Pharmacogenetics in type 2 diabetes: Influence on response to oral hypoglycemic agents

Pharmacogenomics and Personalized Medicine

Volumn 9, Issue , 2016, Pages 17-29

  Dawed, Adem Yesuf ^a   Zhou, Kaixin ^a   Pearson, Ewan Robert ^a  

^a UNIVERSITY OF DUNDEE   (United Kingdom)

Author keywords

Oral hypoglycemic agents; Pharmacodynamics; Pharmacogenetics; Pharmacokinetics; Response; Type 2 diabetes

Indexed keywords

GLITAZONE DERIVATIVE; HEMOGLOBIN A1C; INCRETIN; METFORMIN; MITIGLINIDE; ORAL ANTIDIABETIC AGENT; SULFONYLUREA DERIVATIVE;

ANTIDIABETIC ACTIVITY; CATALYSIS; DRUG ABSORPTION; DRUG EFFICACY; DRUG METABOLISM; GASTROINTESTINAL TOXICITY; GENETIC ASSOCIATION; GENETIC POLYMORPHISM; GENETIC VARIABILITY; GENOTYPE; HEMOGLOBIN BLOOD LEVEL; HUMAN; HYDROPHILICITY; INSULIN RELEASE; LIFESTYLE; LIFESTYLE MODIFICATION; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PHARMACODYNAMICS; PHARMACOGENETICS; PHENOTYPE; REVIEW; SINGLE NUCLEOTIDE POLYMORPHISM;

EID: 84963654003     PISSN: None     EISSN: 11787066     Source Type: Journal    
DOI: 10.2147/PGPM.S84854     Document Type: Review

References (117)

1. Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res Clin Pract. 2010;87(1):4-14.
2. International Diabetes Federation (IDF). IDF Diabetes Atlas. 6th ed. Brussels: International Diabetes Federation; 2013.
3. Casagrande SS, Fradkin JE, Saydah SH, Rust KF, Cowie CC. The prevalence of meeting A1C, blood pressure, and LDL goals among people with diabetes, 1988-2010. Diabetes Care. 2013;36(8):2271-2279.
4. Becker ML, Pearson ER, Tká I. Pharmacogenetics of oral antidiabetic drugs. Int J Endocrinol. 2013;2013:686315.
5. DeFronzo RA, Stonehouse AH, Han J, Wintle ME. Relationship of baseline HbA1c and efficacy of current glucose-lowering therapies: a meta-analysis of randomized clinical trials. Diabetic Med. 2010;27(3):309-317.
6. Ho PM, Rumsfeld JS, Masoudi FA, et al. Effect of medication nonadherence on hospitalization and mortality among patients with diabetes mellitus. Arch Intern Med. 2006;166(17):1836-1841.
7. Zhou K, Donnelly L, Yang J, et al. Heritability of variation in glycaemic response to metformin: a genome-wide complex trait analysis. Lancet Diabetes Endocrinol. 2014;2(6):481-487.
8. Zhou K, Bellenguez C, Spencer CC, et al. Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes. Nat Genet. 2011;43(2):117-120.
9. Vella A. Pharmacogenetics for type 2 diabetes: practical considerations for study design. J Diabetes Sci Technol. 2009;3(4):705-709.
10. Watanabe I, Tomita A, Shimizu M, et al. A study to survey susceptible genetic factors responsible for troglitazone-associated hepatotoxicity in Japanese patients with type 2 diabetes mellitus. Clin Pharmacol Ther. 2003;73(5):435-455.
11. Kumashiro R, Kubota T, Koga Y, et al. Association of troglitazone-induced liver injury with mutation of the cytochrome P450 2C19 gene. Hepatol Res. 2003;26(4):337-342.
12. Donnelly LA, Doney AS, Hattersley AT, Morris AD, Pearson ER. The effect of obesity on glycaemic response to metformin or sulphonylureas in Type 2 diabetes. Diabet Med. 2006;23(2):128-133.
13. Ong CR, Molyneaux LM, Constantino MI, Twigg SM, Yue DK. Long-term efficacy of metformin therapy in nonobese individuals with type 2 diabetes. Diabetes Care. 2006;29(11):2361-2364.
