Disease relevance of S 852

• However, in biopsies obtained at hyperinsulinemia, A0.5 was 0.30 +/- 0.05 vs. 0.20 +/- 0.02 mM before and after gliclazide therapy, P less than .04.(ABSTRACT TRUNCATED AT 250 WORDS)[1]
• Current status of non-insulin-dependent diabetes mellitus (type II): management with gliclazide [2].
• Oral treatment of diabetes mellitus: the contribution of gliclazide [3].
• Overall, the specific hemobiologic actions of gliclazide appear to offset or retard the progression of diabetic retinopathy and may have the advantage of lowering the incidence of preproliferative retinopathy [4].
• This study evaluated the effectiveness and selectivity of gliclazide treatment on retinal leukostasis of diabetic rats in vivo [5].

Psychiatry related information on S 852

• Once-daily dosing with gliclazide MR should improve patient compliance, an important factor in long-term glycaemic control [6].

High impact information on S 852

• Arginine-stimulated insulin and somatostatin release is enhanced by the sulfonylurea gliclazide [7].
• We therefore concluded that gliclazide inhibits glucagon release by a direct action on the pancreatic A cell [7].
• Eight subjects with NIDDM underwent three 8-week periods in a randomized crossover design of therapy with diet alone, sulfonylurea (gliclazide), or insulin (ultralente) [8].
• Release of amylin from perfused rat pancreas in response to glucose, arginine, beta-hydroxybutyrate, and gliclazide [9].
• Gliclazide treatment was associated with improved glycemic control and enhanced pancreatic beta-cell responses to meal stimulation [1].

Chemical compound and disease context of S 852

• Effective and selective prevention of retinal leukostasis in streptozotocin-induced diabetic rats using gliclazide [5].
• CONCLUSIONS: For the same improvement in glycemic control, pioglitazone and metformin produce favorable changes in HDL and LDL subfractions compared with gliclazide in overweight type 2 diabetic patients [10].
• Favorable effects of pioglitazone and metformin compared with gliclazide on lipoprotein subfractions in overweight patients with early type 2 diabetes [10].
• Mean plasma glucose levels are significantly reduced over a 24-hour period in patients with type 2 diabetes mellitus treated with gliclazide MR once daily, in both fasting and postprandial states [11].
• A postmarketing study involving 114 office practices provides the largest body of clinical experience to date in Canada with the second-generation sulfonylurea gliclazide in the treatment of non-insulin-dependent diabetes mellitus (NIDDM) [12].

Biological context of S 852

• This study examined the effect of gliclazide on tissue-type plasminogen activator (t-PA)-related fibrinolysis in 23 Type I diabetic patients without residual beta-cell function and 17 Type II diabetic patients initially treated with tolbutamide [13].
• A small pilot trial of an oral hypoglycemic agent, gliclazide, is reported, providing evidence for a specific action of this drug on thromboxane synthesis and platelet aggregation [14].
• Hence, this permitted an examination of the vascular effects of gliclazide in diabetic rabbits exclusive of metabolic effects [15].
• The cardiovascular effects of glibenclamide, gliclazide and carbutamide were studied on myocardial contractile force, cardiac output, mean arterial pressure and heart rate in 43 intact, 14 pancreatectomized and 18 adrenalectomized dogs [16].
• The QSAR analysis supports the hypothesis of a free radical mechanism of action of sulphonylurea derivatives previously suggested for gliclazide [17].

Anatomical context of S 852

• This enhanced effect of insulin after gliclazide treatment was not accompanied by increased monocyte or erythrocyte insulin binding, which suggests that it was due to potentiation of postbinding insulin-sensitive pathways [18].
• Modalities of gliclazide-induced Ca2+ influx into the pancreatic B-cell [19].
• The gliclazide-induced increase in 45Ca efflux is thought to reflect a stimulation of 40Ca influx into islet cells; it is suppressed in the absence of extracellular Ca2+ or in the presence of the organic CA2/-antagonist verapamil [19].
• Gliclazide, a sulphonylurea, was reported to reduce leukocyte adhesion to endothelial cells in hyperglycaemia in vitro, thus suggesting possible selective efficacy of this sulphonylurea in preventing leukostasis in diabetic patients [5].
• AIMS/HYPOTHESIS: To investigate the tissue specificity of gliclazide for cloned beta-cell, cardiac and smooth muscle ATP-sensitive K-channels (K(ATP) channels) [20].

Associations of S 852 with other chemical compounds

• In conclusion, gliclazide alone has an immediate stimulatory effect on glucose uptake by skeletal muscle and together with insulin has an additive effect on muscle glucose uptake [21].
• The effects of four sulphonylureas (gliclazide, glibenclamide, chlorpropamide and glipizide) on insulin binding and insulin action were studied in vitro using primary cultured rat hepatocytes [22].
• CONCLUSION/INTERPRETATION: Glimepiride appeared to be a more potent ADP-induced platelet aggregation inhibitor in vitro than gliclazide [17].
• After gliclazide therapy in both the n5-STZ gliclazide responder group and the n0-STZ group: (a) in vitro glucose-induced insulin secretion was increased three- to fivefold; (b) the response to arginine, which is increased in diabetic rats, was amplified by two- to threefold; (c) insulin release in response to gliclazide was unchanged [23].
• In an artificial system, hypoglycaemic sulphonamides, such as gliclazide, stimulate the translocation of calcium into or across a hydrophobic immiscible domain, a process enhanced by the antibiotic ionophore A 23187 and antagonized by suloctidil [24].

Gene context of S 852

• The high-affinity site on SUR1 was thus about 40-fold more sensitive to gliclazide than to tolbutamide (Ki approximately 2 micromol/l) [20].
• CONCLUSIONS: Gliclazide administration to NIDDM patients inhibits the increased adhesiveness of diabetic monocytes to endothelial cells and reduces the production of TNF-alpha by these cells [25].
• These effects were inhibited by antioxidants including gliclazide and vitamins C and E. On the basis of the stimulatory effect of AGEs on vascular endothelial growth factor (VEGF) secretion by retinal endothelial cells, the role of this growth factor as mediator of AGE-induced monocyte adhesion to BRECs was next investigated [26].
• Treatment with gliclazide could not restore p38 phosphorylation in insulin-resistant cells [27].
• Although insulin receptor substrate-1 tyrosine phosphorylation was unaffected by gliclazide treatment, phosphatidylinositol 3-kinase activity was partially restored by treatment with gliclazide [27].

Analytical, diagnostic and therapeutic context of S 852

• Gliclazide (30 micro mol/l) inhibited glucagon release by 54% in the perfusion experiments, whereas the somatostatin response was nearly abolished [7].
• Development of macroangiopathy in sand rats (Psammomys obesus), an animal model of non-insulin-dependent diabetes mellitus: effect of gliclazide [28].
• The high concentrations of glycerides and fatty acids in the aorta were significantly decreased towards normal values and histology showed that the gliclazide strongly inhibited the development of aortic and particularly coronary lesions induced by the atherogenic diet [29].
• Pharmacokinetic curves for gliclazide by CE and HPLC were superimposable [30].
• Measurement of gliclazide in plasma by radial compression reversed-phase liquid chromatography [31].

References