Drugs online research references
Res Commun Chem Pathol Pharmacol. 1981 Jul;33(1):21-31.
Metformin-induced lactic acidosis: potentiation by ethanol.
Dubas TC, Johnson WJ.
Although lactic acidosis has been recognized as a potential hazard in biguanide therapy, this complication has been claimed to be extremely rare with dimethylbiguanide (DMBG) (metformin). In the present studies, using the fasted guinea pig, DMBG (125-500 mg/kg i.p.) caused marked dose-related changes in both plasma glucose (43-88% reduction) and blood lactate (3.5-13 fold increase). Lactate/pyruvate ratios were substantially increased. While i.p. doses of 100 mg/kg of DMBG or of 1 g/kg of ethanol produced no changes in plasma glucose, lactate or pyruvate, the two drugs administered conjointly at the indicated doses produced a 53% decrease in plasma glucose and 2 and 10-fold increases in pyruvate and lactate levels respectively, and correspondingly, an increase in the lactate/pyruvate ratio. Ethanol decay curves indicated that DMBG did not significantly influence the disappearance of ethanol from the blood. These results indicate that: (1) doses of DMBG which produce hypoglycemia are associated with lactic acidosis, and (2) this effect of DMBG can be markedly potentiated by ethanol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7268205&dopt=Abstract
Diabet Med. 1998 Apr;15(4):290-6.
Beta-cell deterioration determines the onset and rate of progression of secondary dietary failure in type 2 diabetes mellitus: the 10-year follow-up of the Belfast Diet Study.
Levy J, Atkinson AB, Bell PM, McCance DR, Hadden DR.
Diabetes Research Laboratories, Radcliffe Infirmary, Oxford, UK.
Secondary failure of plasma glucose control following initial successful response to diet therapy may be due to dietary indiscretion, or to progression of the intrinsic diabetic condition. We report a 10-year prospective natural history study of 432 newly diagnosed diabetic patients aged 40-69 years undertaken to assess the effect of intensive dietary management, where patients were transferred to insulin, or oral hypoglycaemic therapy (tolbutamide, metformin) by predetermined criteria of weight and plasma glucose. Secondary failure to diet therapy occurred in 41 patients in years 2-4, 67 patients in years 5-7, and 51 patients in years 8-10; 173 patients remained on diet alone until death or the end of the study. Continuation on diet alone was associated with a lower ongoing fasting plasma glucose, greater beta-cell function assessed by an oral glucose tolerance test at 6 months, and increasing age. The rate of rise of fasting plasma glucose was inversely related to the duration of successful dietary therapy, but mean weight remained constant in all groups while on diet alone. The ongoing fall in beta-cell function assessed by HOMA modelling closely mirrored the progressive rise in fasting plasma glucose: there was no change in mean insulin sensitivity in any of the groups.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9585393&dopt=Abstract
Biochem Pharmacol. 1998 Nov 1;56(9):1145-50.
Prevention of dexamethasone-induced insulin resistance by metformin.
Thomas CR, Turner SL, Jefferson WH, Bailey CJ.
Department of Medicine, ST. Thomas' Hospital, London, UK.
This study investigates the effect of the antidiabetic drug metformin on dexamethasone-induced hyperglycaemia and insulin resistance in mice. Normal mice were treated with dexamethasone (2.5 mg/kg/day p.o.) plus metformin (250 mg/kg/day p.o.) and pair-fed to those receiving dexamethasone alone. Metformin reduced the extent of dexamethasone-induced hyperglycaemia and decreased insulin resistance as indicated by an improved insulin-hypoglycaemia test. Metformin-treated mice also showed increased basal glucose uptake into isolated diaphragm (by 38%), soleus (by 19%) and deep (red) quadriceps (by 31%). Measurements in the quadriceps showed that the increase in glucose uptake occurred without increasing either the mRNA levels or total cellular membrane abundance of the GLUT1 or GLUT4 glucose transporter isoforms. Thus metformin can ameliorate dexamethasone-induced hyperglycaemia and insulin resistance in part by increasing glucose disposal into skeletal muscle. Since this was achieved in quadriceps muscle without increasing mRNA or total membrane abundance of GLUT1 or GLUT4, it is possible that metformin might influence the intrinsic activity of glucose transporters, as well as altering their intracellular translocation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9802324&dopt=Abstract
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