Disease relevance of Maninil

• Eighteen percent of the patients given metformin and glyburide had symptoms compatible with hypoglycemia, as compared with 3 percent in the glyburide group and 2 percent in the metformin group [1].
• A comparison of glyburide and insulin in women with gestational diabetes mellitus [2].
• However, neither glibenclamide nor hyperglycemia affected vasoconstrictor responses to moderate hypoxia or KCl, indicating that effects during severe hypoxia were not due to nonspecific potentiation of vasoconstriction [3].
• Finally, studies in livers from rats with endotoxin- or estrogen-induced cholestasis show that glybenclamide retains its stimulatory effects on bile flow and bicarbonate excretion even under these conditions [4].
• We studied the molecular mechanisms underlying this effect and whether glibenclamide could restore cholangiocyte secretion in cystic fibrosis [5].

Psychiatry related information on Maninil

• However, cognitive function was better preserved during hypoglycaemia in the glibenclamide-treated arm, particularly four-choice reaction time which deteriorated at a plasma glucose 2.5 mmol/l compared with 3.0 mmol/l with diazoxide (P = 0.015) and 2.9 mmol/l with placebo (P = 0.114) [6].
• Glibenclamide alone or in combination with morphine did not affect locomotor activity [7].
• The influence of vinpocetine on glibenclamide steady state plasma levels was investigated in 18 patients suffering from type II diabetes and symptoms of dementia [8].
• CONCLUSIONS: The study demonstrates that patient compliance with once-daily gliclazide MR is significantly better than with twice-daily glibenclamide [9].
• A patient with schizoaffective disorder with non-insulin-dependent diabetes mellitus (NIDDM) treated with sertraline, risperidone and glyburide who developed hypoglycemia is presented [10].

High impact information on Maninil

• The women were randomly assigned between 11 and 33 weeks of gestation to receive glyburide or insulin according to an intensified treatment protocol [2].
• Hypoxic vasodilation in isolated, perfused guinea pig hearts can be prevented by glibenclamide, a blocker of adenosine triphosphate (ATP)-sensitive potassium channels, and can be mimicked by cromakalim, which opens ATP-sensitive potassium channels [11].
• Hypoglycemia from glipizide and glyburide [12].
• Concomitant with this change, basal C-peptide and free insulin values increased with glyburide therapy, but this pharmacological agent did not alter the ability of the patient's erythrocytes to bind insulin [13].
• We report here that both ATP and glibenclamide sensitivities of the 30 pS K channel in TAL cells were absent in mice lacking CFTR and in mice homozygous for the deltaF508 mutation [14].

Chemical compound and disease context of Maninil

• Hypoglycemia from glipizide and glyburide [15].
• CONCLUSIONS: Therapy with glyburide or once-per-day NPH insulin provides a similar degree of glucose control in patients with non-insulin-dependent diabetes mellitus [16].
• Sensitivity of a renal K+ channel (ROMK2) to the inhibitory sulfonylurea compound glibenclamide is enhanced by coexpression with the ATP-binding cassette transporter cystic fibrosis transmembrane regulator [17].
• The data indicate that glibenclamide enhances whereas pinacidil reduces myocardial damage caused by ischemia/reperfusion [18].
• Compounds acting on the pancreatic sulfonylurea receptor (SUR) to increase (e.g., glibenclamide) or decrease (e.g., diazoxide) [Ca2+]i cause corresponding increases and decreases in weight gain [19].

Biological context of Maninil

• When the process of insulin-induced receptor loss (or down regulation) was studied in the presence of glyburide, the drug exerted a marked inhibitory effect on this regulatory process [20].
• Measurements of cAMP, cytosolic pH, and Ca2+ in isolated bile duct cells suggest that glybenclamide directly activates Na+-K+-2Cl- cotransport, rather than other transporters or conventional second-messenger systems that link to secretory pathways in these cells [4].
• RESULTS: In cirrhotic rats, glibenclamide (5, 20, 30 mg/kg but not 2.5 mg/kg) significantly increased vascular resistance in portal and systemic territories [21].
• Glyburide therapy resulted in significant reduction in fasting serum glucose levels; in PMNLs, this treatment resulted in a significant reduction in [Ca2+]i levels, a significant increase in ATP content, and a significant improvement of phagocytosis [22].
• However, glibenclamide did not impair the increases of coronary blood flow, myocardial oxygen consumption, and systolic wall thickening that occurred during exercise [23].

