Drugs online research references
Metabolism. 1990 Apr;39(4):425-35.
Effect of metformin treatment on insulin action in diabetic rats: in vivo and in vitro correlations.
Rossetti L, DeFronzo RA, Gherzi R, Stein P, Andraghetti G, Falzetti G, Shulman GI, Klein-Robbenhaar E, Cordera R.
Division of Diabetes, University of Texas Health Science Center, San Antonio 78284.
The mechanism (both at the whole body and cellular level) by which metformin improves insulin sensitivity has yet to be defined. In the present study, we examined in vivo insulin-mediated whole-body glucose disposal, glycogen synthesis, hepatic glucose production, and insulin secretion, as well as in vitro muscle insulin receptor tyrosine kinase activity in eight control, eight neonatal streptozotocin diabetic rats, and eight diabetic rats before and after treatment with metformin. Ten weeks after birth diabetic rats had higher fasting (132 + 5 v 101 + 2 mg/dL) and postmeal (231 + 10 v 133 + 3) plasma glucose levels compared with controls (P less than .001). Metformin treatment was followed by a significant decrease in the growth rate and normalized glucose tolerance without enhancing the deficient insulin response. Insulin-mediated glucose uptake in diabetic versus control rats was reduced (P less than .01) during the high-dose (15.4 + 0.6 v 18.3 + 1.0 mg/kg.min) insulin clamp study and was increased to values greater (P less than .05) than controls following metformin treatment. Muscle glycogen synthetic rate in vivo, measured by incorporation of 3H-3-glucose radioactivity, was diminished by 25% (P less than .01) in diabetic rats, restored to normal values with metformin, and correlated closely (r = .82, P less than .002) with total-body glucose uptake during the insulin clamp in all three groups. Insulin receptor tyrosine kinase activity, measured in partially purified insulin receptors, was reduced in diabetic rats and increased to supernormal levels after metformin. The decrease in muscle tyrosine kinase activity in diabetic versus control animals was entirely accounted for by a reduction in maximal velocity (Vmax) (32 v 45 pmol/mg.min, P less than .01) and increased to supernormal levels following metformin (91 pmol/mg.min, P less than .001) without any change in affinity (Km). Muscle tyrosine kinase activity was closely correlated with both the muscle glycogen synthetic rate (r = .82, P less than .002) and total-body insulin-mediated glucose disposal (r = .64, P less than .01) in vivo. The close correlation between in vivo insulin action, muscle glycogen synthesis, and muscle insulin receptor tyrosine kinase activity is consistent with an important role of the enzyme in the insulin resistance of diabetes and its improvement following metformin treatment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2157941&dopt=Abstract
Int J Clin Pharmacol Ther Toxicol. 1989 Jun;27(6):285-8.
Hemodialysis in the treatment of lactic acidosis in diabetics treated by metformin: a study of metformin elimination.
Lalau JD, Andrejak M, Moriniere P, Coevoet B, Debussche X, Westeel PF, Fournier A, Quichaud J.
Department of Internal Medicine - Endocrinology, Centre Hospitalier Regional et Universitaire, Amiens, France.
The aim of this study was to determine the characteristics of metformin elimination by dialysis. For this purpose we report the kinetic parameters during dialysis and the metformin clearance (i.e. dialysance) in four patients presenting with lactic acidosis which occurred on metformin therapy. We also studied metformin elimination in two chronically hemodialyzed diabetic patients inadvertently maintained on metformin therapy and in two chronically hemodialyzed non-diabetic patients who took a single dose of metformin before a dialysis session. Analysis of plasma concentration-time curves showed a biphasic pattern of metformin - elimination, according to a two-compartment model. We demonstrate that metformin may be removed even after reaching an equilibrium between blood and dialysate levels in a recirculating system, suggesting a storage of metformin in a deep compartment with a gradient of concentration between this compartment and the blood. Lastly, metformin dialysance appears satisfactory (68 ml/min) even in the case of relatively low blood flow; this value reached 170 ml/min under good hemodynamic conditions. In conclusion, hemodialysis efficiently removes metformin and corrects metabolic acidosis in patients with metformin-induced lactic acidosis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2500402&dopt=Abstract
Curr Med Res Opin. 1979;6(3):201-3.
Stopping phenformin treatment in a diabetic clinic.
Shee CD, Medd WE.
Phenformin was stopped in 35 patients attending a diabetic clinic. In 4 patients where phenformin alone had been used, subsequent diabetic control was easily maintained with diet or a sulphonylurea. Thirty-one patients had been taking phenformin with a sulphonylurea and 17 (55%) later required insulin. Larger doses of a sulphonylurea were usually needed in the other patients. It is suggested that metformin is probably the biguanide of choice now and should be considered in carefully selected diabetics.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=520025&dopt=Abstract
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