Drugs online research references
Gerontology. 1980;26(4):188-99.
Chronic lathyrism and atheromatosis in the rat. Protective effect of metformin.
Bouissou H, Thiers JC, Douste-Blazy L, Pieraggi MT, Julian M.
Chronic administration of beta-aminopropionitrile fumarate (BAPN) (1 g/kg/day for 9 weeks) produced morphological changes of the aorta wall and in dermis, and biochemical changes of the aortic wall in the rat. Chronic administration of BAPN did not produce plasma lipid abnormalities such as those due to hyperlipidic diet. 9 weeks of BAPN followed by 10 months of a hyperlipidic diet increased the aortic cholesterol level and induced atheroma. The diet alone only produced an endothelial lipid overload and increased the aortic cholesterol level but less than BAPN and hyperlipidic diet together. Addition of metformin to BAPN prevented the formation of atheromatous lesions in the aorta and minimized the level of lipids in the aortic wall and of the dermis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7372099&dopt=Abstract
Farmaco [Sci]. 1983 Apr;38(4):248-54.
Effect of metformin on blood glucose, insulin and C-peptide responses to glucagon in non-insulin dependent diabetics.
Ferlito S, Del Campo F, Di Vincenzo S, Damante G, Coco R, Branca S, Fichera C.
Since the C-peptide Radioimmuno active/Immuno Reactive Insulin (CPR/IRI) molar ratio is considered as an index of insulin hepatic extraction and tissue receptor binding, the AA. investigated the effects of metformin on this index after glucagon infusion in non-insulin dependent diabetics. Fourteen lean subjects (aged 48 to 67 years, mean 54 +/- 7) with non-insulin dependent diabetes were studied. At 9.00 a.m. each subject after overnight fasting, underwent glucagon infusion (1 mg i.v. diluted in 250 ml of saline, infused at a rate of 8.3 gamma/min for 2 hours); blood specimen were obtained at --15, 0, 30, 60, 90, 120 min. This test was repeated after a five-day treatment with metformin (1.5 g per os). For each sample plasma glucose by glucose oxidase method, plasma insulin and C-peptide by Radio Immuno Assay (RIA) method were determined. After treatment with metformin the hyperglycemia induced by glucagon was not influenced; nevertheless insulin and C-peptide plasma levels showed an evident reduction while CPR/IRI molar ratio was unchanged. The AA. suppose an indirect effect of metformin upon beta cells, namely a less pancreatic insulin requirement, mediated by an improvement of glucose utilization.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6345193&dopt=Abstract
J Clin Endocrinol Metab. 1983 Oct;57(4):713-8.
Metformin normalizes insulin binding to monocytes from obese nondiabetic subjects and obese type II diabetic patients.
Trischitta V, Gullo D, Pezzino V, Vigneri R.
In order to evaluate the in vivo effects of biguanides on the insulin receptor, we have studied insulin binding to circulating monocytes of six normal controls, eight obese nondiabetic subjects, and six obese type II diabetic patients, both before and after 4 days of treatment with the biguanide metformin (850 mg twice daily orally). Before drug administration, 125I-insulin binding to monocytes was decreased in obese subjects and diabetic patients. After metformin administration, an increase in insulin binding to peripheral monocytes was observed in seven of eight obese nondiabetic subjects (3.57 +/- 0.43 to 4.69 +/- 0.59% bound at 10(7) monocytes, mean +/- SEM, P less than 0.01) and in all diabetic patients (3.21 +/- 0.21 to 5.22 +/- 0.34, P less than 0.01). Scatchard plots indicated that the increased binding was due to an increase in the receptor number. In contrast, no significant change in insulin binding was found in normal controls after metformin administration (5.31 +/- 0.14 and 4.70 +/- 0.12). These studies indicate that metformin normalizes the binding of insulin to its receptor in obese subjects and diabetic patients. It is suggested, therefore, that the action of metformin on the insulin receptor may be one of the mechanisms of the antidiabetic effect of this drug.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6350337&dopt=Abstract
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