Drugs online research references
Clin Ter. 1992 Dec;141(12):483-92.
[Median-term (4 months) treatment with glibenclamide + metformin substituting for glibenclamide + fenformin lowers the lacticemia levels in type-2 diabetics (NIDDM)]
[Article in Italian]
Velussi M, Cernigoi AM, Viezzoli L, Caffau C.
Centro Antidiabetico, Presidio Ospedaliero di Monfalcone.
60 NIDDM patients, mean age (68 +/- 3 years), BMI (25 +/- 5.1 kg/m2), fasting blood glucose (FG) (170 +/- 10 mg/dl), mean daily blood glucose (MDBG) (180 +/- 10 mg/dl), daily glycosuria (GLU) (15.6 +/- 9 g/24 hours), HbA1c (7.9 +/- 0.6%), basal (1.2 +/- 0.2 ng/ml) and stimulated (3.89 +/- 1.3 mg/ml) C peptide (CP) treated by ASS (7.5 +/- 75 mg), after a strict 4 months follow-up period, were assigned to G + M treatment (7.5 +/- 1.500 mg) during a 4 months period. During G+M treatment FG (171 +/- 13 at t0 to 165 +/- 11 mg/dl: p < 0.01 at t4) varied significantly. MDBG (180 +/- 10 at t0 to 175 +/- 12 mg/dl at t4:p < 0.05), GLU (16 +/- 9 at t0 to 11 + 6 g/24 hours at t4; p < 0.01), HbA1c (8.1 +/- 0.4 at t0 to 7.6 +/- 0.3% at t4; p < 0.01). Basal CP remained unchanged in G+M period and varied significantly during ASS period (1.3 +/- 0.3 ng/ml at t4; p < 0.01) and stimulated CP (unchanged during ASS) was reduced during G+M (4.19 +/- 0.4 to 4.04; p < 0.05). Highly significant variations were observed for LAC (28.4 +/- 2.1 at t0 to 14.9 +/- 0.6 mg/dl: p < 0.01 during G+M treatment). G+M therapy was found to be more effective and safer than ASS therapy in regard to glucose metabolism and lactate production in a selected group of NIDDM patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1493670&dopt=Abstract
Diabetologia. 1980 Aug;19(2):93-6.
The effect of metformin treatment on gastric acid secretion and gastrointestinal hormone levels in normal subjects.
Molloy AM, Ardill J, Tomkin GH.
Gastric acid secretion and gastrointestinal hormone levels were measured in healthy non-diabetic subjects after metformin treatment (1.5 g/day). The maximum acid output was increased from 15.7 +/- 3.9 mmol/h (mean +/- SEM) to 30.0 +/- 7.1 mmol/h (p < 0.05) and the peak acid output was increased from 16.4 +/- 4.1 mmol/h to 31.7 +/- 7.2 mmol/h (p < 0.05) after two weeks treatment. Serum insulin, gastric inhibitory polypeptide and secretin levels were normal. After treatment for one week, however, there was a significant increase in fasting vasoactive intestinal peptide (VIP) from 83 +/- 6 ng/1 to 102 +/- 9 ng/1 (p < 0.02) and in stimulated VIP from 58 +/- 5 ng/1 to 79 +/- 5 ng/1 (p < 0.05). Stimulated glucagon-like immunoreactivity (GLI) was also increased from 82 +/- 10 ng/1 to 174 +/- 24 ng/1 (p < 0.01) after one week's treatment. It is suggested that metformin acts as a weak histamine agonist.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7418969&dopt=Abstract
Acta Diabetol Lat. 1990 Apr-Jun;27(2):139-55.
Low dose metformin in the treatment of type II non-insulin-dependent diabetes: clinical and metabolic evaluations.
Gregorio F, Ambrosi F, Marchetti P, Cristallini S, Navalesi R, Brunetti P, Filipponi P.
Cattedra di Malattie del Ricambio, Universita di Perugia, Italy.
Low doses of metformin (500 mg twice daily) were administered to 20 diabetic patients, combined with the original sulfonylurea treatment which had become ineffective even at full dosage. After 1 and 5 weeks, the effects of the drug on glycemic control, blood intermediate metabolites and monocyte insulin receptors were monitored. Metformin clearly improved glycemic control by reducing both fasting blood glucose from 189.88 +/- 21.11 mg/dl to 131.12 +/- 16.02 mg/dl after 1 week and to 130.11 +/- 13.29 mg/dl after 5 weeks (p less than 0.025 both after 1 and 5 weeks); the diurnal blood glucose average fell from 235.33 +/- 24.11 mg/dl to 174.66 +/- 23.45 mg/dl (p less than 0.0025) after 1 week and to 177.65 +/- 21.71 mg/dl (p less than 0.0005) after 5 weeks. Consequently both blood glycosylated hemoglobin (p = n.s. after 1 week, p less than 0.025 after 5 weeks) and serum fructosamine (p less than 0.0025 after both 1 and 5 weeks) also decreased after metformin treatment. No change in plasma insulin and C-peptide levels was reported and no modification in diurnal rhythms of blood lactate, pyruvate, alanine glycerol and beta-OH-butyrate was detected at any time during metformin treatment. All the changes documented in the binding values were already complete at the end of the first week; insulin binding to monocytes increased slightly but significantly (p less than 0.05) and the number of receptors per cell rose (p less than 0.05) but could not be correlated to any index of glycemic control. These data suggest that the antidiabetic action of metformin is neither related to its lactate-increasing activity nor does it depend upon its inducing an increase in insulin binding values. This metformin-related hypoglycemic effect might be the result, at least in part, of a reduced oxidative phosphorylation without inhibition of hepatic gluconeogenesis and/or of decreased hepatic glucose output. Moreover, our data are also consistent with the hypothesis that metformin might affect insulin action at a post-receptor level.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2198745&dopt=Abstract
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