Copyright © 2008 Sharon Cresci. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

1. C. Dreyer, G. Krey, H. Keller, F. Givel, G. Helftenbein, and W. Wahli, “Control of the peroxisomal $\beta$-oxidation pathway by a novel family of nuclear hormone receptors,” Cell, vol. 68, no. 5, pp. 879–887, 1992. View at Publisher · View at Google Scholar
2. O. Braissant, F. Foufelle, C. Scotto, M. Dauça, and W. Wahli, “Differential expression of peroxisome proliferator-activated receptors (PPARs): tissue distribution of PPAR-$\alpha$, -$\beta$, and -$\gamma$ in the adult rat,” Endocrinology, vol. 137, no. 1, pp. 354–366, 1996. View at Publisher · View at Google Scholar
3. C.-H. Chew, M. R. Samian, N. Najimudin, and T. S. Tengku-Muhammad, “Molecular characterisation of six alternatively spliced variants and a novel promoter in human peroxisome proliferator-activated receptor $\alpha$,” Biochemical and Biophysical Research Communications, vol. 305, no. 2, pp. 235–243, 2003. View at Publisher · View at Google Scholar
4. L. Fajas, D. Auboeuf, E. Raspé, et al., “The organization, promoter analysis, and expression of the human PPAR$\gamma$ gene,” Journal of Biological Chemistry, vol. 272, no. 30, pp. 18779–18789, 1997. View at Publisher · View at Google Scholar
5. A. Fredenrich and P. A. Grimaldi, “PPAR $\delta$: an uncompletely known nuclear receptor,” Diabetes & Metabolism, vol. 31, no. 1, pp. 23–27, 2005. View at Publisher · View at Google Scholar
6. P. M. Barger, J. M. Brandt, T. C. Leone, C. J. Weinheimer, and D. P. Kelly, “Deactivation of peroxisome proliferator-activated receptor-$\alpha$ during cardiac hypertrophic growth,” Journal of Clinical Investigation, vol. 105, no. 12, pp. 1723–1730, 2000.
7. F. Djouadi, C. J. Weinheimer, J. E. Saffitz, et al., “A gender-related defect in lipid metabolism and glucose homeostasis in peroxisome proliferator-activated receptor $\alpha$-deficient mice,” Journal of Clinical Investigation, vol. 102, no. 6, pp. 1083–1091, 1998.
8. B. N. Finck, X. Han, M. Courtois, et al., “A critical role for PPAR$\alpha$-mediated lipotoxicity in the pathogenesis of diabetic cardiomyopathy: modulation by dietary fat content,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 3, pp. 1226–1231, 2003. View at Publisher · View at Google Scholar · View at PubMed
9. M. Guerre-Millo, C. Rouault, P. Poulain, et al., “PPAR-$\alpha$-null mice are protected from high-fat diet-induced insulin resistance,” Diabetes, vol. 50, no. 12, pp. 2809–2814, 2001. View at Publisher · View at Google Scholar
10. J. M. Huss, F. H. Levy, and D. P. Kelly, “Hypoxia inhibits the peroxisome proliferator-activated receptor $\alpha$/retinoid X receptor gene regulatory pathway in cardiac myocytes: a mechanism for ${\text{O}}_2$-dependent modulation of mitochondrial fatty acid oxidation,” Journal of Biological Chemistry, vol. 276, no. 29, pp. 27605–27612, 2001. View at Publisher · View at Google Scholar · View at PubMed
11. J. M. Huss and D. P. Kelly, “Nuclear receptor signaling and cardiac energetics,” Circulation Research, vol. 95, no. 6, pp. 568–578, 2004. View at Publisher · View at Google Scholar · View at PubMed
12. J. M. Huss and D. P. Kelly, “Mitochondrial energy metabolism in heart failure: a question of balance,” Journal of Clinical Investigation, vol. 115, no. 3, pp. 547–555, 2005. View at Publisher · View at Google Scholar
13. T. Lemberger, B. Desvergne, and W. Wahli, “Peroxisome proliferator-activated receptors: a nuclear receptor signaling pathway in lipid physiology,” Annual Review of Cell and Developmental Biology, vol. 12, pp. 335–363, 1996. View at Publisher · View at Google Scholar · View at PubMed
14. T. Lemberger, R. Saladin, M. Vázquez, et al., “Expression of the peroxisome proliferator-activated receptor $\alpha$ gene is stimulated by stress and follows a diurnal rhythm,” Journal of Biological Chemistry, vol. 271, no. 3, pp. 1764–1769, 1996. View at Publisher · View at Google Scholar
15. T. C. Leone, C. J. Weinheimer, and D. P. Kelly, “A critical role for the peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) in the cellular fasting response: the PPAR$\alpha$-null mouse as a model of fatty acid oxidation disorders,” Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 13, pp. 7473–7478, 1999. View at Publisher · View at Google Scholar
16. S. Cresci, L. D. Wright, J. A. Spratt, F. N. Briggs, and D. P. Kelly, “Activation of a novel metabolic gene regulatory pathway by chronic stimulation of skeletal muscle,” American Journal of Physiology—Cell Physiology, vol. 270, no. 5, pp. C1413–C1420, 1996.
