Drugs online research references
Pharmacol Toxicol. 1997 Jul;81(1):7-12.
Cardiovascular actions of chronic intracerebroventricular administration of metformin in normotensive rats.
Andersen D, Haugan K, Sorensen AM, Christensen S, Petersen JS.
Department of Pharmacology, Panum Institute, University of Copenhagen, Denmark.
Acute intracerebroventricular administration of the antihyperglycaemic agent metformin (0.25-1 mg) elicits sympathoinhibitory responses in spontaneously hypertensive rats. However, cardiovascular actions of chronic intracerebroventricular metformin administration are unknown. To define the dose-response relationship during chronic intracerebroventricular metformin administration, mean arterial pressure, heart rate, and locomotor activity were measured continuously by radiotelemetry in 40 normotensive rats. After a 10 day control period, an intracerebroventricular cannula was implanted and connected to an osmotic minipump which delivered metformin in the following doses: 0 [saline]. 0.01, 0.1, 1, and 10 mg/day. LD50 was 1.5 mg/day. Metformin, 1 mg/day attenuated the nocturnal, physiological increase in mean arterial pressure (-7.3 +/- 1.6% versus before metformin), produced behavioural changes and tended to increase locomotor activity. Lower doses of intracerebroventricular metformin (0.1 and 0.01 mg/day) did not affect mean arterial pressure, heart rate or locomotor activity. In conclusion, chronic intracerebroventricular administration of high dose metformin (1.0 mg/day) attenuates the nocturnal, physiological increase in mean arterial pressure. These findings are compatible with a toxic, sympathoinhibitory action of high doses of metformin intracerebroventricularly.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9258978&dopt=Abstract
Cytokine. 1998 Jan;10(1):66-9.
Metformin increases circulating tumour necrosis factor-alpha levels in non-obese non-diabetic patients with coronary heart disease.
Carlsen SM, Waage A, Grill V, Folling I.
Section of Endocrinology, University Hospital of Trondheim, Norway.
Metformin reduces insulin resistance and hyperinsulinaemia, as well as lipid levels and body weight. The mechanisms behind these effects are likely to involve intracellular insulin signalling. Recent evidence implicates tumour necrosis factor-alpha (TNF-alpha) as a modulatory factor on insulin resistance. The present investigation was undertaken to clarify whether metformin affects TNF-alpha and soluble TNF receptor levels. Sixty non-diabetic men with coronary heart disease were treated with diet and lifestyle advice and lovastatin 40 mg/day during a 4-week run-in period. During this period TNF-alpha and soluble TNF receptor p75 remained unchanged, whereas soluble TNF receptor p55 increased by 8% (P < 0.05). Twelve weeks of metformin treatment increased TNF-alpha by 33% (P < 0.05). This effect was restricted to non-obese patients in whom TNF-alpha increased by 68% (P < 0.01). Soluble TNF receptors p55 and p75 remained unchanged in the whole group, whereas soluble TNF receptor p55 increased by 11% (P < 0.05) in non-obese patients. Since metformin reduces insulin resistance both in obese and non-obese subjects but increases TNF-alpha levels only in the latter, it is concluded that the drug does not exert its effect on insulin resistance through regulation of circulating TNF-alpha levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9505147&dopt=Abstract
J Clin Endocrinol Metab. 1994 Mar;78(3):549-54.
Effects of a reduction in circulating insulin by metformin on serum dehydroepiandrosterone sulfate in nondiabetic men.
Nestler JE, Beer NA, Jakubowicz DJ, Beer RM.
Department of Internal Medicine, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
Evidence suggests that hyperinsulinemic insulin resistance may reduce serum levels of the adrenal steroid dehydroepiandrosterone (DHEA) sulfate in humans. This study was conducted to assess the influence of physiological concentrations of insulin on serum adrenal steroid levels by lowering circulating insulin in nondiabetic men through the administration of the biguanide metformin. A total of 28 nondiabetic men were studied. The study group consisted of 16 obese and hypertensive men, and the control group of 12 nonobese and normotensive men. The men were studied at baseline and after the oral administration of 500 mg metformin, 3 times daily, for 21 days. Metformin administration resulted in significant reductions in serum insulin levels and concurrent increases in serum DHEA sulfate levels in both groups of men. The mean fasting serum DHEA sulfate concentration rose by 48% in the obese hypertensive men (from 5.9 +/- 0.8 to 8.7 +/- 0.7 mumol/L; P < 0.02) and by 80% in the nonobese normotensive men (from 3.5 +/- 0.5 to 6.3 +/- 0.9 mumol/L; P < 0.05). When the results from both groups were combined, changes in serum DHEA sulfate levels (i.e. day 21 value minus day 0 value) correlated positively with baseline fasting serum insulin levels (r = 0.44; P = 0.02; n = 28). Moreover, changes in fasting serum DHEA sulfate levels correlated inversely with changes in fasting serum insulin levels (r = -0.38; P < 0.05; n = 28). These findings lend further credence to the idea that insulin acts as a physiological regulator of DHEA sulfate metabolism and lowers circulating DHEA sulfate concentrations in men.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8126125&dopt=Abstract
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