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Micronase (Glyburide)

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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.


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.


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.


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


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.


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.

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Hydrogen sulfide (H2S), the colorless gas with the smell of rotten eggs, has been regarded as a novel gaseous signaling molecule. Although H2S has been proved been involved into the cardiovascular functions, the cardiovascular functions of H2S within the nucleus tractus solitarii (NTS) are not clear. Unilateral microinjection of NaHS (2 to 200 pmol), a H2S donor, into the NTS caused transient and dose-dependent hypotension and bradycardia (P<0.01). Microinjection of CBS allosteric activator S-ademetionine (SAM) into the NTS also produced significant decreases in BP (from 101 +/- 8 to 82 +/- 7 mmHg, P < 0.01) and HR (from 469 +/- 16 to 449 +/- 14 bpm, P<0.01), which was very similar to those of NaHS. Pretreatment with hydroxylamine, a CBS inhibitor, failed to affect the cardiovascular functions of intra-NTS NaHS. However, pretreatment with glibenclamide (10 nmol), a KATP channel blocker, eliminated the on BP (from -23 +/- 4 to -5 +/- 1 mmHg, P<0.01) and HR (from -24 +/- 2 to -5 +/- 1 bpm, P<0.01) by 78% and 79%, respectively, of intra-NTS NaHS (20 pmol). Likewise, pretreatment with kynurenic acid (Kyn, 5 nmol) also attenuated the effects of NaHS on BP (from -29 +/- 3 to -12 +/- 3 mmHg, P<0.01) and HR (from -19 +/- 2 to -9 +/- 2 bpm, P<0.01) by 59% and 53%, respectively, of intra-NTS NaHS (20 pmol). These data support the hypothesis that endogenous H2S produces cardiovascular inhibition functions in the NTS, mainly mediated by KATP channels regulation or/and glutamate receptors.

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NLRP3 inflammasome in colonic mucosa, macrophages, and colonic epithelial cells were analysed by western blotting. The NLRP3 inflammasome components were studied by sucrose density gradient fractionation, chemical cross-linking, and co-immunoprecipitation. The role of NLPR3 inflammasome in the pathogenesis of colitis was extensively evaluated in IL-10(-/-) mice, using a specific NLPR3 inflammasome inhibitor glyburide.

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1. The types of K+ channel which determine the membrane potential of arcuate artery smooth muscle cells were investigated by patch-clamp recording from isolated cells and lumenal diameter measurements from intact pressurized renal arcuate arteries. 2. Single cells had a mean resting potential of -38 mV and were depolarized by 130 mM K+ but not by the Cl- channel blocker 4,4'-diisothiocyanatostilbene-2, 2'-disulphonic acid (DIDS). 3. Iberiotoxin did not affect the resting potential but inhibited spontaneous transient hyperpolarizations. Iberiotoxin or 1 mM tetraethylammonium (TEA+) constricted intact arteries. 3,4-Diaminopyridine (3,4-DAP)-sensitive delayed rectifier K+ (KV) channel current was elicited by depolarization but 3,4-DAP did not affect the resting potential or induce constriction in the intact artery. 4. A voltage-independent K+ current was inhibited by >= 0.1 mM barium (Ba2+) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain. In six out of ten cells, 1 mM Ba2+ depolarized the resting potential, while in the other cells the potential was resistant to all of the K+ channel blockers and ouabain. Ba2+ (0.1-1 mM) constricted the intact artery, but 10 microM Ba2+, 1 microM glibenclamide or 100 nM apamin had no effect. 5. The data suggest that resting potential is determined by background K+ channels, one type being Ba2+ sensitive and voltage independent, and another type being poorly defined due to its resistance to any inhibitor. Large conductance Ca2+-activated K+ (BKCa) and KV channels do not determine the resting potential but have separate functions to underlie transient Ca2+-induced hyperpolarizations and to protect against depolarization past about -30 mV.

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These findings suggest that microvascular native and stimulated collaterals respond to activation of ATP-sensitive K+ channels and acetylcholine similar to non-collaterals of similar size. Thus, changes in reactivity of collaterals to activation of ATP-sensitive K+ channels are not related to changes in the ability of the vessels to respond to vasodilators but may primarily be determined by a change in the distribution of collateral vessel size.

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Most evidence for a key role of calcium entry in hypoxia-induced renal damage stems from studies with calcium channel blockers. In proximal tubules, a primary site of renal ischaemic injury, only phenyl-alkylamines, especially verapamil, have been studied. In the present study the effect of the dihydropyridine felodipine on hypoxic injury in isolated rat proximal tubules was investigated. To discriminate between the block of calcium entry and other effects, the enantiomers and a non-calcium blocking derivative of felodipine (H186/86) were included. Cell membrane injury was assessed by measuring the release of lactate dehydrogenase (LDH). At high concentrations (100 microM) felodipine, H186/86 and the two enantiomers all protected rat proximal tubules against hypoxia-induced injury to the same extent. Absence of extracellular calcium did not offer protection, but rather enhanced hypoxic injury. All dihydropyridines used increased the intracellular potassium concentration during normoxia. Felodipine attenuated the hypoxia-induced loss of cellular potassium. We have tried to mimic the effects of felodipine by using potassium channel blockers. The potassium channel blockers quinidine and glibenclamide afforded some protection against hypoxic injury, although their effects on cellular potassium were equivocal. We conclude that the dihydropyridine calcium channel blocker felodipine protects rat proximal tubules against hypoxic injury via a calcium-independent mechanism. We propose that high levels of intracellular potassium and attenuation of potassium loss during hypoxia are important in this protection.

