Heterozygous variants of multidrug and toxin extrusions (MATE1 and MATE2-K) have little influence on the disposition of metformin in diabetic patients
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Scheen, 1996, Clinical pharmacokinetics of metformin, Clin Pharmacokinet, 30, 359, 10.2165/00003088-199630050-00003
Terada, 2008, Physiological and pharmacokinetic roles of H+/organic cation antiporters (MATE/SLC47A), Biochem Pharmacol, 75, 1689, 10.1016/j.bcp.2007.12.008
Takane, 2008, Polymorphism in human organic cation transporters and metformin action, Pharmacogenomics, 9, 415, 10.2217/14622416.9.4.415
Tsuda, 2009, Targeted disruption of the multidrug and toxin extrusion 1 (Mate1) gene in mice reduces renal secretion of metformin, Mol Pharmacol, 75, 1280, 10.1124/mol.109.056242
Kajiwara, 2009, Identification of multidrug and toxin extrusion (MATE1 and MATE2-K) variants with complete loss of transport activity, J Hum Genet, 54, 40, 10.1038/jhg.2008.1
Chen, 2009, Genetic variants in multidrug and toxic compound extrusion-1, hMATE1, alter transport function, Pharmacogenomics J, 9, 127, 10.1038/tpj.2008.19
Becker, 2009, Genetic variation in the multidrug and toxin extrusion 1 transporter protein influences the glucose-lowering effect of metformin in patients with diabetes: a preliminary study, Diabetes, 58, 745, 10.2337/db08-1028
Tzvetkov, 2009, The effects of genetic polymorphisms in the organic cation transporters OCT1, OCT2, and OCT3 on the renal clearance of metformin, Clin Pharmacol Ther, 86, 299, 10.1038/clpt.2009.92
Sparreboom, 2004, Diflomotecan pharmacokinetics in relation to ABCG2 421C>A genotype, Clin Pharmacol Ther, 76, 38, 10.1016/j.clpt.2004.03.003