Drugs online research references
J Pharm Pharmacol. 1985 Nov;37(11):821-3.
Postreceptor effect of metformin on insulin action in mice.
Lord JM, Puah JA, Atkins TW, Bailey CJ.
To investigate the possibility that metformin (dimethylbiguanide) modifies insulin-mediated glucose metabolism by an effect that is independent of insulin receptor binding, glycogenesis and insulin binding were measured in soleus muscles isolated from streptozocin diabetic mice after treatment with 60 mg kg-1 metformin daily for 10 weeks. This dose of metformin increased insulin-stimulated glycogenesis but did not affect insulin binding in the soleus muscles of streptozocin diabetic mice. The results suggest that metformin can influence postreceptor sites of insulin action independently of insulin receptor binding.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2867167&dopt=Abstract
J Clin Endocrinol Metab. 1986 Oct;63(4):898-905.
Mechanism of action of metformin: insulin receptor and postreceptor effects in vitro and in vivo.
Fantus IG, Brosseau R.
Metformin (Met) is a biguanide oral hypoglycemic agent used in the treatment of noninsulin-dependent diabetes mellitus (NIDDM). To define whether the glucose-lowering effects are mediated via alterations of insulin receptors, the effects of Met in vitro in rat adipocytes and in vivo in patients with poorly controlled NIDDM were studied. In vitro exposure of rat adipose tissue to metformin for 20 h resulted in a significant increase in insulin binding (mean +/- SEM percent specific [125I]insulin bound per 10(5) adipocytes: control, 1.35 +/- 0.13; Met, 1.69 +/- 0.18; P less than 0.02). No change occurred after 2 h of exposure or less. In contrast, after only 1 h of preincubation. Met alone stimulated [U-14C]glucose oxidation by 58 +/- 15.5% (P less than 0.01). Met did not stimulate glucose oxidation in the presence of a high insulin concentration. For the in vivo studies, oral glucose tolerance tests and monocyte [125I]insulin binding assays were performed before and after 7 days of Met treatment (2 g/day) in 18 patients with poorly controlled NIDDM. All patients responded to Met with a decrease in fasting and postglucose plasma glucose concentrations, but no change in insulin concentrations [pre-Met vs. post-Met: fasting plasma glucose, 210 +/- 10 vs. 157 +/- 11 mg/dl (P less than 0.001); fasting plasma insulin, 20.3 +/- 3.1 vs. 18.4 +/- 2.0 microU/ml]. When insulin binding was examined, 8 patients with decreased binding each responded to Met with a 50% or greater increase (group 1), while 10 patients with normal binding had no increase after treatment (group 2). However, both groups had similar lowering of glucose concentrations [fasting plasma glucose: group 1, 205 +/- 19 vs. 153 +/- 20 (P less than 0.001); group 2, 214 +/- 11 vs. 160 +/- 13 (P less than 0.001)]. We conclude that 1) Met has an acute insulin-like effect in vitro independent of its ability to increase insulin binding; 2) Met acts in vivo predominantly at a postreceptor site to lower plasma glucose; 3) the glucose-lowering effect is independent of pretreatment insulin binding status; and 4) the increase in insulin binding after Met treatment in patients with NIDDM and low insulin binding occurs without changes in insulin concentrations.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3745404&dopt=Abstract
Paroi Arterielle. 1979 Dec;5(4):209-18.
Comparative effects of metformin and phenformin on the progression and regression of cholesterol induced athreosclerosis in rabbits.
Marquie G.
This work was undertaken to determine the comparative effects of metformin and phenformin on the development and the regression of atherosclerosis in cholesterol fed rabbits: 1. Both compounds reduced very significantly the elevated lipid content of plasma induced by a high cholesterol diet, they limited and sometimes suppressed the appearance of lipid deposits in the liver. Only metformin prevented the development of aortic and coronary lesions. 2. In rabbits fed a cholesterol enriched diet for a period of 2 months, followed by a normal diet during 12 months, both compounds accelerated the sponanteous regression of hyperlipidemia and of the excess lipids in the liver, observed in the corresponding controls. Only metformin promoted a marked elimination of arterial lipids and displayed a protective action against coronary atherosclerosis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=554975&dopt=Abstract
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