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Intermediate developmental delay, epilepsy and neonatal diabetes mellitus (DEND) syndrome as a result of a 59V>M Kir6.2 mutation.

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To evaluate the role of potassium channels in the regulation of coronary hemodynamics in experimental hypercholesterolemia.

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In order to investigate the different factors related to the development of steroid diabetes (SDM) in patients with rheumatic diseases, we studied 27 patients with SDM, and 27 age- and sex-matched controls who also received therapy with glucocorticoids. In every case, family history of DM, body mass index, associated treatment, steroid dose and treatment duration were studied; fasting serum insulin, "C" peptide, growth hormone and glucagon levels were measured.

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Oxygen free radicals have been suggested to be a contributory factor in diabetes complications. The aim of this study was to examine the effects of glyburide on the antioxidant enzyme activities in the heart tissue of diabetic rats. We investigated the activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) in the hearts of both control and streptozotocin-induced diabetic rats. In the heart of diabetic rats, the activity of total superoxide dismutase decreased significantly (p < 0.005), whereas the activity of catalase and glutathione peroxidase increased to a large extent (p < 0.0001 and p = 0.05, respectively) at the end of the fourth week compared with the control group. Glyburide treatment of diabetic rats for 4 weeks corrected the changes observed in diabetic heart. In addition, blood glucose levels of untreated diabetic rats decreased following the glyburide treatment. These results demonstrate that the sulfonylurea glyburide is capable of exerting direct insulin-like effect on heart superoxide dismutase, catalase and glutathione peroxidase activities of diabetic rats in vivo.

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2-(4'-Hydroxybenzeneazo)benzoic acid is a spectrophotometric probe which shows absorption spectrum changes upon binding to protein. Difference absorption spectra of this probe were used as an indirect measurement of the binding of selected sulfonylurea and phenothiazine drugs to bovine serum albumin. The results obtained using the spectrophotometric probe were similar to data obtained from other methods, especially fluorescent methods. Of the four sulfonylureas studied, tolbutamide showed the highest binding affinity, followed by glyburide, glipizide, and acetohexamide, in that order. The data collected for phenothiazine drugs indicated that chlorpromazine has the highest affinity, followed in order by trifluoperazine, perphenazine, fluphenazine, and promazine. Correlation of these results with chemical composition indicated that the interaction of phenothiazine drugs with bovine serum albumin was of a hydrophobic nature.

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Atrial dilation and rapid pacing reduce atrial effective refractory periods (AERPs), thereby increasing the susceptibility to sustained atrial fibrillation (AF) in Langendorff-perfused rabbit hearts. It is unclear whether similar pathophysiologic mechanisms are operative in short-term electrophysiologic changes caused by dilation and rapid pacing. Therefore, we analyzed whether both forms of short-term electrophysiologic changes are similarly affected by pharmacologic interventions acting on different potential mechanisms underlying these changes.

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Neonatal diabetes mellitus (NDM) is a rare but important condition affecting approximately 1 in 100,000 newborns. Permanent form requires life-long treatment with difficulties in long-term compliance and metabolic complications. Exact genetic diagnosis can enable improved outcome and patient satisfaction by switching insulin injection to oral sulfonylureas. Successful cases have been reported with most experience on the KCNJ11-mutated permanent form. Here we report a successful experience in an ABCC8-mutated infant with permanent NDM.

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Using a series of functional criteria, we wished to evaluate the K+ conductance mechanism and the cyclic GMP mechanism implicated in the actions of nicorandil (NIC) as a vasodilator. In rabbit isolated superior mesenteric artery, NIC exhibited two relaxation dose-response curves (DRCs): one with a lower IC50 of 4.8 x 10(-6) M for norepinephrine (NE 5 microM) contraction, and another with a higher IC50 of 1.4 x 10(-4) M for 80 mM K+ contraction. K+ channel blockers (TEA 1-10 mM), Ba2+ (0.1-0.5 mM), glyburide (1 microM), and increased [K+]ex (20 mM), all caused significant attenuations in the ability of NIC to relax NE contraction, but did not influence the ability of NIC to relax high-K+ contraction. Pretreatment with 5 microM methylene blue, a guanylate cyclase inhibitor, produced a pronounced inhibition of nitroglycerine (NTG) relaxation, but only a marginal inhibitory effect on the NIC relaxation DRC for NE contraction. Functional studies demonstrated that the inhibitory effect of NIC on NE-sensitive intracellular Ca2+ release occurred in the same concentration range as that required for relaxation of 80 mM K+ contractions (10(-5)-10(-3) M). Furthermore, NIC also caused increases in cellular cyclic GMP levels at this higher concentration range. Finally, NIC relaxation of NE contraction was not prone either to self-tolerance (30 mM NIC preexposure) or cross-tolerance (0.55 mM NTG preexposure) development. In contrast, a modest but significant degree of self-tolerance to NIC could be demonstrated under high-K+ contraction condition. These studies thus show the existence of both cellular mechanisms for NIC in the same vascular preparation and further show that these two mechanistic components are separate and independent. The K+ channel-dependent component occurs at lower concentrations, is blocked by K+ channel blockers, is not inhibited by methylene blue, is not associated with increases in cyclic GMP, and is not prone to tolerance development. In this, NIC resembles other K+ channel openers. The cyclic GMP-dependent component is evident at relatively higher concentrations, is associated with inhibition of [Ca2+]i release, is associated with increases in cyclic GMP levels, and is prone to tolerance development. In this, NIC resembles other nitrovasodilators. A combination of these characteristics of the actions of NIC may contribute to the differences in the acute versus chronic hemodynamic profile of NIC.

