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Daniels, M.A.* ; Kan, C.* ; Willmes, D.M. ; Ismail, K.* ; Pistrosch, F. ; Hopkins, D.* ; Mingrone, G.* ; Bornstein, S.R. ; Birkenfeld, A.L.

Pharmacogenomics in type 2 diabetes: Oral antidiabetic drugs.

Pharmacogenomics J. 16, 399-410 (2016)
Verlagsversion DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Type 2 diabetes mellitus (T2DM) is a fast progressing disease reaching pandemic proportions. T2DM is specifically harmful because of its severe secondary complications. In the course of the disease, most patients require treatment with oral antidiabetic drugs (OADs), for which a relatively large number of different options are available. The growing number of individuals affected by T2DM as well as marked interindividual differences in the response to treatment call for individualized therapeutic regimens that can maximize treatment efficacy and thus reduce side effects and costs. A large number of genetic polymorphisms have been described affecting the response to treatment with OADs; in this review, we summarize the most recent advances in this area of research. Extensive evidence exists for polymorphisms affecting pharmacokinetics and pharmacodynamics of biguanides and sulfonylureas. Data on incretin-based medications as well as the new class of sodium/glucose cotransporter 2 (SGLT2) inhibitors are just starting to emerge. With diabetes being a known comorbidity of several psychiatric disorders, we also review genetic polymorphisms possibly responsible for a common treatment response in both conditions. For all drug classes reviewed here, large prospective trials are necessary in order to consolidate the existing evidence and derive treatment schemes based on individual genetic traits.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Organic Cation Transporter-2; Transcription-factor-7-like-2 Tcf7l2 Gene; Single Nucleotide Polymorphisms; Glycosylated Hemoglobin A1c; Iranian Population Relation; Genome-wide Association; Insulin-resistance; Therapeutic Response; Ppar-gamma; Rosiglitazone Response
ISSN (print) / ISBN 1470-269X
e-ISSN 1473-1150
Quellenangaben Band: 16, Heft: 5, Seiten: 399-410 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)