Drugs online research references
Metabolism. 1989 May;38(5):466-70.
Effect of sulfonylureas on hepatic glycogen metabolism: activation of glycogen phosphorylase.
Mojena M, Marcos ML, Monge L, Feliu JE.
Servicio de Endocrinologia Experimental, Universidad Autonoma de Madrid, Spain.
In hepatocytes isolated from fed rats, both tolbutamide and glipizide caused a dose-dependent activation of glycogen phosphorylase, possibly by a Ca2+-mediated mechanism. Maximal effects (about twofold) were already obtained when drugs were used at 0.5 mmol/L, the calculated concentrations of tolbutamide and glipizide responsible for the half-maximal effects being 60 and 30 mumol/L, respectively. The activation of glycogen phosphorylase caused the mobilization of glycogen and increased the cellular concentration of hexose 6-phosphates (glucose 6-phosphate plus fructose 6-phosphate) and that of fructose 2,6-bisphosphate. Under the influence of sulfonylureas, glucose formation was slightly stimulated while the rate of L-lactate production was more markedly incremented, indicating that sulfonylureas canalize the metabolic flux coming from glycogen mainly to the glycolytic pathway. These results suggest that a glycogenolytic action of sulfonylureas could collaborate to raise hepatic fructose 2,6-bisphosphate concentration in the fed animal.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2725285&dopt=Abstract
Rev Clin Esp. 1989 Jun;185(1):24-32.
[Glipizide in the treatment of non-insulin-dependent diabetes mellitus]
[Article in Spanish]
Luis Iriarte J.
We present the results of a large study (1.282 patients) carried out in non insulin dependent diabetic patients recruited in the frame of primary care, and treated with Glipizide during 1985 and 1986. We have basically evaluated the overall efficacy of the treatment during 6 1/2 months, with a variable dose of Glipizide established in accordance with the patient's needs, starting with a minimum dose of 2.5 mg (10-30 min. before meals), according to the glycemic control reached. Tolerance was evaluated by laboratory tests and adverse events recorded. In most (83%) of the non insulin dependent diabetic cases previously controlled only with diet, the treatment with Glipizide affords a satisfactory glycemic control, as well as in most of the cases previously treated with other oral hypoglycemias (63%). The median decrease of hyperglycemia has been very significant, with plasma levels under 140 mg/dl (fasting plasma glycemic values), and under 175 mg/dl (postprandial plasma glycemic values), with normal HbA1 levels (less than 8%). This decrease is higher in initial fasting glycemia greater than or equal to 200 mg/dl. Side-effects were scarce (4.2%), mostly gastro-intestinal in previously treated patients (2.7%), with only 2.1% hypoglycemia, usually mild and transient. Treatment with Glipizide went on in 95% of previously untreated patients and in 90% of patients with previous oral hypoglycemias, with a mean daily dose of 10 mg (2 tablets).
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2772334&dopt=Abstract
Eur J Pharmacol. 1987 Aug 11;140(2):157-69.
A binding site for [3H]glipizide in the rat cerebral cortex.
Lupo B, Bataille D.
Centre CNRS-INSERM de Pharmacologie-Endocrinologie, C.C.I.P.E., Montpellier, France.
[3H]glipizide, a 2nd generation hypoglycemic sulfonylurea, binds specifically to rat cerebral cortex membranes in a time- and temperature-dependent way. The binding is saturable and reversible. The maximal binding capacity is 110 fmol/mg protein and the dissociation constant 1.5 nM. The binding site was destroyed by proteolytic and lipolytic enzymes suggesting a lipoprotein nature. Active analogs of sulfonylureas are characterized by IC50 values in the cerebral cortex which parallel their insulinotropic activity. In the cerebral cortex, adenylate cyclase was not stimulated by glipizide but sulfonylureas could inhibit, at high doses, the cAMP-dependent phosphodiesterase. This central binding site for glipizide displays the characteristics of the recognition moiety of a biological receptor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2822437&dopt=Abstract
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