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Intrapulmonary veins (PVs) contribute to pulmonary vascular resistance, but the mechanisms controlling PV tone are poorly understood. Although smooth muscle cell (SMC) K(+) channels regulate tone in most vascular beds, their role in PV tone is unknown. We show that voltage-gated (K(V)) and inward rectifier (K(ir)) K(+) channels control resting PV tone in the rat. PVs have a coaxial structure, with layers of cardiomyocytes (CMs) arrayed externally around a subendothelial layer of typical SMCs, thus forming spinchterlike structures. PVCMs have both an inward current, inhibited by low-dose Ba(2+), and an outward current, inhibited by 4-aminopyridine. In contrast, PVSMCs lack inward currents, and their outward current is inhibited by tetraethylammonium (5 mM) and 4-aminopyridine. Several K(V), K(ir), and large-conductance Ca(2+)-sensitive K(+) channels are present in PVs. Immunohistochemistry showed that K(ir) channels are present in PVCMs and PV endothelial cells but not in PVSMCs. We conclude that K(+) channels are present and functionally important in rat PVs. PVCMs form sphincters rich in K(ir) channels, which may modulate venous return both physiologically and in disease states including pulmonary edema.

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In rats with cirrhosis, the glibenclamide-induced vasoconstriction indicates that a vasodilator tone due to KATP channel opening existed under baseline conditions. Moreover, this study suggests that the control of vascular tone by KATP channels is altered in cirrhosis.

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Sulphonylureas have remained the mainstay of oral therapy for type 2 (non-insulin-dependent) diabetes mellitus (NIDDM). They stimulate insulin release from pancreatic beta cells. Pharmacokinetic differences between the various sulphonylureas are of clinical importance in terms of the time to onset of action, timing of drug administration in relation to food intake, magnitude and duration of the glucose-lowering effect and the risk of serious hypoglycaemia. Recent studies with improved analytical sensitivity have shown that the elimination half-life of glibenclamide is longer than previously thought and that 2 metabolites of glibenclamide have significant hypoglycaemic activity. Furthermore, single dose studies in healthy volunteers using an integrated pharmacokinetic-pharmacodynamic model have identified clear concentration-effect relationships for both glibenclamide and its metabolites after oral and intravenous administration. Under multiple dose conditions, kinetic-dynamic relations have been identified with shorter-acting drugs in dosages that give discontinuous sulphonylurea exposure. However, at continuous exposure, i.e. sustained 24-hour therapeutic concentrations in plasma, there is evidence indicating the development of tolerance, which may be caused by downregulation of beta cell sensitivity. As more sophisticated concentration-effect studies appear, it has become evident that currently recommended maximum daily doses of many sulphonylureas are too high.

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Administrative databases that only capture records for benefit-approved prescriptions may underestimate exposure because they do not capture non-benefit prescriptions. Using a natural experiment, we illustrate the impact of automating a prior-authorization policy on the completeness of drug exposure.

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Our study demonstrates that there are no differences in glycemic control or pregnancy outcomes when OHAs were compared with insulin.

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Cerebral arterioles were dilated during topical ACh infusion. After smoking, 10 M ACh constricted cerebral arterioles (-7.7±1.8%). After smoking, in the nicorandil-pretreatment group, 10 M ACh dilated cerebral pial arterioles by 10.5±3.0%. When given before nicorandil infusion, glibenclamide, but not L-NAME, abolished the preventive effects of nicorandil against smoking-induced endothelial dysfunction in pial vessels.

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The main purpose of this paper is to describe the relationship between serum concentrations of glibenclamide and its main metabolites and the effects on blood glucose levels, the clinically most relevant parameter to assess in diabetes.

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The vasorelaxant actions of adenosine 5'-triphosphate (ATP)-dependent K+ channel openers and sodium nitroprusside in isolated thoracic aorta and pulmonary artery of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats (14-18 weeks old) were investigated. Cumulative addition of sodium nitroprusside and different ATP-dependent K+ channel openers (pinacidil, cromakalim, nicorandil, 2-(2"(1",3"-dioxolone)-2-methyl-4-(2'-oxo-1'-pyrrolidinyl)-6-nitro -2H-1-benzopyren (KR-30450) and aprikalim) to these preparations caused a concentration-dependent relaxation of noradrenaline-pre-contracted aorta and pulmonary artery from both strains. The relative order of relaxation potency, estimated by comparing the IC50, was sodium nitroprusside > KR-30450 > aprikalim > or = cromakalim > pinacidil > nicorandil in pulmonary artery and aorta from both strains. At high concentrations (> or =1 microM), cromakalim, aprikalim and KR-30450 produced a greater percentage relaxation in SHR aorta than in WKY aorta. However, there was no apparent difference between SHR and WKY in the relaxation response to all drugs tested on the pulmonary artery. The effects of cromakalim, aprikalim, pinacidil and KR-30450 observed in aorta and pulmonary artery were significantly attenuated by 3 microM glibenclamide. 6-Anilino-5,8-quinolinequinone (LY 83583, 1 microM), a soluble guanylate cyclase inhibitor, abolished the vasorelaxant effects of nicorandil and sodium nitroprusside. In conclusion, sodium nitroprusside and ATP-dependent K+ channel openers cause relaxation of noradrenaline-pre-contracted aorta and pulmonary artery from both strains. However, all the drugs tested failed to cause selective relaxation of the pulmonary artery relative to the thoracic aorta.