14. Miyazaki Y, De Filippis E, Bajaj M, Wajcberg E, Glass LC, Triplitt C. Predictors of improved glycemic control with rosiglitazone therapy in type 2 diabetic patients: a practical approach for the primary care physician. Br J Diabetes Vasc Dis. 2005;5:28-35.
15. Kim YM, Cha BS, Kim DJ, et al. Predictive clinical parameters for therapeutic efficacy of rosiglitazone in Korean type 2 diabetes mellitus. Diabetes Res Clin Pract. 2005;67:43-52.
16. Scheen AJ. Drug interactions of clinical importance with antihyperglycaemic agents: an update. Drug Saf. 2005;28(7):601-631.
17. Dujic T, Zhou K, Donnelly LA, Tavendale R, Palmer CN, Pearson ER. Association of organic cation transporter 1 with intolerance to metformin in type 2 diabetes: a GoDARTS Study. Diabetes. 2015;64(5):1786-1793.
18. Niemi M, Backman JT, Neuvonen M, Neuvonen PJ. Effects of gemfibrozil, itraconazole, and their combination on the pharmacokinetics and pharmacodynamics of repaglinide: potentially hazardous interaction between gemfibrozil and repaglinide. Diabetologia. 2003;46:347-351.
19. Goswami S, Yee SW, Stocker S, et al. Genetic variants in transcription factors are associated with the pharmacokinetics and pharmacodynamics of metformin. Clin Pharmacol Ther. 2014;96(3):370-379.
20. DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med. 1999;131(4):281-303.
21. Han TH, Everett RS, Proctor WR, et al. Organic cation transporter 1 (OCT1/mOct1) is localized in the apical membrane of Caco-2 cell monolayers and enterocytes. Mol Pharmacol. 2013;84(2):182-189.
22. Han TK, Proctor WR, Costales CL, Cai H, Everett RS, Thakker DR. Four cation-selective transporters contribute to apical uptake and accumulation of metformin in Caco-2 cell monolayers. J Pharmacol Exp Ther. 2015;352(3):519-528.
23. Müller J, Lips KS, Metzner L, Neubert RH, Koepsell H, Brandsch M. Drug specificity and intestinal membrane localization of human organic cation transporters (OCT). Biochem Pharmacol. 2005;70(12):1851-1860.
24. Graham GG, Punt J, Arora M, et al. Clinical pharmacokinetics of metformin. Clin Pharmacokinet. 2011;50(2):81-98.
25. Kimura N, Masuda S, Tanihara Y, et al. Metformin is a superior substrate for renal organic cation transporter OCT2 rather than hepatic OCT1. Drug Metab Pharmacokinet. 2005;20(5): 379-386.
26. Otsuka M, Matsumoto T, Morimoto R, Arioka S, Omote H, Moriyama Y. A human transporter protein that mediates the final excretion step for toxic organic cations. Proc Natl Acad Sci USA. 2005;102(50):17923-17928.
27. Pernicova I, Korbonits M. Metformin-mode of action and clinical implications for diabetes and cancer. Nat Rev Endocrinol. 2014;10(3):143-156.
28. Foretz M, Hébrard S, Leclerc J, et al. Metformin inhibits hepatic gluconeogenesis in mice independently of the LKB1/AMPK pathway via a decrease in hepatic energy state. J Clin Invest. 2010;120(7):2355-2369.
29. Miller RA, Chu Q, Xie J, Foretz M, Viollet B, Birnbaum MJ. Biguanides suppress hepatic glucagon signalling by decreasing production of cyclic AMP. Nature. 2013;494(7436):256-260.
30. Madiraju AK, Erion DM, Rahimi Y, et al. Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase. Nature. 2014;510(7506):542-546.
31. Maruthur NM, Gribble MO, Bennett WL, et al. The pharmacogenetics of type 2 diabetes: a systematic review. Diabetes Care. 2014;37:876-886.
32. Nies AT, Koepsell H, Damme K, Schwab M. Organic cation transporters (OCTs, MATEs), in vitro and in vivo evidence for the importance in drug therapy. Handb Exp Pharmacol. 2011;(201): 105-167.