Anatomical context of Maninil

• We examined the immunofluorescence and ultrastructural changes of insulin-producing B cells in the center and at the periphery of islets of Langerhans during in vivo stimulation by glucose and glibenclamide [24].
• Insulin- and glyburide-stimulated changes in cytosolic free calcium concentrations [( Ca2+]i) were studied in gluteal adipocytes obtained from six obese women (139 +/- 3% ideal body wt) and six healthy, normal weight age- and sex-matched controls [25].
• When glyburide was added to monolayers of human fibroblasts, a dose-dependent increase in the number of cell surface receptors was observed with a maximum effect (19% increase) seen at 1 microgram/ml glyburide [20].
• Stimulation of bile duct epithelial secretion by glybenclamide in normal and cholestatic rat liver [4].
• Both a short (90 min) stimulation by glucose in vitro and a prolonged (2.5 d) stimulation by glibenclamide in vivo raise the number of gap junctions; in addition, the glibenclamide stimulation causes an increase in the size of individual gap junctions [26].

Associations of Maninil with other chemical compounds

• RESULTS: Stimulation of cholangiocyte secretion by glibenclamide and tolbutamide required Cl - and was mediated by the sulfonylurea receptor 2B [5].
• Effects of an agonist (Y-26763, intra-arterially) and an inhibitor (glibenclamide, intravenously) of KATP channels were tested [27].
• This study aimed to examine hemodynamic responses to glibenclamide, a KATP channel blocker, and to aprikalim, a vasodilator activating KATP channels, in normal and cirrhotic rats [21].
• Cyclosporin A, rifamycin SV, rifampicin, and glibenclamide cis-inhibited Bsep-mediated bile salt transport to similar extents as ATP-dependent taurocholate transport in cLPM vesicles [28].
• Sulfonylurea and particularly glibenclamide are potent blockers of ATP-regulated K+ channels in insulin-secreting cells [29].

Gene context of Maninil

• Here, we show that beta(2) is the major adrenergic receptor isoform expressed in airway epithelia and that it colocalizes with CFTR at the apical membrane. beta(2)AR stimulation increases CFTR activity, in airway epithelial cells, that is glybenclamide sensitive [30].
• The putative ABCA1 inhibitor glyburide and antisense oligonucleotides directed against ABCA1 mRNA significantly reduced apoE secretion from THP1 macrophages and HMDM [31].
• 1) In PANC-1 cells, cAMP causes parallel activation of Cl- channels and of HCO3- extrusion by DIDS-sensitive and Na+-independent Cl-/HCO3- exchange, both effects being inhibited by Cl- channel blockers NPPB and glibenclamide [32].
• SUR1, the typical pancreatic SUR isoform, shows much higher affinity for glibenclamide but considerably lower affinity for most openers than SUR2 [33].
• Moreover, HL activity was significantly lower after insulin than after glibenclamide (HL 247.2 +/- 22.3 vs. 263.5 +/- 22.6 mU/ml, P < 0.05) [34].

Analytical, diagnostic and therapeutic context of Maninil

• Molecular cloning of a glibenclamide-sensitive, voltage-gated potassium channel expressed in rabbit kidney [35].
• Glyburide or insulin for metabolic control in non-insulin-dependent diabetes mellitus. A randomized, double-blind study [16].
• When glibenclamide was applied from the onset of reperfusion, the persistent APD shortening was significantly suppressed [36].
• The aim of this study was to establish whether glibenclamide, a selective KATP channel blocker, abolishes the ischemic preconditioning observed in humans during coronary angioplasty following repeated balloon inflations [37].
• METHODS AND RESULTS: Twenty consecutive patients undergoing one-vessel coronary angioplasty were randomized to receive 10 mg oral glibenclamide or placebo [37].

References