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“Association of the CD36 gene with impaired glucose tolerance, impaired fasting glucose, type-2 diabetes, and lipid metabolism in essential hypertensive patients”, vol. 11, pp. 2163-2170, 2012.
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Aitman TJ, Glazier AM, Wallace CA, Cooper LD, et al. (1999). Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. Nat. Genet. 21: 76-83.
http://dx.doi.org/10.1038/5013
PMid:9916795
Almgren T, Wilhelmsen L, Samuelsson O, Himmelmann A, et al. (2007). Diabetes in treated hypertension is common and carries a high cardiovascular risk: results from a 28-year follow-up. J. Hypertens. 25: 1311-1317.
http://dx.doi.org/10.1097/HJH.0b013e328122dd58
PMid:17563546
Bokor S, Legry V, Meirhaeghe A, Ruiz JR, et al. (2010). Single-nucleotide polymorphism of CD36 locus and obesity in European adolescents. Obesity 18: 1398-1403.
http://dx.doi.org/10.1038/oby.2009.412
PMid:19893500
Coburn CT, Knapp FF Jr, Febbraio M, Beets AL, et al. (2000). Defective uptake and utilization of long chain fatty acids in muscle and adipose tissues of CD36 knockout mice. J. Biol. Chem. 275: 32523-32529.
http://dx.doi.org/10.1074/jbc.M003826200
PMid:10913136
Gurnell M, Savage DB, Chatterjee VK and O'Rahilly S (2003). The metabolic syndrome: peroxisome proliferator-activated receptor gamma and its therapeutic modulation. J. Clin. Endocrinol. Metab. 88: 2412-2421.
http://dx.doi.org/10.1210/jc.2003-030435
PMid:12788836
Hajri T and Abumrad NA (2002). Fatty acid transport across membranes: relevance to nutrition and metabolic pathology. Annu. Rev. Nutr. 22: 383-415.
http://dx.doi.org/10.1146/annurev.nutr.22.020402.130846
PMid:12055351
Han XX, Chabowski A, Tandon NN, Calles-Escandon J, et al. (2007). Metabolic challenges reveal impaired fatty acid metabolism and translocation of FAT/CD36 but not FABPpm in obese Zucker rat muscle. Am. J. Physiol. Endocrinol. Metab. 293: E566-E575.
http://dx.doi.org/10.1152/ajpendo.00106.2007
PMid:17519284
Harasim E, Kalinowska A, Chabowski A and Stepek T (2008). The role of fatty-acid transport proteins (FAT/CD36, FABPpm, FATP) in lipid metabolism in skeletal muscles. Postepy Hig. Med. Dosw. 62: 433-441.
Lepretre F, Vasseur F, Vaxillaire M, Scherer PE, et al. (2004). A CD36 nonsense mutation associated with insulin resistance and familial type 2 diabetes. Hum. Mutat. 24: 104.
http://dx.doi.org/10.1002/humu.9256
PMid:15221799
Love-Gregory L, Sherva R, Sun L, Wasson J, et al. (2008). Variants in the CD36 gene associate with the metabolic syndrome and high-density lipoprotein cholesterol. Hum. Mol. Genet. 17: 1695-1704.
http://dx.doi.org/10.1093/hmg/ddn060
PMid:18305138 PMCid:2655228
Ma X, Bacci S, Mlynarski W, Gottardo L, et al. (2004). A common haplotype at the CD36 locus is associated with high free fatty acid levels and increased cardiovascular risk in Caucasians. Hum. Mol. Genet. 13: 2197-2205.
http://dx.doi.org/10.1093/hmg/ddh233
PMid:15282206
Noel SE, Lai CQ, Mattei J, Parnell LD, et al. (2010). Variants of the CD36 gene and metabolic syndrome in Boston Puerto Rican adults. Atherosclerosis 211: 210-215.
http://dx.doi.org/10.1016/j.atherosclerosis.2010.02.009
PMid:20223461 PMCid:2923842
Osei K, Rhinesmith S, Gaillard T and Schuster D (2004). Impaired insulin sensitivity, insulin secretion, and glucose effectiveness predict future development of impaired glucose tolerance and type 2 diabetes in pre-diabetic African Americans: implications for primary diabetes prevention. Diabetes Care 27: 1439-1446.
http://dx.doi.org/10.2337/diacare.27.6.1439
PMid:15161801
Pontiroli AE, Pizzocri P, Caumo A, Perseghin G, et al. (2004). Evaluation of insulin release and insulin sensitivity through oral glucose tolerance test: differences between NGT, IFG, IGT, and type 2 diabetes mellitus. A cross-sectional and follow-up study. Acta Diabetol. 41: 70-76.
http://dx.doi.org/10.1007/s00592-004-0147-x
PMid:15224208
Pravenec M and Kurtz TW (2002). Genetics of Cd36 and the hypertension metabolic syndrome. Semin. Nephrol. 22: 148-153.
http://dx.doi.org/10.1053/snep.2002.2002.30218
PMid:11891508
Susztak K, Ciccone E, McCue P, Sharma K, et al. (2005). Multiple metabolic hits converge on CD36 as novel mediator of tubular epithelial apoptosis in diabetic nephropathy. PLoS Med. 2: e45.
http://dx.doi.org/10.1371/journal.pmed.0020045
PMid:15737001 PMCid:549593
Wang X and Snieder H (2010). Genome-wide association studies and beyond: what's next in blood pressure genetics? Hypertension 56: 1035-1037.
http://dx.doi.org/10.1161/HYPERTENSIONAHA.110.157214
PMid:21060002
Yamauchi T, Hara K, Maeda S, Yasuda K, et al. (2010). A genome-wide association study in the Japanese population identifies susceptibility loci for type 2 diabetes at UBE2E2 and C2CD4A-C2CD4B. Nat. Genet. 42: 864-868.
http://dx.doi.org/10.1038/ng.660
PMid:20818381
Zhou X, Wang Y, Zhang Y, Gao P, et al. (2010). Association of CAPN10 gene with insulin sensitivity, glucose tolerance and renal function in essential hypertensive patients. Clin. Chim. Acta 411: 1126-1131.
http://dx.doi.org/10.1016/j.cca.2010.04.012
PMid:20406624
“Association of KCNJ11 with impaired glucose regulation in essential hypertension”, vol. 10, pp. 1111-1119, 2011.