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Gestational diabetics who fail dietary therapy after 30 weeks gestation or have fasting blood sugars <110 mg/dl and 1-hour postprandials <140 mg/dl do well on glyburide therapy.

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Interstitial lung disease (ILD) may be caused by a wide panel of recognized drugs. Despite the increasing number of reports in the literature, high-lightings of ILD related to oral hypoglycemic drugs are very infrequent.  Herein, we describe the case of a 78-yr-old Caucasian diabetic woman who developed mild dyspnoea at rest, asthenia and fever while on treatment with oral metformin (2000 mg/day) and glibenclamide (12.5 mg/day). On hospital admission, pulmonary function testing (PFT), chest x-ray and thorax high resolution computed tomography (HRCT) were consistent with a diagnosis of ILD. The patient's clinical conditions significantly improved soon after the initiation of insulin therapy instead of oral anti-diabetics due to poor glycemic control. After excluding other known etiologies, the significant improvement in PFT along with the complete resolution of the radiologic findings in the absence of any additional therapeutic effort at 3 months suggested the causal link between previous oral hypoglycemic therapy and lung toxicity. Clinicians should always consider the role of drugs as causative agent in the diagnostic work-up of patients with suspected ILD. To our knowledge, this is the second report in the literature of a case of ILD related to the treatment with high doses of anti-diabetic drugs in a poorly controlled diabetic woman.

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1. The effect of BTS 67 582, a novel antidiabetic agent, has been evaluated on plasma glucose and plasma insulin in normal and streptozotocin-induced diabetic rats. 2. BTS 67 582 (3 to 300 mg kg-1, p.o.) caused a dose- and time-dependent reduction in plasma glucose and an increase in plasma insulin in both fasted and glucose-loaded normal rats. The ED50 for the glucose lowering effect of BTS 67 582 in fasted rats was 37.6, 18.4 and 18.5 mg kg-1 at 1, 2 and 4 h after administration respectively. 3. In streptozotocin-induced (50 mg kg-1, i.v.) diabetic rats, BTS 67 582 (37-147 mg kg-1, p.o.) caused significant reductions of plasma glucose following a glucose load, whereas glibenclamide (100 mg kg-1, p.o.) was ineffective. BTS 67 582 significantly increased plasma insulin compared to controls whereas glibenclamide did not. 4. BTS 67 582 did not displace [3H]-glibenclamide from its binding sites in rat brain, guinea-pig ventricle or the HIT-T15 insulinoma beta-cell line. BTS 67 582 does not therefore appear to modulate its action via an effect on the 'sulphonylurea' receptor. 5. In fasted rats, the glucose lowering effect of BTS 67 582 (100 mg kg-1 p.o.) and glibenclamide (1 mg kg-1, p.o.) were antagonized by diazoxide (30 mg kg-1, i.p.). In addition BTS 67 582, like glibenclamide, caused a dose-dependent rightward shift of cromakalim-induced relaxation of noradrenaline precontracted rat aortic strips, suggesting the involvement of KATP channels. 6. In summary, BTS 67 582 produces a blood glucose-lowering effect in normal and streptozotocin-induced diabetic rats associated with increased insulin concentrations. This effect appears to be due to a blockade of ATP-sensitive potassium channel activity via a different binding site to that of glibenclamide.

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Despite oral hypoglycaemic medications being the most commonly used pharmacological treatments for type 2 diabetes, research is limited on their comparative safety, particularly their effects on overall mortality. We compared mortality risk with monotherapy initiation of four oral hypoglycaemic medications in a nationwide cohort of US veterans with type 2 diabetes.

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1. The role of ATP sensitive potassium channels in the analgesic activity of prolactin (PRL) was studied in mice using glibenclamide and minoxidil, a blocker and an opener of these channel, respectively. 2. Pre-treatment with glibenclamide attenuated the analgesic activity of PRL while treatment with minoxidil potentiated the activity. 3. It is concluded that PRL, similar to morphine, utilizes ATP sensitive potassium channels in eliciting the analgesic response.

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In 28 type II diabetics with secondary failure of sulfonylurea treatment, the efficacy and safety of combined therapy with insulin and glibenclamide were investigated. Patients were randomized in two groups and treated for 16 weeks either with insulin Novo Protaphan HM Penfill (100 IU/ml "bed time") and 10 mg of glibenclamide in the morning (group A), or with insulin Novo Actraphan HM Penfill 100 IU/ml in the morning combined with two 5 mg doses of glibenclamide at lunchtime and in the evening (group B). Subsequently a dropout trial of sulfonylurea was performed in half of the patients. Mean blood glucose levels were lowered in the whole group of patients from 13.5 +/- 1.8 mmol/l to 8.8 +/- 2.3 mmol/l after 8 weeks and 8.7 +/- 1.8 mmol/l after 16 weeks, and the HbAlc from 10.1 +/- 1.2% to 8.4 +/- 1.0% and 7.8 +/- 1.0% respectively. After a glibenclamide dropout period of one or two weeks in 14 of the patients, the mean blood glucose level rose significantly by 2.8 +/- 2.6 mmol/l. Only 2 patients did not show this increase. The mean insulin consumption was 13 +/- 3 IU after 8 weeks and 14 +/- 5 IU after 16 weeks respectively, and the incidence of hypoglycemia one in 12 weeks of treatment. The combination of glibenclamide and insulin (administered with the Novo Pen injector) is a safe and effective form of therapy in secondary failure of sulfonylurea, and is well accepted due to the mild start into insulin therapy.

