Disease relevance of Glurenorm

• A study was made of the effects of acute or chronic treatment of rabbits with 10 mg gliquidone (Glurenorm)/kg body weight on erythrocyte insulin receptors [1].
• In the present study we evaluated the effects of gliquidone, a second-generation compound, on several metabolic parameters in 22 patients with untreated newly-diagnosed type II (noninsulin-dependent) diabetes mellitus [2].
• Gliquidone contributes to improvement of type 2 diabetes mellitus management : a review of pharmacokinetic and clinical trial data [3].
• Importantly, in the light of the well documented consequences of increased bodyweight and the large growth in obesity worldwide, gliquidone is not associated with significant bodyweight gain.Thus, gliquidone is a sulfonylurea with proven efficacy and good safety and metabolic profiles that is only rarely associated with hypoglycaemia [3].
• Irradiation with a SOL 3 apparatus (solar simulating irradiation) revealed hemolysis in the presence of chlorpropamide, glipizide, gliquidone, glymidine and tolbutamide (all in the concentration 10(-3) mol/l) [4].

Psychiatry related information on Glurenorm

• 3. Tetraethylammonium (TEA; 1-5 microg per mouse i.c.v.), apamin (10 ng per mouse i.c.v.), charybdotoxin (1 microg per mouse i.c.v.), gliquidone (3 microg per mouse i.c.v.) and glibenclamide (1 microg per mouse i.c.v.), administered 20 min before the training session, prevented the potassium channel opener-induced amnesia [5].

High impact information on Glurenorm

• RESULTS: The most pronounced inhibition of platelet aggregation was by glimepiride, gliclazide, gliquidone, glibenclamide and compound 2A [6].
• During the second 24 h of this period, the hepatocytes were incubated with or without gliquidone (5 mg/l) [7].
• The most active of these compounds, gliquidone, is shown to be as potent as pioglitazone at inducing PPARgamma target gene expression [8].
• 1. The effect of intracerebroventricular (i.c.v.) administration of different potassium channel blockers (tetraethylammonium, apamin, charybdotoxin, gliquidone), potassium channel openers (pinacidil, minoxidil, cromakalim) and aODN to mKv1.1 on immobility time was evaluated in the mouse forced swimming test, an animal model of depression [9].
• Three potassium-channel blocking agents, quinine, 4-aminopyridine and gliquidone, were tested for their action on the increase in [K+]e, induced by inhalation of 100% N2 for 0.5 min [10].

Chemical compound and disease context of Glurenorm

• The monoethyl, monopropyl and monoisopropyl esters of succinic acid, administered intravenously at the dose of 2 micromol/g body weight, were found to increase the insulinotropic action of gliquidone (0.2 nmol/g body weight) in anaesthetized rats [11].
• The duration of action and the pharmacokinetics of gliquidone (1-cyclohexyl-3-[[4-[2-(3,4-dihydro-7-methoxy-4,4-dimethyl-1, 3-dioxo-2(1H)-isochinolyl)ethyl]phenyl]-sulfonyl]-urea, AR-DF 26 SE, CAS 33342-05-1, Glurenorm, Beglynor) were investigated in 32 patients with non-insulin-dependent (type 2) diabetes mellitus over 16 h [12].

Biological context of Glurenorm

• The data indicate that there are different binding sites for glibenclamide and gliquidone in RIN m5F cells [13].
• Interference of the sulphonylurea antidiabeticum gliquidone with mitochondrial bioenergetics in the rat under in vitro conditions [14].
• The study ascertained the utility of HP-beta-CD in enhancing the oral bioavailability of gliquidone, and points towards a strong influence of the preparation method on the physicochemical properties [15].
• Duration of action and pharmacokinetics of the oral antidiabetic drug gliquidone in patients with non-insulin-dependent (type 2) diabetes mellitus [12].
• Besides the uncoupling effect, gliquidone and glibenclamide caused a direct inhibition of ATP-as well as DNP-stimulated oxygen consumption [14].

Anatomical context of Glurenorm

• Effect of gliquidone on insulin binding to rabbit erythrocytes [1].
• The non-sulfonylurea moiety of gliquidone mimics the effects of the parent molecule on pancreatic B-cells [16].
• The data suggest that UL-DF 9 and gliquidone decrease the K+ permeability of the B-cell membrane, thereby causing a depolarization which leads to activation of voltage-dependent Ca channels and Ca2+ influx, and thus eventually increase insulin release [16].
• In contrast, gliquidone caused a marked and dose-dependent stimulation of acid production in gastric glands incubated under basal conditions and potentiated the stimulatory effect of both histamine and carbachol [17].
• Extrapancreatic action of sulphonylureas: effect of gliquidone on insulin and glucagon binding to rat liver plasma membranes [18].

Associations of Glurenorm with other chemical compounds

• Without causing significant changes in cellular levels of cyclic adenosine monophosphate (cAMP), the addition of either glibenclamide or gliquidone to isolated rat hepatocytes caused a transient dose- and Ca(2+)-dependent activation of glycogen phosphorylase [19].
• Effects of gliquidone on D-glucose metabolism in rat pancreatic islets depend on hexose concentration [20].
• Immunohistochemical localization of islets of Langerhans of streptozotocin (65 mg/kg, ip) induced diabetic + glurenorm (10 mg/kg, po) treated female albino rats revealed increase in number of beta cells and insulin immunoreactivity of beta cells [21].
• We describe insulin binding and insulin-mediated RNA synthesis on seven human fibroblasts strains in culture initiated from skin biopsies in the presence of three oral antidiabetic agents, Metformin, Gliquidone, and a non-sulfonylurea antidiabetic drug (B X DF 591 ZW), which belong to different chemical classes [22].
• The hypoglycaemic sulphonylurea gliquidone and glibenclamide exerted a partial uncoupling effect on mitochondrial respiration of liver under in vitro conditions using various citrate cycle intermediates as substrates [14].

Gene context of Glurenorm

• 6. The reversal potential of the anoxic hyperpolarization was unaffected by tetrodotoxin (TTX) but was significantly altered by application of the ATP-sensitive K+ channel (KATP) blocker gliquidone [23].
• Application of gliquidone additionally resulted in a significantly smaller hypoxia-induced decline in paired-pulse inhibition [23].
• The effect of gliquidone, an ATP-dependent K+ (KATP) channel blocker, on morphine-induced hypermotility in mice was studied [24].
• After 6 but not 1 month of gliquidone therapy we also found an increase in the activity of hexokinase in circulating mononuclear leukocytes [2].
• We concluded that gliquidone is an effective oral hypoglycemic agent for treating patients with NIDDM [25].

Analytical, diagnostic and therapeutic context of Glurenorm

• After treatment of ob/ob mice with ARDF-26 (Gliquidon; Boehringer Ingelheim Ltd) the concentration of liver membrane insulin receptors was increased 5 fold [26].
• Gliquidone (Glurenorm) and glibenclamide were compared in a cross-over study of 20 non insulin dependent diabetics [27].
• Glurenorm was administered to one diabetic and one control group separately, from days 14 to 42 [28].

References