33. Tzvetkov MV, Vormfelde SV, Balen D, et al. The effects of genetic polymorphisms in the organic cation transporters OCT1, OCT2, and OCT3 on the renal clearance of metformin. Clin Pharmacol Ther. 2009;86(3):299-306.
34. Christensen MM, Brasch-Andersen C, Green H, et al. The pharmacogenetics of metformin and its impact on plasma metformin steady-state levels and glycosylated hemoglobin A1c. Pharmacogenet Genomics. 2011;21(12):837-850. [Erratum in Pharmacogenet Genomics. 2015;25(1):48-50].
35. Shu Y, Brown C, Castro RA, et al. Effect of genetic variation in the organic cation transporter 1, OCT1, on metformin pharmacokinetics. Clin Pharmacol Ther. 2008;83(2):273-280.
36. Zhou K, Donnelly LA, Kimber CH, et al. Reduced-function SLC22A1 polymorphisms encoding organic cation transporter 1 and glycemic response to metformin: a GoDARTs study. Diabetes. 2009;58(6):1434-1439.
37. Davis R, Giacomini K, Yee SW, Jenkins G, McCarty CA, Wilke RA. PS1-10: response to metformin and genetic variants of organic cation and multidrug and toxin extrusion transporters. Clin Med Res. 2010;8(3-4):191.
38. Becker ML, Visser LE, van Schaik RH, Hofman A, Uitterlinden AG, Stricker BH. Genetic variation in the organic cation transporter 1 is associated with metformin response in patients with diabetes mellitus. Pharmacogenomics J. 2009;9(4):242-247.
39. Jablonski KA, McAteer JB, de Bakker PI, et al; Diabetes Prevention Program Research Group. Common variants in 40 genes assessed for diabetes incidence and response to metformin and lifestyle intervention in the diabetes prevention program. Diabetes. 2010;59(10): 2672-2681.
40. Tarasova L, Kalnina I, Geldnere K, et al. Association of genetic variation in the organic cation transporters OCT1, OCT2 and multidrug and toxin extrusion 1 transporter protein genes with the gastrointestinal side effects and lower BMI in metformin-treated type 2 diabetes patients. Pharmacogenet Genomics. 2012;22(9):659-666.
41. Song IS, Shin HJ, Shim EJ, et al. Genetic variants of the organic cation transporter 2 influence the disposition of metformin. Clin Pharmacol Ther. 2008;84(5):559-562.
42. Shikata E, Yamamoto R, Takane H, et al. Human organic cation transporter (OCT1 and OCT2) gene polymorphisms and therapeutic effects of metformin. J Hum Genet. 2007;52(2):117-122.
43. Hou W, Zhang D, Lu W, et al. Polymorphism of organic cation transporter 2 improves glucose-lowering effect of metformin via influencing its pharmacokinetics in Chinese type 2 diabetic patients. Mol Diagn Ther. 2015;19(1):25-33.
44. Chen Y, Li S, Brown C, et al. Effect of genetic variation in the organic cation transporter 2 on the renal elimination of metformin. Pharmacogenet Genomics. 2009;19(7):497-504.
45. Christensen MM, Pedersen RS, Stage TB, et al. A gene-gene interaction between polymorphisms in the OCT2 and MATE1 genes influences the renal clearance of metformin. Pharmacogenet Genomics. 2013;23(10):526-534.
46. Kajiwara M, Terada T, Ogasawara K, et al. Identification of multidrug and toxin extrusion (MATE1 and MATE2-K) variants with complete loss of transport activity. J Hum Genet. 2009;54(1):40-46.
47. Choi JH, Yee SW, Ramirez AH, et al. A common 5'-UTR variant in MATE2-K is associated with poor response to metformin. Clin Pharmacol Ther. 2011;90(5):674-684.
48. He R, Zhang D, Lu W, et al. SLC47A1 gene rs2289669 G. A variants enhance the glucose-lowering effect of metformin via delaying its excretion in Chinese type 2 diabetes patients. Diabetes Res Clin Pract. 2015;109(1):57-63.
