Drugs online research references
Exp Mol Pathol. 1990 Oct;53(2):140-51.
Diabetic microangiopathy in KK mice. VI. Effect of glycemic control on renal glycoprotein metabolism and established glomerulosclerosis.
Reddi AS, Velasco CA, Reddy PR, Khan MY, Camerini-Davalos RA.
Department of Medicine, UMD-New Jersey Medical School, Newark 07103-2757.
Twenty-three nonobese KK mice with abnormal tolerance to glucose, hyperinsulinemia with insulin resistance and human diabetic-like nephropathy were treated with either saline (12 mice) or glipizide, an oral hypoglycemic compound, 1 mg/kg, (11 mice) from 120 to 360 days of age. These mice develop significant increases in mesangial volume and matrix by 40 days of age. Oral glucose tolerance (OGTT), glucosyltransferase and N-acetyl-beta-glucosaminidase (enzymes involved in synthesis and degradation of kidney glycoproteins, respectively) in the kidney and serum, 24-hr proteinuria, and light microscopy studies of the kidney were performed. Glipizide-treated mice improved their OGTT. There was no difference in body weight; however, a 16% decrease (P less than 0.05) in kidney weight was observed in glipizide-treated mice. Both enzymes were significantly increased in the kidneys of mice treated with glipizide. No difference in serum enzymes was found between the two groups of mice. About 58% of the saline-treated mice had moderate glomerulosclerosis. By contrast, only 27% of glipizide-treated mice had moderate glomerulosclerosis. Also, a significant decrease in proteinuria was found in glipizide-treated mice. These data suggest that glipizide improves glucose metabolism, decreases kidney size, prevents kidney glycoprotein and mesangial matrix accumulation, and reduces proteinuria in type II diabetic KK mice. This indicates that good glycemic control prevents further progression of established diabetic nephropathy in animals.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2148155&dopt=Abstract
Biochem Int. 1990 Sep;21(6):1125-34.
Modulation of glucose metabolism by sulfonylureas in primary cultures of adult rat hepatocytes.
Lopez-Alarcon L, Melian E, Berbil-Bautista PR, Guijarro C, Feliu JE.
Servicio de Bioquimica Experimental, Hospital Puerta de Hierro, Universidad Autonoma de Madrid, Spain.
Addition of tolbutamide (0.1-5 microM) or glipizide (0.05-5 microM) to primary cultures of adult rat hepatocytes caused a dose-dependent increase of fructose 2,6-bisphosphate concentration. This effect was accompanied by a stimulation of the rate of L-lactate production and by an acceleration of the metabolic flux through the reaction catalysed by 6-phosphofructo 1-kinase. Moreover, the continuous presence of tolbutamide during the first 26 hours of culture mimicked long-term insulin effects by raising fructose 2,6-bisphosphate levels and the rate of L-lactate formation. Glucokinase, 6-phosphofructo 1-kinase and total 6-phosphofructo 2-kinase activities were not found to be significantly different in hepatocytes cultured either in the presence or in the absence of sulfonylurea.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2150480&dopt=Abstract
Diabetes Care. 1990 Aug;13 Suppl 3:2-8.
Characterization and significance of sulfonylurea receptors.
Siconolfi-Baez L, Banerji MA, Lebovitz HE.
Department of Medicine, State University of New York, Brooklyn 11203.
This study describes and characterizes a putative sulfonylurea receptor. The radioligand used was [3H]glipizide (9 Ci/mmol). The beta-cell plasma membranes were derived from a transplantable rat insulinoma generated by subcutaneous injection of RINm5F cells and purified by ultracentrifugation on a 15-55% sucrose gradient. Specific binding of [3H]glipizide to purified beta-cell plasma membranes was determined to be maximal at temperatures of 4-23 degrees C, pH 7.3, and an incubation of 2 h. Scatchard analysis indicated a single binding site with Kd = 7 nM and sulfonylurea binding of 0.93 pmol/mg membrane protein. Displacement of [3H]glipizide from the purified beta-cell plasma membranes by various sulfonylureas and their analogues correlated well with their known hypoglycemic and insulin-releasing activities. Various agents, including nutrients, agents affecting Ca2+ flux, gastrointestinal hormones, and pancreatic hormones, had no effect on [3H]glipizide binding to the beta-cell plasma membranes. Putative sulfonylurea receptors on beta-cell and brain cell plasma membranes have been reported by several groups of investigators. Sulfonylurea binding to the beta-cell is hypothesized to close an ATP-sensitive K+ channel, which leads to depolarization of the membrane and activation of a voltage-dependent Ca2+ channel.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2209340&dopt=Abstract
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