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The pharmacogenetics of metformin and its impact on plasma metformin steady-state levels and glycosylated hemoglobin A1c
University of So Denmark.
Odense University Hospital.
Linköpings universitet, Institutionen för medicin och hälsa, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
University of So Denmark.
Vise andre og tillknytning
2011 (engelsk)Inngår i: Pharmacogenetics & Genomics, ISSN 1744-6872, E-ISSN 1744-6880, Vol. 21, nr 12, s. 837-850Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective The aim of this study was to evaluate the effect of genetic variations in OCT1, OCT2, MATE1, MATE 2, and PMAT on the trough steady-state plasma concentration of metformin and hemoglobin A1c (Hb1Ac). less thanbrgreater than less thanbrgreater thanMethod The South Danish Diabetes Study was a 2 x 2 x 2 factorial, prospective, randomized, double-blind, placebo-controlled, multicentre study. One hundred and fifty-nine patients received 1 g of metformin, twice daily continuously, and 415 repeated plasma metformin measurements were obtained after 3, 6, and 9 months of treatment. less thanbrgreater than less thanbrgreater thanResults The mean trough steady-state metformin plasma concentration was estimated to be 576 ng/ml (range, 54-4133 ng/ml, rho = 0.55) and correlated to the number of reduced function alleles in OCT1 (none, one or two: 642, 542, 397 ng/ml; P = 0.001). The absolute decrease in Hb1Ac both initially and long term was also correlated to the number of reduced function alleles in OCT1 resulting in diminished pharmacodynamic effect of metformin after 6 and 24 months. less thanbrgreater than less thanbrgreater thanConclusion In a large cohort of type 2 diabetics, we either confirm or show for the first time: (a) an enormous 80-fold) variability in trough steady-state metformin plasma concentration, (b) OCT1 activity affects metformin steady-state pharmacokinetics, and (c) OCT1 genotype has a bearing on HbA1c during metformin treatment.

sted, utgiver, år, opplag, sider
Lippincott, Williams and Wilkins , 2011. Vol. 21, nr 12, s. 837-850
Emneord [en]
MATE1, MATE2, metformin, OCT1, OCT2, personalized medicine, pharmacogenetics, PMAT, steady state, type 2 diabetes
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Identifikatorer
URN: urn:nbn:se:liu:diva-72648DOI: 10.1097/FPC.0b013e32834c0010ISI: 000296799900008OAI: oai:DiVA.org:liu-72648DiVA, id: diva2:461148
Merknad
Funding Agencies|A.J. Andersen og Hustrus Fond|01737-0005|A.P. Moeller Foundation for the Advancement of Medical Science|09034|Region of Southern Denmark|09/12913|Tilgjengelig fra: 2011-12-02 Laget: 2011-12-02 Sist oppdatert: 2017-12-08

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