49. Tká I, Klimáková L, Javorský M, et al. Pharmacogenomic association between a variant in SLC47A1 gene and therapeutic response to metformin in type 2 diabetes. Diabetes Obes Metab. 2013;15(2): 189-191.
50. Becker ML, Visser LE, van Schaik RH, Hofman A, Uitterlinden AG, Stricker BH. 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. 2009;58(3):745-749.
51. Stocker SL, Morrissey KM, Yee SW, et al. The effect of novel promoter variants in MATE1 and MATE2 on the pharmacokinetics and pharmacodynamics of metformin. Clin Pharmacol Ther. 2013;93(2): 186-194.
52. Becker ML, Visser LE, van Schaik RH, Hofman A, Uitterlinden AG, Stricker BH. Interaction between polymorphisms in the OCT1 and MATE1 transporter and metformin response. Pharmacogenet Genomics. 2010;20(1):38-44.
53. van Leeuwen N, Nijpels G, Becker ML, et al. A gene variant near ATM is significantly associated with metformin treatment response in type 2 diabetes: a replication and meta-analysis of five cohorts. Diabetologia. 2012;55(7):1971-1977.
54. Zhou Y, Guo Y, Ye W, et al. rs11212617 is associated with metformin treatment response in type 2 diabetes in Shanghai local Chinese population. Int J Clin Pract. 2014;68(12):1462-1466.
55. Florez JC, Jablonski KA, Taylor A, et al; Diabetes Prevention Program Research Group. The C allele of ATM rs11212617 does not associate with metformin response in the diabetes prevention program. Diabetes Care. 2012;35(9):1864-1867.
56. Desai NR, Shrank WH, Fischer MA, et al. Patterns of medication initiation in newly diagnosed diabetes mellitus: quality and cost implications. Am J Med. 2012;125(3):302.e1-302.e7.
57. Kirchheiner J, Roots I, Goldammer M, et al. Effect of genetic polymorphisms in cytochrome p450 (CYP) 2C9 and CYP2C8 on the pharmacokinetics of oral antidiabetic drugs: clinical relevance. Clin Pharmacokinet. 2005;44(12):1209-1225.
58. Xu H, Murray M, McLachlan AJ. Influence of genetic polymorphisms on the pharmacokinetics and pharmacodynamics of sulfonylurea drugs. Curr Drug Metab. 2009;10:643-658.
59. Shyng S, Nichols CG. Octameric stoichiometry of the KATP channel complex. J Gen Physiol. 1997;110(6):655-664.
60. Goldstein JA. Clinical relevance of genetic polymorphisms in the human CYP2C subfamily. Br J Clin Pharmacol. 2001;52(4):349-355.
61. Kirchheiner J, Brockmöller J, Meineke I, et al. Impact of CYP2C9 amino acid polymorphisms on glyburide kinetics and on the insulin and glucose response in healthy volunteers. Clin Pharmacol Ther. 2002;71(4):286-296.
62. Yin OQ, Tomlinson B, Chow MS. CYP2C9, but not CYP2C19, polymorphisms affect the pharmacokinetics and pharmacodynamics of glyburide in Chinese subjects. Clin Pharmacol Ther. 2005;78(4): 370-377.
63. Shon JH, Yoon YR, Kim KA, et al. Effects of CYP2C19 and CYP2C9 genetic polymorphisms on the disposition of and blood glucose lowering response to tolbutamide in humans. Pharmacogenetics. 2002;12(2):111-119.
64. Wang R, Chen K, Wen SY, Li J, Wang SQ. Pharmacokinetics of glimepiride and cytochrome P450 2C9 genetic polymorphisms. Clin Pharmacol Ther. 2005;78(1):90-92.
65. Zhang Y, Si D, Chen X, et al. Influence of CYP2C9 and CYP2C19 genetic polymorphisms on pharmacokinetics of gliclazide MR in Chinese subjects. Br J Clin Pharmacol. 2007;64(1):67-74.
66. Zhou K, Donnelly L, Burch L, et al. Loss-of-function CYP2C9 variants improve therapeutic response to sulfonylureas in type 2 diabetes: a Go-DARTS study. Clin Pharmacol Ther. 2010;87(1):52-56.
