Drugs online research references
Rev Invest Clin. 1992 Jan-Mar;44(1):71-6.
Combination daytime chlorpropamide-metformin/bedtime insulin in the treatment of secondary failures in non insulin dependent diabetes.
Aguilar CA, Wong B, Gomez-Perez FJ, Rull JA.
Departamento de Diabetes y Metabolismo de Lipidos, Instituto Nacional de la Nutricion Salvador Zubiran, Mexico, D.F.
OBJECTIVES. To determine the effectiveness of the combination therapy with daytime chlorpropamide-metformin and bedtime NPH insulin in the treatment of secondary failures in NIDDM and to study its effects on insulin secretion. DESIGN. Non randomized open study with a duration of two months. The patients were followed six months after ending the study. INSTITUTION. Department of Diabetes and Lipid Metabolism. Instituto Nacional de la Nutricion "Salvador Zubiran", Mexico City. CHARACTERISTICS OF THE PATIENTS. Nine patients (seven women and two men) were included. All had NIDDM and secondary failure to antidiabetic oral drugs. Their fasting plasma glucose was 14.5 +/- 2 mM/L and their HbA1c 13.37 +/- 2.9%. At the entry and at the end of the study a 5h-OGTT was done with assays of plasma glucose and C-peptide. TREATMENT. Chlorpropamide (375 mg/day) plus metformin (1200 mg/day) and bedtime insulin (0.1 U/kg/day). RESULTS. After two months on combination therapy, fasting plasma glucose and HbA1c levels were remarkably improved (decreases of 7.3 +/- 0.6 and 9.1 +/- 1.02 respectively, p less than 0.002). The insulin dose was small (6.77 +/- 2.09 U/day). Side effects were minimal and infrequent. During the 5h-OGTT, the mean glucose area under the curve also decreased. The insulin secretion did not change but the C-peptide/glucose ratio increased. At the end of the study, the insulin dose was tapered off and stopped when possible. The four patients with the best glycemic control during the study were able to suspend the bedtime insulin and maintain a good control six months after the insulin suspension. CONCLUSIONS. The combination therapy is useful in the treatment of secondary failures in NIDDM. Its advantages are the very low mean daily insulin dose needed, the low incidence of side effects and, if a HbA1c less than 8.7% is achieved, the restoration of oral antidiabetic drugs efficacy. The very low insulin dose used in this study could be explained by complementary effects of metformin and bedtime insulin on hepatic glucose output and a putative decrease in peripheral resistance attributable both to sulfonylurea and metformin.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1523352&dopt=Abstract
Chem Phys Lipids. 1992 Oct;62(3):229-37.
On the mechanism of cholesterol interaction with apolipoproteins A-I and E.
Klimov AN, Kozhevnikova KA, Klueva NN, Belova EV.
Department of Biochemistry, Institute of Experimental Medicine of the Russian Academy of Medical Sciences, St. Petersburg.
It is shown that cholesterol may interact with some substances containing the guanidine group (guanidine itself, arginine, metformin and dodecylguanidine bromide) and with arginine-rich proteins--apoproteins A-I and E. In the latter case the interaction produces the formation of cholesterol-apoprotein complexes. Analysis of such complexes has shown that one apo A-I molecule binds 17-22 and one apo E molecule binds 30-35 sterol molecules, which approximately corresponds to the amount of arginine residues in these proteins. Formation of cholesterol-apoprotein complexes has been suggested to occur due to: (1) formation of hydrogen bond and/or ion-dipole interaction between cholesterol hydroxyl and guanidine groups of the apoprotein arginine residues and (2) hydrophobic interaction of the cholesterol aliphatic chain with nonpolar side chains of the amino acids occupying the third position from arginine in the protein molecule.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1468123&dopt=Abstract
J Pharmacol Exp Ther. 1997 May;281(2):618-23.
Effects of adrenergic, cholinergic and ganglionic blockade on acute depressor responses to metformin in spontaneously hypertensive rats.
Muntzel MS, Abe A, Petersen JS.
Department of Biological Sciences, Lehman College, Bronx, New York, USA.
Metformin lowers blood pressure in humans and in experimental animal models. To determine the mechanism of acute metformin-induced hypotension, we measured changes in mean arterial pressure (MAP) and heart rate (HR) during metformin alone (0, 10, 50, 100 mg/kg i.v.; n = 10) and during concomitant alpha adrenergic (phentolamine, 5 mg/kg; n = 5), beta adrenergic (propranolol, 3 mg/kg; n = 6), muscarinic (atropine, 200 micrograms/kg; n = 7), ganglionic (hexamethonium, 30 mg/kg; n = 11), nitric oxide synthase (NG-methyl-L-arginine acetate salt, 15 mg/ kg; n = 9) and combination ganglionic plus alpha adrenergic plus beta adrenergic (n = 6) blockade in spontaneously hypertensive rats (SHR). Responses to metformin alone were also assessed in normotensive Wistar-Kyoto rats (n = 6). In SHRs, metformin elicited depressor responses accompanied by tachycardia (100 mg/kg; delta MAP, -26 +/- 3 mm Hg; delta HR, +49 +/- 12 bpm). Depressor responses in Wistar-Kyoto rats were significantly attenuated (100 mg/kg; delta MAP, -9 +/- 4 mm Hg; P < .01). Hypotensive actions of metformin in SHRs were abolished and reversed into pressor responses by hexamethonium (100 mg/kg; delta MAP, +24 +/- 6 mm Hg), phentolamine (100 mg/kg; delta MAP, +62 +/- 10 mm Hg) and by combination ganglionic plus adrenergic (100 mg/kg; delta MAP, +62 +/- 10 mm Hg) blockade. Neither propranolol, atropine nor NG-methyl-L-arginine acetate salt affected hypotensive responses to metformin. We conclude that acute intravenous metformin administration decreases MAP by causing withdrawal of sympathetic activity. The increase in MAP uncovered by hexamethonium and phentolamine suggests that the original depressor response to metformin is buffered by mechanisms unrelated to the autonomic nervous system.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9152364&dopt=Abstract
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