Literature DB >> 27555891

Pharmacogenetic studies update in type 2 diabetes mellitus.

Shalini Singh1, Kauser Usman1, Monisha Banerjee1.   

Abstract

Type 2 diabetes mellitus (T2DM) is a silent progressive polygenic metabolic disorder resulting from ineffective insulin cascading in the body. World-wide, about 415 million people are suffering from T2DM with a projected rise to 642 million in 2040. T2DM is treated with several classes of oral antidiabetic drugs (OADs) viz. biguanides, sulfonylureas, thiazolidinediones, meglitinides, etc. Treatment strategies for T2DM are to minimize long-term micro and macro vascular complications by achieving an optimized glycemic control. Genetic variations in the human genome not only disclose the risk of T2DM development but also predict the personalized response to drug therapy. Inter-individual variability in response to OADs is due to polymorphisms in genes encoding drug receptors, transporters, and metabolizing enzymes for example, genetic variants in solute carrier transporters (SLC22A1, SLC22A2, SLC22A3, SLC47A1 and SLC47A2) are actively involved in glycemic/HbA1c management of metformin. In addition, CYP gene encoding Cytochrome P450 enzymes also play a crucial role with respect to metabolism of drugs. Pharmacogenetic studies provide insights on the relationship between individual genetic variants and variable therapeutic outcomes of various OADs. Clinical utility of pharmacogenetic study is to predict the therapeutic dose of various OADs on individual basis. Pharmacogenetics therefore, is a step towards personalized medicine which will greatly improve the efficacy of diabetes treatment.

Entities:  

Keywords:  Genetic variants; Oral antidiabetic drugs; Personalized medicine; Pharmacogenetics; Type 2 diabetes mellitus

Year:  2016        PMID: 27555891      PMCID: PMC4980637          DOI: 10.4239/wjd.v7.i15.302

Source DB:  PubMed          Journal:  World J Diabetes        ISSN: 1948-9358


  143 in total

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10.  Heparin impairs skeletal muscle glucose uptake by inhibiting insulin binding to insulin receptor.

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