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micronase drug interactions 2017-03-18

We have recently demonstrated that adult rat ventricular myocytes maintained in a high glucose (HG) culture medium exhibit abnormalities in excitation-contraction coupling similar to myocytes from diabetic rats. Metformin, an insulin-sensitizing biguanide, enhances peripheral insulin action and lowers blood pressure in hyperinsulinemic animals, but its direct impact on cardiac function is not fully understood. To examine the role of metformin on HG-induced cardiac dysfunction at the cellular level, normal adult ventricular myocytes were cultured for 1 day in a serum-free insulin-containing medium with either normal glucose (5.5 mmol/l glucose) or HG (25.5 mmol/l glucose) in the presence or absence of metformin or the sulfonylurea glyburide. Mechanical properties were evaluated using a high-speed video-edge detection system, and intracellular Ca2+ transients were recorded in fura-2-loaded myocytes. As previously reported, culturing myocytes in HG depresses peak shortening, prolongs time to 90% relengthening, and slows Ca2+ transient decay. Culturing cells with metformin (50 micromol/l) prevented the HG-induced buy micronase abnormalities in relaxation without ameliorating depressed peak-shortening amplitudes. Incubation of the cells with metformin also prevented slower intracellular Ca2+ clearing induced by HG. However, the HG-induced relaxation defects were not improved by glyburide (50-300 micromol/l). Interestingly, metformin also improved HG-induced relaxation abnormalities in the absence of insulin, whereas it failed to protect against HG in the presence of the tyrosine kinase inhibitor genistein (50 micromol/l). These data demonstrate that, unlike glyburide, metformin provides cardioprotection against HG-induced abnormalities in myocyte relaxation, perhaps through tyrosine kinase-dependent changes in intracellular Ca2+ handling, independent of its insulin sensitizing action.

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Isolated Langendorff-perfused rat hearts were subjected to three different studies to determine: Study 1, whether a single intermittent cross-clamp buy micronase fibrillation episode (10 min) and reperfusion (10 min) before prolonged ischemia acts as a preconditioning trigger for protection; Study 2, whether cardioprotection induced by intermittent cross-clamp fibrillation alone (no prolonged ischemia) involves a preconditioning mechanism; Study 3, whether intermittent cross-clamp fibrillation cardioprotection can be prevented by targeting putative components of the preconditioning mechanism (protein kinase C or the mitochondrial ATP-sensitive potassium (K(ATP)) channel). Hearts were reperfused (60 min) and recovery of function (left ventricular developed pressure measured using an intraventricular balloon) and myocardial injury (creatine kinase leakage) were measured.

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1. Recombinant ATP-sensitive K+ channels (KATP channels) were heterologously expressed in the NIH3T3 mouse cell line, and the electrophysiological properties were studied using patch-clamp techniques. 2. The NIH3T3 cell lines transfected with the inwardly rectifying K+ channel Kir6.1 alone or with both Kir6.1 and cystic fibrosis transmembrane conductance regulator (CFTR) exhibited time-independent K+ currents with weak inward rectification. In contrast, no measurable K+ conductance was observed in mock-transfected cells or in cells transfected with CFTR alone. Regardless of co-transfection with Kir6.1, the transfection with CFTR produced a Cl- conductance that was activated by cell dialysis with cAMP (1 mM). The conductance was reversibly suppressed by glibenclamide (30 microM). 3. Whole-cell currents at +60 mV were blocked in a concentration-dependent manner by Ba2+ ions with similar IC50 values: 89.3 +/- 23.3 microM (Kir6.1 alone) and 67.3 +/- 24.9 microM (Kir6.1-CFTR). 4. The currents recorded from Kir6. 1-transfected cells were not affected by glibenclamide, whereas glibenclamide did inhibit the conductance expressed in cells co-transfected with CFTR (IC50 = 35.9 buy micronase +/- 6.6 microM). 5. In the cell-attached mode with a 150 mM K+ pipette solution, both Kir6.1- and Kir6.1-CFTR-transfected cells displayed a class of K+ channels showing weak inward rectification and a slope conductance of 50.7 +/- 1.0 and 52.4 +/- 4.9 pS, respectively. 6. In the inside-out mode, the single-channel currents recorded from both types of cells were not inhibited by intracellular ATP (1 mM). However, glibenclamide was found to block the single-channel activities in the co-transfected cells.

