Drugs online research references
Am J Surg. 1989 Jan;157(1):103-8.
Effect of glipizide on the surgically altered pancreas.
Barr JD, Parish ES, Krusch DA, Farris AH, Freedlender AH, Kaiser DL, Hanks JB.
Department of Surgery, University of Virginia Medical Center, Charlottesville 22908.
Surgical alterations of the pancreas affect peripheral glucose, insulin, and glucagon levels with accompanying changes in carbohydrate metabolism. The sulfonylurea glipizide has been used to treat insulin-deficient states; however, its mechanism is not completely known. We hypothesized that glipizide would correct postoperative changes in glucose handling in a way that would allow more complete understanding of the drug's action. Two surgical groups (Group 1:80 percent proximal pancreatectomy; Group 2: proximal pancreatectomy plus splenocaval diversion) were compared with a healthy control group (Group 3). We have concluded that glipizide may have affected basal insulin sensitivity in the control group and Group 2 animals without affecting insulin secretion in response to oral or intravenous glucose stimulation. Glipizide does not correct the alterations in glucose handling or insulin secretion after reduction in beta-cell mass.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2642663&dopt=Abstract
Biochem Pharmacol. 1989 Apr 15;38(8):1217-29.
Control of insulin secretion by sulfonylureas, meglitinide and diazoxide in relation to their binding to the sulfonylurea receptor in pancreatic islets.
Panten U, Burgfeld J, Goerke F, Rennicke M, Schwanstecher M, Wallasch A, Zunkler BJ, Lenzen S.
Institute of Pharmacology and Toxicology, University of Gottingen, Federal Republic of Germany.
Sulfonylureas inhibit an ATP-dependent K+ channel in the B-cell plasma membrane and thereby initiate insulin release. Diazoxide opens this channel and inhibits insulin release. In mouse pancreatic islets, we have explored whether other targets for these drugs must be postulated to explain their hypo- or hyperglycaemic properties. At non-saturating drug concentrations the rates of increase in insulin secretion declined in the order tolbutamide = meglitinide greater than glipizide greater than glibenclamide. The same rank order was observed when comparing the rates of disappearance of insulin-releasing and K+ channel-blocking effects. The different kinetics of response depend on the lipid solubility of the drugs, which controls their penetration into the intracellular space. Allowing for the different kinetics, the same maximum secretory rates were caused by saturating concentrations of tolbutamide, meglitinide, glipizide and glibenclamide. A close correlation between insulin-releasing and K+ channel-blocking potencies of these drugs was observed. The relative potencies of tolbutamide, meglitinide, glipizide and glibenclamide corresponded well to their relative affinities for binding to islet-cell membranes, suggesting that the binding site represents the sulfonylurea receptor. The biphasic time-course of dissociation of glibenclamide binding indicates a complex receptor-drug interaction. For diazoxide there was no correlation between affinity of binding to the sulfonylurea receptor and potency of inhibition of insulin secretion. Thus, opening or closing of the ATP-dependent K+ channel by diazoxide or sulfonylureas, respectively, appears to be due to interaction with different binding sites in the B-cell plasma membrane. The free concentrations of tolbutamide, glipizide, glibenclamide and diazoxide which are effective on B-cells are in the range of therapeutic plasma concentrations of the free drugs. It is concluded that the hypo- and hyperglycaemic effects of these drugs result from changing the permeability of the ATP-dependent K+ channel in the B-cell plasma membrane.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2650685&dopt=Abstract
Am J Manag Care. 1999 Aug;5(8):1007-24.
A short-term cost-of-treatment model for type 2 diabetes: comparison of glipizide gastrointestinal therapeutic system, metformin, and acarbose.
Ramsdell JW, Grossman JA, Stephens JM, Botteman MF, Arocho R.
Department of Medicine, University of California, San Diego, USA.
OBJECTIVE: To compare, from a managed care perspective, the 3-year costs of 3 first-line monotherapy strategies in type 2 diabetes patients: glipizide gastrointestinal therapeutic system (GITS), metformin, and acarbose. STUDY DESIGN: A Markov model, with a Monte Carlo simulation, was developed to compare the costs to achieve full glycemic control (hemoglobin A1c of < or = 7%) with each first-line strategy. PATIENTS AND METHODS: The patient population for the model was assumed to be all newly diagnosed type 2 diabetes patients eligible for monotherapy with an oral agent. Each monotherapy could be succeeded by add-on treatments. The model included the costs of routine medical care and supplies, medication, adverse events, and treatment failures. RESULTS: Using a Monte Carlo simulation, the mean 3-year cumulative costs per patient were $4971, $5273, and $5311 for glipizide GITS, metformin, and acarbose first-line strategies, respectively. The main cost drivers were drug prices. Mean 3-year cost savings for first-line glipizide GITS were $301 over metformin and $340 over acarbose. Between 83% and 85% of all simulations showed cost savings with glipizide GITS compared with the other agents. CONCLUSIONS: The model suggests first-line monotherapy with glipizide GITS should result in desirable short-term economic benefits for managed care. Because the model incorporates recommended glycemic goals and performed well in sensitivity analyses, it should be applicable to a variety of clinical practices and useful for economic assessments of new therapies. Results of this model should be verified prospectively in typical care settings.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10558125&dopt=Abstract
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