67. Becker ML, Visser LE, Trienekens PH, Hofman A, van Schaik RH, Stricker BH. Cytochrome P450 2C9 *2 and *3 polymorphisms and the dose and effect of sulfonylurea in type II diabetes mellitus. Clin Pharmacol Ther. 2008;83(2):288-292.
68. Suzuki K, Yanagawa T, Shibasaki T, Kaniwa N, Hasegawa R, Tohkin M. Effect of CYP2C9 genetic polymorphisms on the efficacy and pharmacokinetics of glimepiride in subjects with type 2 diabetes. Diabetes Res Clin Pract. 2006;72(2):148-154.
69. Hattersley AT, Ashcroft FM. Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy. Diabetes. 2005;54(9):2503-2513.
70. Pearson ER, Flechtner I, Njølstad PR, et al; Neonatal Diabetes International Collaborative Group. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir62 mutations. N Engl J Med. 2006;355(5):467-477.
71. Lang VY, Fatehi M, Light PE. Pharmacogenomic analysis of ATP-sensitive potassium channels coexpressing the common type 2 diabetes risk variants E23K and S1369A. Pharmacogenet Genomics. 2012;22(3):206-214.
72. Zhang H, Liu X, Kuang H, Yi R, Xing H. Association of sulfonylurea receptor 1 genotype with therapeutic response to gliclazide in type 2 diabetes. Diabetes Res Clin Pract. 2007;77(1):58-61.
73. Feng Y, Mao G, Ren X, et al. Ser1369Ala variant in sulfonylurea receptor gene ABCC8 is associated with antidiabetic efficacy of gliclazide in Chinese type 2 diabetic patients. Diabetes Care. 2008;31(10):1939-1944.
74. Li Q, Chen M, Zhang R, et al. KCNJ11 E23K variant is associated with the therapeutic effect of sulphonylureas in Chinese type 2 diabetic patients. Clin Exp Pharmacol Physiol. 2014;41(10):748-754.
75. Javorsky M, Klimcakova L, Schroner Z, et al. KCNJ11 gene E23K variant and therapeutic response to sulfonylureas. Eur J Intern Med. 2012;23(3):245-249.
76. Gloyn AL, Hashim Y, Ashcroft SJ, et al; UK Prospective Diabetes Study (UKPDS 53). Association studies of variants in promoter and coding regions of beta-cell ATP-sensitive K-channel genes SUR1 and Kir62 with Type 2 diabetes mellitus (UKPDS 53). Diabet Med. 2001;18(3):206-212.
77. Sesti G, Laratta E, Cardellini M, et al. The E23K variant of KCNJ11 encoding the pancreatic beta-cell adenosine 5'-triphosphate-sensitive potassium channel subunit Kir62 is associated with an increased risk of secondary failure to sulfonylurea in patients with type 2 diabetes. J Clin Endocrinol Metab. 2006;91(6):2334-2339.
78. Ragia G, Tavridou A, Petridis I, Manolopoulos VG. Association of KCNJ11 E23K gene polymorphism with hypoglycemia in sulfonylurea-treated type 2 diabetic patients. Diabetes Res Clin Pract. 2012;98(1):119-124.
79. Shu L, Sauter NS, Schulthess FT, Matveyenko AV, Oberholzer J, Maedler K. Transcription factor 7-like 2 regulates beta-cell survival and function in human pancreatic islets. Diabetes. 2008;57(3):645-653.
80. Grant SF, Thorleifsson G, Reynisdottir I, et al. Variant of transcription factor 7-like 2 (TCF7L2) gene confers risk of type 2 diabetes. Nat Genet. 2006;38(3):320-323.
81. Pearson ER, Donnelly LA, Kimber C, et al. Variation in TCF7L2 influences therapeutic response to sulfonylureas: a GoDARTs study. Diabetes. 2007;56(8):2178-2182.
82. Schroner Z, Javorsky M, Tkacova R, et al. Effect of sulphonylurea treatment on glycaemic control is related to TCF7L2 genotype in patients with type 2 diabetes. Diabetes Obes Metab. 2011;13(1):89-91.