micronase 5 mg 2015-01-05

Albeit controversial, it has been suggested by several authors that nitric oxide (NO) serves as a permissive factor in the cerebral blood flow response to systemic hypercapnia. Potassium channels are important regulators of cerebrovascular tone and may be modulated by a basal perivascular NO level. To elucidate the functional targets of the proposed NO modulation during hypercapnia-induced vasodilation, the authors performed experiments in isolated, cannulated, and pressurized rat middle cerebral arteries (MCA). Extracellular pH was reduced from 7.4 to 7.0 in the extraluminal bath to induce NO dependent vasodilation. Acidosis increased vessel diameter by 35 +/- 10%. In separate experiments, ATP-sensitive potassium channels (KATP) were blocked by extraluminal application of glibenclamide (Glib), Ca2+-activated potassium channels (KCa) by tetraethylammonium (TEA), voltage-gated potassium channels (Kv) by 4-aminopyridine, and inward rectifier potassium channels (KIR) by BaCl2. Na+-K+-ATP-ase was inhibited by ouabain. Application of TEA slightly constricted the arteries at pH 7.4 and slightly but significantly attenuated the vasodilation to acidosis. Inhibition of the other potassium channels or Na+-K+-ATP-ase had no effect. Combined blockade of KATP and KCa channels further reduced resting diameter, and abolished acidosis induced vasodilation. The authors conclude that mainly KCa channels are active under resting conditions. KATP and KCa channels are responsible for vasodilation to acidosis. Activity of one of these potassium buy micronase channel families is sufficient for vasodilation to acidosis, and only combined inhibition completely abolishes vasodilation. During NO synthase inhibition, dilation to the KATP channel opener pinacidil or the KCa channel opener NS1619 was attenuated or abolished, respectively. The authors suggest that a basal perivascular NO level is necessary for physiologic KATP and KCa channel function in rat MCA. Future studies have to elucidate whether this NO dependent effect on KATP and KCa channel function is a principle mechanism of NO induced modulation of cerebrovascular reactivity and whether the variability of findings in the literature concerning a modulatory role of NO can be explained by different levels of vascular NO/cGMP concentrations within the cerebrovascular tree.

micronase tablets 2017-12-26

Obesity is associated with impaired functional hyperemic response. We have shown that ATP-sensitive potassium (K(ATP)) channels are important in mediating functional vasodilation. Adipocyte-derived factors (ADFs) can alter vascular tone via opening K(ATP) channels. We hypothesize that, in an animal model of obesity, ADFs will decrease basal arteriolar tone by opening K(ATP) channels, resulting in an attenuated functional vasodilation. We used wild-type (WT) mice and ob(-)/ob(-) mice (ob) to test this hypothesis. The spinotrapezius muscle was prepared for the microcirculatory observation of arcade arterioles, and we measured buy micronase the vasodilatory responses to muscle stimulation. The basal arteriolar diameter was larger in ob mice compared with WT mice. The K(ATP) channel inhibitor glibenclamide (10 microM) decreased arteriolar diameter in ob mice with no effect in WT mice. The increase in arteriolar diameter induced by muscle stimulation was attenuated in ob mice compared with WT mice. To determine the mechanisms for the opening of K(ATP) channels, fat was collected from the ob mice, subcutaneous fat from around the spinotrapezius muscle (OBSF) or visceral fat (OBVF) and was incubated in physiological saline solution (PSS). The vasodilatory responses to the fat-conditioned PSS were determined in WT mice. Treatment with OBSF- or OBVF -conditioned PSS increased the arteriolar diameters in WT mice, a dilation that was inhibited by glibenclamide. The absolute diameters induced by muscle stimulation were not altered by the fat-conditioned PSS. These results suggest that, in ob mice, local ADFs reduce the functional vasodilatory capability via opening K(ATP) channels.

micronase brand name 2017-06-06

The present study investigated whether activation of vasodilatory mechanisms masks the involvement of endothelin in hypoxic pulmonary buy micronase vasoconstriction. Rat intrapulmonary arteries were mounted in microvascular myographs. In arteries with endothelium and contracted with phenylephrine, hypoxia, evoked by exchanging 5% CO2 in air for CO2 in N2, caused a transient contraction followed by a sustained contraction. Hypoxia evoked relaxation in preparations without endothelium. An inhibitor of ATP-sensitive K+ channels (KATP), glibenclamide (10 microM), blunted hypoxic relaxation in arteries without endothelium and enhanced the sustained hypoxic vasoconstriction in arteries with endothelium. Hypoxic contraction was more pronounced in endothelin compared with phenylephrine-contracted preparations in the absence, but not in the presence of glibenclamide. Antagonism of the endothelin ETA and ETB receptors with SB217242 or the combination of BQ123 and BQ788 inhibited endothelin and hypoxic contraction, but the latter only in the presence of glibenclamide. An inhibitor of nitric oxide (NO) synthase, N-nitro-L-arginine (100 microM), evoked contractions, which were left unaltered by SB217242 in hypoxic conditions. In conclusion, hypoxic contraction is mediated in part by an unknown endothelium-derived contractile factor and incubation with glibenclamide shows endothelin enhances hypoxic contraction in part through inhibition of KATP channels. Moreover, inhibition of NO formation in pulmonary arteries does not change endothelin receptor activation in severe hypoxia.

