Drugs online research references
Diabetes Res. 1986 Jul;3(6):293-300.
Effects of glipizide on various consecutive insulin secretory stimulations in patients with type 2 diabetes.
Ahren B, Lundquist I, Schersten B.
Immunoreactive insulin (IRI) and C-peptide secretory responses to consecutive stimulations with terbutaline, glucagon, glucose and a standard meal were investigated in fasted subjects with newly diagnosed, untreated Type 2 diabetes with and without concomitant administration of the sulphonylurea agent glipizide (5 mg). Basal concentrations of blood glucose were 8.7 +/- 0.8 mmol/l without glipizide, and 6.6 +/- 0.5 mmol/l with glipizide (p less than 0.01). This difference in prestimulation glucose levels persisted throughout the study. It was found that glipizide potentiated the IRI and C-peptide secretion in response to terbutaline (125 micrograms i.v.). The absolute IRI and C-peptide secretory responses to glucagon (250 micrograms i.v.) were of similar magnitudes with or without glipizide, despite the lower blood glucose concentrations after glipizide. Allowing for the lower blood glucose, IRI and C-peptide responses to glucagon were potentiated by glipizide. Glucose (6 g i.v.) exerted no IRI or C-peptide secretory effect in these patients either without or with glipizide. The changes in blood glucose concentration after injection of glucagon were not altered by glipizide. On the contrary, the terbutaline-induced increment in blood glucose concentration was inhibited by glipizide and the glucose elimination rate after glucose injection was slightly enhanced by glipizide; effects explained by the higher plasma insulin levels. After meal ingestion, the absolute IRI and C-peptide secretory responses were slightly enhanced by glipizide. Glipizide had no effect on the meal-induced changes in blood glucose concentrations. In conclusion, glipizide had the ability to cause an absolute potentiation of beta 2-adrenoceptor-stimulated and meal-induced insulin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3530592&dopt=Abstract
Metabolism. 1987 Feb;36(2 Suppl 1):12-6.
Clinical pharmacology of sulfonylureas.
Melander A.
Sulfonylureas seem to have similar mechanisms of action, including an acceleration and increase of insulin secretion, an increase of the systemic availability of insulin, and probably indirectly, an increase of insulin action. Sulfonylureas may postpone the development of impaired glucose tolerance (IGT) to manifest non-insulin-dependent diabetes mellitus (NIDDM), and all NIDDM subjects should benefit from sulfonylurea treatment except those in whom insulin secretion has been attenuated. The most effective use is the combination of diet restriction and sulfonylurea introduced in NIDDM subjects soon after transition from IGT to NIDDM. A simple screening procedure has been devised to find the subjects at this early stage. Newer sulfonylureas, such as glipizide and glyburide, are more potent than the older ones, such as tolbutamide and chlorpropamide. During chronic treatment, glipizide and glyburide seem to be equally effective in reducing blood glucose levels, and they do so without causing a chronic elevation of insulin secretion, signifying that they do not increase the risk of pancreatic B cell exhaustion. Glipizide has rapid and complete absorption, as well as a rapid distribution and elimination. This may explain why it is less liable than other sulfonylureas to provoke long-lasting hypoglycemia, which is the major danger when using sulfonylureas. Despite its rapid elimination, 7.5 to 15 mg glipizide can be administered once daily without loss of therapeutic efficacy. This may be due in part to enterohepatic recirculation of the drug in response to meals. The therapeutic efficacy is increased if glipizide is received half an hour before breakfast.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3543616&dopt=Abstract
Metabolism. 1987 Feb;36(2 Suppl 1):17-21.
Determining the most appropriate treatment for patients with non-insulin-dependent diabetes mellitus.
Cooppan R.
Today it is possible, with the available treatment armamentarium, for a physician to rationally choose a strategy to be customized to patients with type II diabetes. The keystone of treatment is a good nutritional plan that provides for proper nutrition as well as appropriate weight loss. Exercise is also a useful adjunct. When diet therapy is unsuccessful, the use of oral sulfonylureas may be indicated. These agents have been shown to stimulate insulin release, to reduce hepatic glucose output, to potentiate insulin action in a postreceptor mechanism, and to have a modest effect in increasing insulin receptors. The first-generation compounds have a 70% success rate within the first 5 years after initiating therapy. However, these agents can have undesirable side effects. The second-generation agents, such as glipizide, offer the advantages of high efficacy, inactive metabolites, nonionic binding, and low reported alcohol flushing. Many patients who fail on first-generation agents may respond to second-generation drugs. Insulin therapy can be used if the patient fails on an oral agent.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3543617&dopt=Abstract
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