controls). In contrast to the effects of glibenclamide, glimepiride treatment (5 mg/kg b.i.d. intraperitoneally) inhibited the enlargement of the left ventricular cavity (15.2 +/- 1.1% vs. 19.9 +/- 1.2% of the left ventricular volume in controls), it did not precipitate scar thinning and did not influence the development of hypertrophy of the non-infarcted myocardium. These results suggest that glimepiride treatment might inhibit the development of left ventricular dilatation after myocardial infarction. Glibenclamide treatment, however, producing a thinning of the scar tissue may further precipitate morphological changes that can contribute to the development of heart failure.

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micronase generic name 2016-08-16

Ion channels expressed in monocytes/macrophages have been tightly attached to atherosclerosis by coupling cellular buy micronase function with electrical activity. However, the function of ATP-sensitive potassium channels (K(ATP)) in atherosclerosis has not been investigated directly. This study was performed to explore its role in atherosclerosis.

micronase drug class 2016-11-08

Several electronic databases were searched, among these buy micronase The Cochrane Library (issue 4, 2009), MEDLINE, EMBASE, CINAHL, SIGLE and LILACS (all up to November 2009), combined with handsearches. No language restriction was used.

micronase 10 mg 2017-12-09

In a large managed care organization, glyburide was at least as effective Cheap Nolvadex Uk as insulin in achieving glycemic control and similar birth weights in women with GDM who failed diet therapy. The increased risk of preeclampsia and phototherapy in the glyburide group warrant further study.

dosage of micronase 2016-08-27

The results indicated that celery seed extract can be effective in controlling hyperglycemia and hyperlipidemia in diabetic rats, and demonstrated its protective effects Sinequan Overdose against pancreatic toxicity resulting from STZ-induction.

micronase dosage 2016-06-21

Sulphonylurea receptors (SURs) serve as regulatory subunits of ATP-sensitive K(+) channels. SURs are members of the ATP-binding cassette (ABC) protein superfamily and contain two conserved nucleotide-binding domains (NBDs) which bind and hydrolyse MgATP; in addition, they carry the binding sites for the sulphonylureas like glibenclamide (GBC) which close the channel and for the K(ATP) channel openers such as P1075. Here we have exchanged the conserved Lys in the Walker A motif by Arg in both NBDs of SUR2B, the regulatory subunit of the vascular K(ATP) channel. Then the effect of the mutation on the ATPase-dependent binding of GBC and P1075 to SUR2B and on the activity of the recombinant vascular (Kir6.1/SUR2B) channel was assessed. Surprisingly, in the absence of MgATP, the mutation weakened binding of P1075 and the extent of allosteric inhibition of GBC binding by P1075. The mutation abolished most, but not all, of the MgATP effects on the binding of GBC and P1075 and prevented nucleotide-induced activation of the channel which relies on SUR reaching the posthydrolytic (MgADP-bound) state; the mutant channel was, however, opened by P1075 at higher concentrations. The data provide evidence that mutant SUR2B binds MgATP but that the posthydrolytic state is insufficiently populated. This suggests that the mutation locks SUR2B in an MgATP-binding prehydrolytic-like state; binding of P1075 may induce a posthydrolytic-like conformation Allegra Kids Dosage to open the channel.

micronase 50 mg 2015-12-31

In cardiac myocytes, lidocaine reduces but mexiletine increases adenosine triphosphate (ATP)-sensitive K+ currents, suggesting that these class Ib antiarrhythmic drugs may differentially modify the activity of ATP-sensitive K+ channels. The effects of lidocaine and mexiletine on arterial relaxations induced by K+ channel openers Ventolin Daily Dosage have not been studied. Therefore, the current study was designed to evaluate whether lidocaine and mexiletine may produce changes in relaxations to the ATP-sensitive K+ channel openers cromakalim and pinacidil in isolated rat thoracic aortas.

micronase tablets 2017-02-21

Even though the administration of sulfonylurea+statin can achieve a greater reduction of total cholesterol and LDL-cholesterol levels and a comparable glucose control compared to PPAR treatment, their administration did not change the plasma adipokine levels significantly. In contrast, a significant greater increase of the plasma concentrations of adiponectin (P<0.0001), a trend to a greater decrease of the plasma resistin levels (P=0.061), a Floxin Medication significantly greater increase of HDL-cholesterol (P=0.002), and a significantly greater reduction of triglyceride levels (P=0.018) were seen in the PPAR group.

micronase drug information 2017-03-29

The aim of the study was to find out which model of insulin therapy in patients with noninsulin-dependent diabetes mellitus with secondary inefficacy of sulphonylurea is most effective for glycemia normalization, inhibition of late complications, prevention of atherosclerosis and better quality of life. In 27 patients aged 40-70 years with a history of diabetes over 3 years, BMI < 30, treated with maximal doses of Euclamine we applied 4 therapeutic models: 1) intensive insulin therapy (M1), 2) two injections of three insulins (M2), 3) Euclamin 20 mg + intermediate insulin (M3), 4) Euclamine 20 mg + intermediate insulin (M4). The study lasted 3 months whereas education was carried out within the first two weeks. The following parameters Nexium Tablet 40mg were evaluated: beta cell reserve (glibenclamide test), peptide C level, HbA1C concentration, glycemia profile, lipids, creatinine level. Foci of infection were eradicated. It was found out that: 1) all models of insulin therapy, produced near normoglycemia, 2) the model of intensive insulin therapy does not generate hyperinsulinism in face of body weight loss and improved lipid profile, 3) the model of intensive insulin therapy shows long-term efficacy in the absence of effects when assessing fasting glycemia state (HbA1C, Schilchtkrull's index, lipid indices), 4) the model combining Euclamine with intermediate insulin is on intermediate step leading to another form of insulin therapy.

micronase 5 mg 2015-04-04

Extracts of pine needles (Pinus densiflora Sieb. et Zucc.) have diverse physiological and pharmacological actions. In this study we show that pine needle extract alters pacemaker currents in interstitial cells of Cajal (ICC) by modulating ATP-sensitive K+ channels and that this effect is mediated by prostaglandins. In whole cell patches at 30 degrees , ICC generated spontaneous pacemaker potentials in the current clamp mode (I = 0), and inward currents (pacemaker currents) in the voltage clamp mode at a holding potential of -70 mV. Pine needle extract hyperpolarized the membrane potential, and in voltage clamp mode decreased both the frequency and amplitude of the pacemaker currents, and increased the resting currents in the outward direction. It also inhibited the pacemaker currents in a dose-dependent manner. Because the effects of pine needle extract on pacemaker currents were the same as those of pinacidil (an ATP-sensitive K+ channel opener) we tested the effect of glibenclamide (an ATP-sensitive K+ channels blocker) on ICC exposed to pine needle extract. The effects of pine needle extract on pacemaker currents were blocked by glibenclamide. To see whether production of prostaglandins (PGs) is involved in the inhibitory effect of pine needle extract on pacemaker currents, we tested the effects of naproxen, a non-selective cyclooxygenase (COX-1 and COX-2) inhibitor, and AH6809, a prostaglandin EP1 and EP2 receptor antagonist. Naproxen and AH6809 blocked the inhibitory effects of pine needle extract on ICC. These results indicate that pine needle extract inhibits the pacemaker currents of ICC by activating ATP-sensitive K+ channels via the production of PGs.