micronase drug class 2017-08-02

The present study examined the antinociceptive effects induced by 2,3-bis(mesitylseleno)propenol, a buy micronase bis-selenide alkene derivate, given orally, in chemical models of pain in rats and mice. Selenide administered orally (p.o.) into the rats caused antinociception against the first and second phases of the formalin test, with mean ID(50) values of 28.17 and 39.68 mg/kg, respectively. The antinociceptive effect caused by selenide (50 mg/kg, p.o.) on the formalin test was reversed by pretreatment with N(G)-L-nitro-arginine methyl ester (L-NAME, a nitric oxide (NO) synthase inhibitor), methylene blue (a non-specific NO/guanylyl cyclase inhibitor) and glibenclamide (an ATP-sensitive K(+) channel inhibitor), but not by atropine (a muscarinic antagonist). Given orally selenide in mice produced an inhibition of glutamate-, histamine- and compound 48/80-induced nociception with mean ID(50) values of 27.58, 36.18 and 44.53 mg/kg, respectively. Moreover, oral treatment with selenide in mice decreased licking -- induced by serotonin (mean ID(50) value of >50 mg/kg). The data show that selenide exerts pronounced systemic antinociception in chemical (formalin, glutamate, histamine, compound 48/80 and serotonin-induced pain) models of nociception. Taken together, these results suggest that the antinociceptive effect of selenide on the formalin test involves the participation of nitric oxide/cyclic GMP/K(+) channel pathways in rats.

micronase dosage 2017-09-12

Glucose control in routine care was better when most patients were treated by buy micronase a diabetes specialist and were exposed to more intense pharmacotherapy.

dosage of micronase 2015-02-19

The objective of the study is to compare adherence of a FDC [Glucovance, a buy micronase FDC of metformin and glyburide] to a 2-pill regimen.

micronase cost 2017-03-16

In 31 anaesthetized dogs the left anterior descending artery was blood-perfused by computer-controlled servo-pump, with real-time arterial perfusion pulse pressure (PP) varied from 40 and 100 mm Hg at a buy micronase constant mean pressure and cardiac workload.

micronase dosing 2016-03-02

Gly may mediate HHPV via activating ERK1/ buy micronase 2 signal transduction pathway.

micronase 50 mg 2016-07-09

The functional buy micronase curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid sinus baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized rats with perfused isolated carotid sinus.

micronase drug information 2017-07-24

The favorable combined changes buy micronase in β-cell function and insulin sensitivity over time with rosiglitazone appear to be responsible for its superior glycemic durability over metformin and glyburide as initial monotherapy in type 2 diabetes.

micronase medication 2016-09-19

We investigated the role of oxidative/nitrosative stress in the Motrin 100 Mg tolerance to ischemia/reperfusion (I/R) injury in BIO14.6 cardiomyopathy hamster hearts at 6 weeks of age. These hearts showed no significant morphologic change and left ventricular (LV) dysfunction. However, expression and activity of iNOS, nitrotyrosine (NT) formation, and protein kinase C (PKC)-epsilon activity were increased in these hearts. When the BIO14.6 hamster hearts were isolated and subjected to 40 min of global ischemia, they showed smaller myocardial necrosis and greater recovery of LV function during reperfusion compared with the control hamster heart. All of these effects were abrogated by prolonged treatment with the antioxidant, 2-mercaptopropionylglycine (MPG). Brief preischemic treatment with MPG or the iNOS inhibitor 1400W also abrogated NT formation and activation of PKC-epsilon and inhibited the tolerance to I/R injury in the BIO14.6 hamster heart. Brief preischemic treatment with the PKC inhibitor chelerythrine or the K(ATP) channel blockers, 5-hydroxydecanoate (5-HD) and glibenclamide, had no effect on iNOS activation and NT formation but inhibited the tolerance to I/R injury in the cardiomyopathic heart. These results suggest that oxidative/nitrosative stress plays a role in the tolerance to I/R injury in the cardiomyopathic heart through activation of PKC and the downstream effectors, K(ATP) channels.

micronase 10 mg 2015-01-14

The intracellular signalling pathways and molecular mechanisms responsible for P2-purinoceptor-mediated chloride (Cl(-)) currents (I(Cl,ATP)) were studied in mouse ventricular myocytes. In standard NaCl-containing extracellular solutions, extracellular ATP (100 microm) activated two different currents, I(Cl,ATP) with a linear I-V relationship in symmetrical Cl(-) solutions, and an Lanoxin Elixir Dosage inwardly rectifying cation conductance (cationic I(ATP)). Cationic I(ATP) was selectively inhibited by Gd(3+) and Zn(2+), or by replacement of extracellular NaCl by NMDG; I(Cl,ATP) was Cl(-) selective, and inhibited by replacement of extracellular Cl(-) by Asp(-); both currents were prevented by suramin or DIDS pretreatment. In GTPgammaS-loaded cells, I(Cl,ATP) was irreversibly activated by ATP, but cationic I(ATP) was still regulated reversibly. GDPbetaS prevented activation of the I(Cl,ATP,) even though pertussis toxin pretreatment did not modulate I(Cl,ATP). These results suggest that activation of I(Cl,ATP) occurs via a G-protein coupled P2Y purinergic receptor. The I(Cl,ATP) persistently activated by GTPgammaS, was inhibited by glibenclamide but not by DIDS, thus exhibiting known pharmacological properties of cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channels. In ventricular cells of cftr(-/-) mice, extracellular ATP activated cationic I(ATP), but failed to activate any detectable I(Cl,ATP). These results provide compelling evidence that activation of CFTR Cl(-) channels in mouse heart are coupled to G-protein coupled P2Y purinergic receptors.

micronase drug form 2015-06-04

By inducing severe endothelial impairment, hypertension and diabetes are two leading causes of morbidity and Imitrex Dosing mortality. Hypertensive patients with concomitant diabetes must take both antihypertensive and hypoglycaemic medications, for which there is a lack of experimental and clinical guidelines. This study aimed to examine the interaction between these two types of medication on the endothelial cell function.

