Drugs online research references
Diabetologia. 1992 May;35(5):490-3.
Expression of the 64 kDa/glutamic acid decarboxylase rat islet cell autoantigen is influenced by the rate of insulin secretion.
Bjork E, Kampe O, Andersson A, Karlsson FA.
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
This study examined the relationship between insulin secretion and expression of the 64 kDa/glutamic acid decarboxylase autoantigen in pancreatic islets. Islets isolated from Wistar rats were cultured for 3 days under different conditions: in 5.5 mmol/l glucose with or without alpha-ketoisocaproic acid or glipizide and in 28 mmol/l glucose with or without diazoxide. The 64 kDa/glutamic acid decarboxylase autoantigen was precipitated from lysates of [35S]-methionine-labelled islets with sera from patients with Type 1 (insulin-dependent) diabetes mellitus and identified by sodium dodecyl sulphate-polyacrylamide gel electrophoresis and fluorography. In parallel, insulin contents of the islets and the media were determined as well as the rates of glucose-stimulated (pro)insulin biosynthesis. alpha-Ketoisocaproic acid and glipizide were found to stimulate the expression of the 64 kDa/glutamic acid decarboxylase autoantigen and also the rate of insulin secretion. Diazoxide on the other hand reduced the rate of the 64 kDa/glutamic acid decarboxylase autoantigen synthesis in parallel with an inhibition of glucose-stimulated insulin release. Under most of the conditions employed, (pro)insulin biosynthesis was not affected. The correlation found between the rate of insulin release and expression of the 64 kDa/glutamic acid decarboxylase autoantigen might provide an explanation for the earlier observed relationship between the functional demands on the Beta cells and their rate of destruction which may result in diabetes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1521732&dopt=Abstract
Eur J Clin Pharmacol. 1992;42(1):77-83.
Long-term effects of glipizide on insulin secretion and blood glucose control in patients with non-insulin-dependent diabetes mellitus.
Bitzen PO, Melander A, Schersten B, Svensson M, Wahlin-Boll E.
Department of Community Health Sciences, Lund University Health Sciences Centre, Dalby, Sweden.
Of 23 patients with non-insulin-dependent diabetes mellitus (NIDDM), whose fasting blood glucose had not reached less than or equal to 6.0 mmol.l-1 after 10 weeks of dietary regulation, 15, who had had a weight reduction of -2.8 kg by dietary control, did achieve a fasting blood glucose less than or equal to 6.0 mmol.l-1 after addition of less than or equal to 20 mg glipizide daily. They had a sustained (greater than or equal to 2 years) increase in meal-induced insulin secretion (32% increase in postprandial C-peptide AUC), and a sustained reduction in postprandial hyperglycaemia (34% reduction in AUC). Ten of the patients took a mean daily dose less than 5 mg (4.8 mg) and had a sustained increase in insulin secretion rate (increased C-peptide slope). The 15 patients had no elevation of basal insulin secretion and no impairment of weight reduction. The remaining 8 subjects, who showed little or no weight reduction on dietary control, had little or no reduction in fasting blood glucose despite long-term treatment with 20 mg glipizide daily, a less sustained increase in meal-induced insulin secretion, a smaller reduction of postprandial hyperglycaemia, and an increase in body weight. On diagnosis the 8 subjects did not differ from the other 15 subjects in age, body weight, blood glucose, HbA1c, C-peptide or insulin, nor in their glucose and insulin responses to a test dose of glipizide; the main reason for the apparent drug failure appeared to be deficient compliance with dietary regulation rather than a primary inability to respond to sulphonylurea treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1541320&dopt=Abstract
Metabolism. 1992 Apr;41(4):420-5.
Glipizide-induced immunomodulation: inhibition of human mononuclear cell stimulation and macrophage-mediated islet cell killing in the BB rat.
Nagy MV, Chan EK, Charles MA.
Department of Medicine, University of California, Irvine 92717.
Intensive insulin treatment, when combined with sulfonylurea drugs, may enhance remissions in new-onset type I diabetic patients. These clinical data suggest that sulfonylurea drugs may have immunosuppressive actions in addition to insulin secretory and sensitivity actions. Thus, studies were conducted in humans to determine if glipizide was immunomodulatory in vitro. Five, 10, and 15 micrograms/mL of phytohemagglutinin (PHA) and concanavalin A (Con A), and 0.5, 1.0, and 1.5 micrograms/mL of pokeweed mitogen (PWM) were incubated with normal human peripheral blood mononuclear cells. Maximum stimulatory indices were 52, 39, and 30 for PHA, Con A, and PWM, respectively. Additional incubations were performed in the presence of 1, 10(1), 10(2), 10(3), 10(4), and 10(5) ng/mL glipizide. Glipizide concentrations inhibiting mitogen stimulation approximately 50% (P less than .01 v nonglipizide control) were 1.0 ng/mL for PWM, 10 ng/mL for Con A, and 10(4) ng/mL for PHA. At higher glipizide levels, inhibition was 90% to 100%. To determine if glipizide immunomodulates diabetes-associated reactions, bio-breeding (BB) diabetic rat splenic macrophage-mediated islet killing was studied. Glipizide at 10(3) ng/mL inhibited islet killing by 60% (P less than .001). These preliminary data suggest that glipizide may have immunomodulatory actions not previously appreciated, and may be related to this drug's putative action in islet cell restoration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1556950&dopt=Abstract
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