83. Javorský M, Babjaková E, Klimáková L, et al. Association between TCF7L2 genotype and glycemic control in diabetic patients treated with gliclazide. Int J Endocrinol. 2013;2013:374858.
84. Holstein A, Hahn M, Körner A, Stumvoll M, Kovacs P. TCF7L2 and therapeutic response to sulfonylureas in patients with type 2 diabetes. BMC Med Genet. 2011;12:30.
85. Bachmakov I, Glaeser H, Fromm MF, König J. Interaction of oral antidiabetic drugs with hepatic uptake transporters: focus on organic anion transporting polypeptides and organic cation transporter 1. Diabetes. 2008;57(6):1463-1469.
86. Niemi M, Backman JT, Kajosaari LI, et al. Polymorphic organic anion transporting polypeptide 1B1 is a major determinant of repaglinide pharmacokinetics. Clin Pharmacol Ther. 2005;77(6): 468-478.
87. Kalliokoski A, Neuvonen M, Neuvonen PJ, Niemi M. Different effects of SLCO1B1 polymorphism on the pharmacokinetics and pharmacodynamics of repaglinide and nateglinide. J Clin Pharmacol. 2008;48(3):311-321.
88. Zhang W, He YJ, Han CT, et al. Effect of SLCO1B1 genetic polymorphism on the pharmacokinetics of nateglinide. Br J Clin Pharmacol. 2006;62(5):567-572.
89. Cheng Y, Wang G, Zhang W, Fan L, Chen Y, Zhou HH. Effect of CYP2C9 and SLCO1B1 polymorphisms on the pharmacokinetics and pharmacodynamics of nateglinide in healthy Chinese male volunteers. Eur J Clin Pharmacol. 2013;69(3):407-413.
90. Kalliokoski A, Backman JT, Neuvonen PJ, Niemi M. Effects of the SLCO1B1*1B haplotype on the pharmacokinetics and pharmacodynamics of repaglinide and nateglinide. Pharmacogenet Genomics. 2008;18(11):937-942.
91. Kirchheiner J, Meineke I, Müller G, et al. Influence of CYP2C9 and CYP2D6 polymorphisms on the pharmacokinetics of nateglinide in genotyped healthy volunteers. Clin Pharmacokinet. 2004;43(4): 267-278.
92. Niemi M, Leathart JB, Neuvonen M, Backman JT, Daly AK, Neuvonen PJ. Polymorphism in CYP2C8 is associated with reduced plasma concentrations of repaglinide. Clin Pharmacol Ther. 2003;74(4):380-387.
93. He YY, Zhang R, Shao XY, et al. Association of KCNJ11 and ABCC8 genetic polymorphisms with response to repaglinide in Chinese diabetic patients. Acta Pharmacol Sin. 2008;29(8):983-989.
94. Inzucchi SE, Bergenstal RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes, 2015: a patient-centered approach. Update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care. 2015;38:140-149.
95. Levin D, Bell S, Sund R, et al; Scottish Diabetes Research Network Epidemiology Group; Diabetes and Cancer Research Consortium. Pioglitazone and bladder cancer risk: a multipopulation pooled, cumulative exposure analysis. Diabetologia. 2015;58(3):493-504.
96. Lewis JM, Ferrara A, Peng T, et al. Risk of bladder cancer among diabetic patients treated with pioglitazone interim report of a longitudinal cohort study. Diabetes Care. 2008;34:916-922.
97. Kalliokoski A, Neuvonen PJ, Niemi M. SLCO1B1 polymorphism and oral antidiabetic drugs. Basic Clin Pharmacol Toxicol. 2010; 107(4):775-781.
98. Kirchheiner J, Thomas S, Bauer S, et al. Pharmacokinetics and pharmacodynamics of rosiglitazone in relation to CYP2C8 genotype. Clin Pharmacol Ther. 2006;80(6):657-667.
99. Aquilante CL, Bushman LR, Knutsen SD, Burt LE, Rome LC, Kosmiski LA. Influence of SLCO1B1 and CYP2C8 gene polymorphisms on rosiglitazone pharmacokinetics in healthy volunteers. Hum Genomics. 2008;3(1):7-16.
