Drugs online research references
Ups J Med Sci. 1980;85(1):74-83.
Effects of gliclazide--a new antidiabetic agent--on blood platelet function in vitro and in vivo.
Arfors KE, Bergqvist D, Tangen O.
The effect of gliclazide on platelet activity was investigated and compared to that of tolbutamide and glipizide. In vitro studies: adenosine diphosphate induced human platelet aggregation was inhibited by gliclazide in high concentrations (0.5--2.0 mg/ml). In the same concentration range tolbutamide exhibited a slightly less pronounced inhibitory effect. Collagininduced human platelet aggregation was inhibited by gliclazide, glipizide and tolbutamide in a concentration range of 0.5--2.0 mg/ml. Gliclazide had a similar effect on rabbit platelets. In vivo studies: Both acute and seven days administration of gliclazide to rabbits resulted in prolonged primary and total hemostatic plug formation time both in arterioles and venules. Similar results were obtained with tolbutamide and glipizide. Experiments with laser-induced platelet plug formation in the rabbit ear chamber demonstrated that 100 mg gliclazide/kg body weight and 25 mg gliclazide/kg body weight during 7 days significantly reduced the number of platelet emboli formed during 10 minutes after laser injury.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7385462&dopt=Abstract
Diabetes. 1995 Jan;44(1):118-24.
Insulin secretagogues, but not glucose, stimulate an increase in [Ca2+]i in the fetal rat beta-cell.
Weinhaus AJ, Poronnik P, Cook DI, Tuch BE.
Department of Medicine, University of Sydney, Australia.
Fetal pancreatic islets release insulin poorly in response to glucose; however, the cellular mechanism for this is controversial. By using fura 2 to measure changes in the cytoplasmic free Ca2+ concentration ([Ca2+]i) in beta-cells, we have examined islets from fetal, neonatal, and adult rats to determine the ability of glucose and other secretagogues to cause an increase in [Ca2+]i. The effects of glucose (20 mmol/l), glyceraldehyde (20 mmol/l), leucine (20 mmol/l), arginine (20 mmol/l), and the channel effectors glipizide (50 mumol/l), BAY K8644 (2 mumol/l), diazoxide (300 mumol/l), and verapamil (20 mumol/l) on changes in [Ca2+]i were studied. In both the fetal and the mature islet, glyceraldehyde, leucine, arginine, glipizide, and BAY K8644 caused an increase in [Ca2+]i. In mature islets, glucose also increased [Ca2+]i; however, in the fetal islet, glucose had no effect on [Ca2+]i. The stimulus-induced increases in [Ca2+]i in fetal and adult islets were both significantly inhibited by the addition of either diazoxide or verapamil. Similar results were obtained when insulin secretion was measured. Our data show that various secretagogues are able to stimulate fetal islets and cause an increase in [Ca2+]i. Glucose, however, fails to cause an increase in [Ca2+]i in the fetal islet. Hence, the immature insulin secretory response to glucose by the fetal islet is due to the inability of the fetal beta-cell to translate glucose stimulation into the increase in [Ca2+]i required for exocytosis of the insulin granule.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7529202&dopt=Abstract
Mol Cell Endocrinol. 1995 Jun;111(2):159-65.
Interleukin-1 beta-induced stimulation of insulin release in mouse pancreatic islets is related to diacylglycerol production and protein kinase C activation.
Eizirik DL, Sandler S, Welsh N, Juntti-Berggren L, Berggren PO.
Department of Medical Cell Biology, Uppsala University, Sweden.
The aim of the present study was to investigate the mechanisms responsible for the acute, stimulatory effects of interleukin-1 beta (rIL-1 beta; 1 ng/ml) on insulin release from mouse pancreatic islets. For this purpose, mouse islets were exposed for 60-120 min to rIL-1 beta and their function and metabolism characterized during this period. The cytokine did not increase insulin release in the presence of 1.7 mM glucose, but both in the presence of 5.6 or 16.7 mM glucose, or 10 mM leucine + 2 mM glutamine, it induced a 60-100% increase in insulin release. Moreover, rIL-1 beta also enhanced the effects of 1 mu/ml glipizide on insulin release, but failed to increase insulin release induced by 30 mM KCl or by glucose plus phorbol ester (TPA; 100 nM). These early stimulatory effects of rIL-1 beta on insulin release were neither accompanied by major increases in glucose or amino acid metabolism, nor by modifications in islet cAMP content, and they were prevented by mannoheptulose, diazoxide or verapamil. rIL-1 beta potentiation of glucose-induced insulin release was not accompanied by modifications in [Ca2+]i, but the cytokine increased diacylglycerol production and induced protein kinase C (PKC) activation. Down-regulation of PKC completely prevented the stimulatory effects of rIL-1 beta on glucose-induced insulin release. In conclusion, rIL-1 beta induces an early stimulation of insulin release in mouse beta-cells by a mechanism independent of glucose metabolism, cAMP generation or modifications in [Ca2+]i. This effect is probably related to diacylglycerol formation and stimulation of PKC.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7556877&dopt=Abstract
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