micronase drug interactions 2016-08-03

Type 2 diabetes is characterized by increased acute phase serum proteins. They are also risk Propecia Vs Generic factors for cardiovascular disease. We wanted to study how improvement of glycemic control with pioglitazone or glibenclamide affects their serum concentrations.

micronase generic name 2015-01-10

A liquid chromatographic-mass spectrometric (LC-MS) method with rapid automated sample preparation was developed and validated for determination of glybenclamide in human serum. Glybenclamide and its deuterated labelled internal standard were extracted from human serum samples by automated solid-phase extraction. The extract was injected into the LC-MS system for analysis. Glybenclamide Prilosec Dosage Forms and its internal standard were measured in multiple ion monitoring mode. The method was validated over a range of 10-1000 ng/ml with good accuracy and precision and was applicable for pharmacokinetic studies.

micronase buy cheap 2017-03-27

Astroglial cells synthesize and release endozepines, a family of neuropeptides derived from diazepam-binding inhibitor (DBI). The authors have recently shown that beta-amyloid peptide (Abeta) stimulates DBI gene expression and endozepine release. The purpose of this study was to determine the mechanism of action of Abeta in cultured rat astrocytes. Abeta(25-35) and the N-formyl peptide receptor (FPR) agonist N-formyl-Met-Leu-Phe (fMLF) increased the secretion of endozepines in a dose-dependent manner with EC(50) value of approximately 2 microM. The stimulatory effects of Abeta(25-35) and the FPR agonists fMLF and N-formyl-Met-Met-Met (fMMM) on endozepine release were abrogated by the FPR antagonist N-t-Boc-Phe-Leu-Phe-Leu-Phe. In contrast, Abeta(25-35) increased DBI mRNA expression through a FPR-independent mechanism. Abeta(25-35) induced a transient stimulation of cAMP formation and a sustained activation of polyphosphoinositide turnover. The stimulatory effect of Abeta(25-35) on endozepine release was blocked by the adenylyl cyclase inhibitor somatostatin, the protein kinase A (PKA) inhibitor H89, the phospholipase C inhibitor U73122, the protein kinase C (PKC) inhibitor chelerythrine and the ATP Altace 20 Mg binding cassette transporter blocker glyburide. Taken together, these data demonstrate for the first time that Abeta(25-35) stimulates endozepine release from rat astrocytes through a FPR receptor positively coupled to PKA and PKC.

micronase 5 mg 2016-02-08

Type 2 diabetes is characterized by tissue resistance to the action of insulin combined with a relative deficiency in insulin secretion. In Mexico, medicinal plants have traditionally been used to control the disease; in this work, we investigate the hypoglycemic effect of Ageratina petiolaris, a plant used in Mexico for the treatment of Zoloft 350 Mg diabetes.

micronase tablets 2015-09-22

CRLA increased the plasma concentration of LA over time in healthy subjects, and CRLA was safe, well tolerated, and effective in reducing plasma fructosamine in patients Zithromax Drug Classification with type 2 diabetes.

micronase brand name 2017-12-04

Patients with type 2 diabetes are at increased susceptibility to a prolonged QT interval. Furthermore, insulin secretagogues, drugs used to treat diabetes, may prolong QT interval and provoke arrhythmias. We evaluated whether secretagogues can affect QTc interval during cardiac stress test in 20 patients with type 2 diabetes treated with secretagogues. ECG stress test was performed Dutasteride Avodart Generic in all patients. QTc interval was calculated both before cardiac stress test (BCST) and at acme of cardiac stress test (ACST). Diabetic patients treated with secretagogues showed longer QTc-ACST values than those treated with metformin only. QTc-ACST values resulted shorter than QTc-BCST values in control group. Diabetic patients treated with secretagogues showed QTc-ACST values significantly longer than QTc-BCST values. In our study, diabetic patients treated with secretagogues did not show the QTc physiologic decrease that is a protective against arrhythmias. These results suggest to evaluate, in these patients, QT length, even during routine cardiac stress test.

micronase drug class 2016-12-28

We compared the effects of dietary treatment (D) and diet plus glibenclamide (DPG), for 3 weeks, on glycemia, insulin secretion and action in 2 groups of non-obese patients with NIDDM matched for fasting plasma glucose level. Fasting glycemia decreased in both groups with greater reductions after DPG (n = 7, 10.0 +/- 0.6 to 6.3 + 0.3 mmol/l, M +/- SEM, P less than 0.02) than after D (n = 7, 10.1 +/- 0.8 to 8.7 +/- 0.7 mmol/l, M +/- SEM, P less than 0.02). The magnitude of day-time elevation of plasma glucose over the fasting level, however, was reduced only after DPG. DPG but not D improved the plasma insulin response to glucose ingestion and in vivo Flagyl Daily Dosage insulin action measured by insulin tolerance test with unaltered erythrocyte 125I-insulin binding. This might indicate potentiation of insulin action at post-receptor binding steps. Improvements in in vivo insulin action and in insulin secretion after DPG closely correlated with decrease in fasting glycemia and reduction in the day-time elevation of plasma glucose levels, respectively. In conclusion, diet improved glycemic control in non-obese patients with NIDDM mainly by reducing fasting glycemia, although the mechanism remains unknown. Glibenclamide added to the diet further decreased fasting glycemia by improving in vivo insulin action and reduced the magnitude of day-time elevation of plasma glucose by enhancing endogenous insulin secretion.