100. Aquilante CL, Kosmiski LA, Bourne DW, et al. Impact of the CYP2C8 *3 polymorphism on the drug-drug interaction between gemfibrozil and pioglitazone. Br J Clin Pharmacol. 2013;75(1):217-226.
101. Tornio A, Niemi M, Neuvonen PJ, Backman JT. Trimethoprim and the CYP2C8*3 allele have opposite effects on the pharmacokinetics of pioglitazone. Drug Metab Dispos. 2008;36(1):73-80.
102. Kalliokoski A, Neuvonen M, Neuvonen PJ, Niemi M. No significant effect of SLCO1B1 polymorphism on the pharmacokinetics of rosiglitazone and pioglitazone. Br J Clin Pharmacol. 2008;65(1): 78-86.
103. Altshuler D, Hirschhorn JN, Klannemark M, et al. The common PPARgamma Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes. Nat Genet. 2000;26(1):76-80.
104. Hsieh MC, Lin KD, Tien KJ, et al. Common polymorphisms of the peroxisome proliferator-activated receptor-gamma (Pro12Ala) and peroxisome proliferator-activated receptor-gamma coactivator-1 (Gly482Ser) and the response to pioglitazone in Chinese patients with type 2 diabetes mellitus. Metabolism. 2010;59(8):1139-1144.
105. Pei Q, Huang Q, Yang GP, et al. PPAR-γ2 and PTPRD gene polymorphisms influence type 2 diabetes patients' response to pioglitazone in China. Acta Pharmacol Sin. 2013;34(2):255-261.
106. Kang ES, Park SY, Kim HJ, et al. Effects of Pro12Ala polymorphism of peroxisome proliferator-activated receptor gamma2 gene on rosiglitazone response in type 2 diabetes. Clin Pharmacol Ther. 2005;78(2):202-208.
107. Bailey SD, Xie C, Do R, et al. Variation at the NFATC2 locus increases the risk of thiazolidinedione-induced edema in the Diabetes REduction Assessment with ramipril and rosiglitazone Medication (DREAM) study. Diabetes Care. 2010;33(10):2250-2253.
108. Drucker DJ, Nauck MA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet. 2006;368(9548):1696-1705.
109. Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. 2007;87(4):1409-1439.
110. Sathananthan A, Man CD, Micheletto F, et al. Common genetic variation in GLP1R and insulin secretion in response to exogenous GLP-1 in nondiabetic subjects: a pilot study. Diabetes Care. 2010;33(9):2074-2076.
111. 't Hart LM, Fritsche A, Nijpels G, et al. The CTRB1/2 locus affects diabetes susceptibility and treatment via the incretin pathway. Diabetes. 2013;62(9):3275-3281.
112. Scheen AJ. Pharmacokinetics, pharmacodynamics and clinical use of SGLT2 inhibitors in patients with type 2 diabetes mellitus and chronic kidney disease. Clin Pharmacokinet. 2015;54(7):691-708.
113. Francke S, Mamidi RN, Solanki B, et al. In vitro metabolism of canagliflozin in human liver, kidney, intestine microsomes, and recombinant uridine diphosphate glucuronosyltransferases (UGT) and the effect of genetic variability of UGT enzymes on the pharmacokinetics of canagliflozin in humans. J Clin Pharmacol. 2015;55(9):1061-1072.
114. Scheen AJ. Pharmacodynamics, efficacy and safety of sodium-glucose co-transporter type 2 (SGLT2) inhibitors for the treatment of type 2 diabetes mellitus. Drugs. 2015;75(1):33-59.
115. van den Heuvel LP, Assink K, Willemsen M, Monnens L. Autosomal recessive renal glucosuria attributable to a mutation in the sodium glucose cotransporter (SGLT2). Hum Genet. 2002;111(6):544-547.
116. Calado J, Soto K, Clemente C, Correia P, Rueff J. Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria. Hum Genet. 2004;114(3):314-316.
117. Rafiq M, Flanagan SE, Patch AM, et al; Neonatal Diabetes International Collaborative Group. Effective treatment with diabetes due to sulfonylurea receptor 1 (SUR1) mutations. Diabetes Care. 2008;32(2):204-209.