Drugs online research references
Int J Clin Pharmacol Ther. 1999 Jul;37(7):319-22.
Bioequivalence of a generic metformin tablet preparation.
Yuen KH, Wong JW, Billa N, Julianto T, Toh WT.
School of Pharmaceutical Sciences, University of Science Malaysia, Penang.
OBJECTIVE: The bioavailability of a generic preparation of metformin (Diabetmin from Hovid Sdn Bhd) was evaluated in comparison with a proprietary product (Glucophage from Lipha Pharma Ltd., UK). PATIENTS AND METHODS: Twenty-four healthy male volunteers participated in the study conducted according to a two-way crossover design. The bioavailability was compared using the parameters total area under the plasma concentration-time curve (AUC0-infinity), peak plasma concentration (Cmax and time to reach peak plasma concentration (Tmax). RESULTS: No statistically significant difference was observed between the values of the two products in all three parameters. Moreover, the 90% confidence interval for the ratio of the logarithmic-transformed AUC0-infinity and Cmax values of Diabetmin over those of Glucophage was found to lie between 0.94-1.03 and 0.94-1.06, respectively, being within the acceptable bioequivalence limit of 0.80-1.25. CONCLUSION: These findings indicate that the two preparations are comparable in the extent and rate of absorption. In addition, elimination rate constant (k(e)) and apparent volume of distribution (Vd) were calculated. There was no statistically significant difference between the values of the two preparations in the k(e) and Vd. Moreover, the values are comparable to those reported in the literature.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10442505&dopt=Abstract
coh.org
Enhanced formation and accumulation of advanced glycation end products (AGEs) have been proposed to play a major role in the pathogenesis of diabetic complications, and atherosclerosis, leading to the development of a range of diabetic complications including nephropathy, retinopathy and neuropathy. Several potential drug candidates as AGE inhibitors have been reported recently. Aminoguanidine is the first drug extensively studied. However, there are no currently available medications known to block AGE formation. We have previously reported a number of novel and structurally diverse compounds as potent inhibitors of glycation and AGE formation. We have now studied several of the existing drugs, which are in therapeutic practice for lowering blood sugar or the treatment of peripheral vascular disease in diabetic patients, for possible inhibitory effects on glycation. We show that that three compounds; pioglitazone, metformin and pentoxifylline are also inhibitors of glycation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11020463&dopt=Abstract
Metabolism. 2001 Sep;50(9):1049-53.
Exercise adds to metformin and acarbose efficacy in db/db mice.
Tang T, Reed MJ.
Shaman Pharmaceuticals, Inc, South San Francisco, CA, USA.
Physical exercise is frequently recommended for the treatment of type 2 diabetes, whether as primary therapy with diet modification or as an adjunct to drug therapy. We hypothesized that mild exercise would enhance the glucose-lowering effects of 2 oral antihyperglycemic drugs, metformin and acarbose, in an animal model of type 2 diabetes. Eight-week-old male C57BL/Ks (db/db) mice were sorted into control and exercise groups and dosed daily for 4 weeks with vehicle, metformin (150 mg/kg/d), or acarbose (40 mg/kg/d). Exercise consisted of swimming (initially 5 min/d and ultimately 1 h/d for the last 2 weeks). Exercise, metformin, and acarbose independently reduced serum glucose concentrations 15% to 25% compared with the respective controls (P <.0001), but the effect on glucose concentration of combining drug therapy with exercise was no greater than the sum of the individual effects. Exercise training independently increased muscle glycogen (30%; P <.05) and liver glycogen (250%; P <.05) levels and slightly reduced serum high-density lipoprotein cholesterol (-8%; P <.05), whereas drug treatment had no effect on these variables. In addition, exercise but not drug treatment prevented the approximately 30% decline in serum insulin concentrations that occurred in the control animals (P <.05). Twenty-four hours after the last drug or exercise treatment, oral glucose tolerance and hemoglobin A1c were not significantly different between groups. Treatment also did not greatly affect triglyceride, glycerol, or total cholesterol concentrations. In conclusion, exercise and drug therapy independently decreased serum glucose in db/db mice, and these effects did not appear to be synergistic. In addition, exercise training maintained serum insulin concentrations and increased tissue glycogen storage. These results suggest that exercise has the potential to add to the efficacy of oral antihyperglycemic drugs. Copyright 2001 by W.B. Saunders Company
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11555837&dopt=Abstract
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