, Cederholm J and Wibell L (1990). Insulin release and peripheral sensitivity at the oral glucose tolerance test. Diabetes Res. Clin. Pract. 10: 167-175.
doi:10.1016/0168-8227(90)90040-Z
De Marco M, de Simone G, Roman MJ, Chinali M, et al. (2009). Cardiovascular and metabolic predictors of progression of prehypertension into hypertension: the strong heart study. Hypertension 54: 974-980.
doi:10.1161/HYPERTENSIONAHA.109.129031
PMid:19720957 PMCid:2776057
Dudbridge F (2003). Pedigree disequilibrium tests for multilocus haplotypes. Genet. Epidemiol. 25: 115-121.
doi:10.1002/gepi.10252
PMid:12916020
Florez JC, Jablonski KA, Kahn SE, Franks PW, et al. (2007). Type 2 diabetes-associated missense polymorphisms KCNJ11 E23K and ABCC8 A1369S influence progression to diabetes and response to interventions in the Diabetes Prevention Program. Diabetes 56: 531-536.
doi:10.2337/db06-0966
PMid:17259403 PMCid:2267937
Gloyn AL, Pearson ER, Antcliff JF, Proks P, et al. (2004). Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N. Engl. J. Med. 350: 1838-1849.
doi:10.1056/NEJMoa032922
PMid:15115830
Hackam DG, Khan NA, Hemmelgarn BR, Rabkin SW, et al. (2010). The 2010 Canadian Hypertension Education Program recommendations for the management of hypertension: part 2 - therapy. Can. J. Cardiol. 26: 249-258.
doi:10.1016/S0828-282X(10)70379-2
Lin YW, Bushman JD, Yan FF, Haidar S, et al. (2008). Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism. J. Biol. Chem. 283: 9146-9156.
doi:10.1074/jbc.M708798200
PMid:18250167 PMCid:2431039
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, et al. (1985). Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 28: 412-419.
doi:10.1007/BF00280883
PMid:3899825
Nielsen EM, Hansen L, Carstensen B, Echwald SM, et al. (2003). The E23K variant of Kir6.2 associates with impaired post-OGTT serum insulin response and increased risk of type 2 diabetes. Diabetes 52: 573-577.
doi:10.2337/diabetes.52.2.573
Ryder E, Gomez ME, Fernandez V, Campos G, et al. (2003). Presence of impaired insulin secretion and insulin resistance in normoglycemic male subjects with family history of type 2 diabetes. Diabetes Res. Clin. Pract. 60: 95-103.
doi:10.1016/S0168-8227(02)00282-6
Saxena R, Voight BF, Lyssenko V, Burtt NP, et al. (2007). Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science 316: 1331-1336.
doi:10.1126/science.1142358
PMid:17463246
Schaid DJ, Rowland CM, Tines DE, Jacobson RM, et al. (2002). Score tests for association between traits and haplotypes when linkage phase is ambiguous. Am. J. Hum. Genet. 70: 425-434.
doi:10.1086/338688
PMid:11791212
Scott LJ, Mohlke KL, Bonnycastle LL, Willer CJ, et al. (2007). A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants. Science 316: 1341-1345.
doi:10.1126/science.1142382
PMid:17463248
Seino S, Iwanaga T, Nagashima K and Miki T (2000). Diverse roles of K(ATP) channels learned from Kir6.2 genetically engineered mice. Diabetes 49: 311-318.
doi:10.2337/diabetes.49.3.311
PMid:10868950
Vaxillaire M, Veslot J, Dina C, Proenca C, et al. (2008). Impact of common type 2 diabetes risk polymorphisms in the DESIR prospective study. Diabetes 57: 244-254.
doi:10.2337/db07-0615
PMid:17977958
Villareal DT, Koster JC, Robertson H, Akrouh A, et al. (2009). Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance. Diabetes 58: 1869-1878.
doi:10.2337/db09-0025
PMid:19491206 PMCid:2712777
Vlasakova Z, Pelikanova T, Karasova L and Skibova J (2004). Insulin secretion, sensitivity, and metabolic profile of young healthy offspring of hypertensive parents. Metabolism 53: 469-475.
doi:10.1016/j.metabol.2003.10.030
PMid:15045694
Yokoi N, Kanamori M, Horikawa Y, Takeda J, et al. (2006). Association studies of variants in the genes involved in pancreatic beta-cell function in type 2 diabetes in Japanese subjects. Diabetes 55: 2379-2386.
doi:10.2337/db05-1203
PMid:16873704
Zeggini E, Weedon MN, Lindgren CM, Frayling TM, et al. (2007). Replication of genome-wide association signals in UK samples reveals risk loci for type 2 diabetes. Science 316: 1336-1341.
doi:10.1126/science.1142364
PMid:17463249