17. I. Inoue, K. Shino, S. Noji, T. Awata, and S. Katayama, “Expression of peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) in primary cultures of human vascular endothelial cells,” Biochemical and Biophysical Research Communications, vol. 246, no. 2, pp. 370–374, 1998. View at Publisher · View at Google Scholar · View at PubMed
18. B. Staels, W. Koenig, A. Habib, et al., “Activation of human aortic smooth-muscle cells is inhibited by PPAR$\alpha$ but not by PPAR$\gamma$ activators,” Nature, vol. 393, no. 6687, pp. 790–793, 1998. View at Publisher · View at Google Scholar · View at PubMed
19. D. C. Jones, X. Ding, and R. A. Daynes, “Nuclear receptor peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) is expressed in resting murine lymphocytes. The PPAR$\alpha$ in T and B lymphocytes is both transactivation and transrepression competent,” Journal of Biological Chemistry, vol. 277, no. 9, pp. 6838–6845, 2002. View at Publisher · View at Google Scholar · View at PubMed
20. T. Imai, R. Takakuwa, S. Marchand, et al., “Peroxisome proliferator-activated receptor $\gamma$ is required in mature white and brown adipocytes for their survival in the mouse,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 13, pp. 4543–4547, 2004. View at Publisher · View at Google Scholar · View at PubMed
21. E. D. Rosen, P. Sarraf, A. E. Troy, et al., “PPAR$\gamma$ is required for the differentiation of adipose tissue in vivo and in vitro,” Molecular Cell, vol. 4, no. 4, pp. 611–617, 1999. View at Publisher · View at Google Scholar
22. B. M. Spiegelman, “Peroxisome proliferator-activated receptor $\gamma$: a key regulator of adipogenesis and systemic insulin sensitivity,” European Journal of Medical Research, vol. 2, no. 11, pp. 457–464, 1997.
23. P. D. G. Miles, Y. Barak, W. He, R. M. Evans, and J. M. Olefsky, “Improved insulin-sensitivity in mice heterozygous for PPAR-$\gamma$ deficiency,” Journal of Clinical Investigation, vol. 105, no. 3, pp. 287–292, 2000.
24. R. S. Ahima and J. S. Flier, “Adipose tissue as an endocrine organ,” Trends in Endocrinology and Metabolism, vol. 11, no. 8, pp. 327–332, 2000. View at Publisher · View at Google Scholar
25. E.-Z. Amri, F. Bonino, G. Ailhaud, N. A. Abumrad, and P. A. Grimaldi, “Cloning of a protein that mediates transcriptional effects of fatty acids in preadipocytes. Homology to peroxisome proliferator-activated receptors,” Journal of Biological Chemistry, vol. 270, no. 5, pp. 2367–2371, 1995. View at Publisher · View at Google Scholar
26. J. M. Peters, S. S. T. Lee, W. Li, et al., “Growths, adipose, brain, and skin alterations resulting from targeted disruption of the mouse peroxisome proliferator-activated receptor $\beta (\delta )$,” Molecular and Cellular Biology, vol. 20, no. 14, pp. 5119–5128, 2000. View at Publisher · View at Google Scholar
27. K. Matsusue, J. M. Peters, and F. J. Gonzalez, “PPAR$\beta$/$\delta$ potentiates PPAR$\gamma$-stimulated adipocyte differentiation,” The FASEB Journal, vol. 18, no. 12, pp. 1477–1479, 2004. View at Publisher · View at Google Scholar · View at PubMed
28. T. Tanaka, J. Yamamoto, S. Iwasaki, et al., “Activation of peroxisome proliferator-activated receptor $\delta$ induces fatty acid $\beta$-oxidation in skeletal muscle and attenuates metabolic syndrome,” Proceedings of the National Academy of Sciences of the United States of America, vol. 100, no. 26, pp. 15924–15929, 2003. View at Publisher · View at Google Scholar · View at PubMed
29. L. Cheng, G. Ding, Q. Qin, et al., “Cardiomyocyte-restricted peroxisome proliferator-activated receptor-$\delta$ deletion perturbs myocardial fatty acid oxidation and leads to cardiomyopathy,” Nature Medicine, vol. 10, no. 11, pp. 1245–1250, 2004. View at Publisher · View at Google Scholar · View at PubMed
30. A. Planavila, J. C. Laguna, and M. Vázquez-Carrera, “Nuclear factor-$\kappa$B activation leads to down-regulation of fatty acid oxidation during cardiac hypertrophy,” Journal of Biological Chemistry, vol. 280, no. 17, pp. 17464–17471, 2005. View at Publisher · View at Google Scholar · View at PubMed
31. A. Planavila, R. Rodríguez-Calvo, M. Jové, et al., “Peroxisome proliferator-activated receptor $\beta$/$\delta$ activation inhibits hypertrophy in neonatal rat cardiomyocytes,” Cardiovascular Research, vol. 65, no. 4, pp. 832–841, 2005. View at Publisher · View at Google Scholar · View at PubMed
32. A. Berkenstam and J. Å. Gustafsson, “Nuclear receptors and their relevance to diseases related to lipid metabolism,” Current Opinion in Pharmacology, vol. 5, no. 2, pp. 171–176, 2005. View at Publisher · View at Google Scholar · View at PubMed
33. G. Benoit, M. Malewicz, and T. Perlmann, “Digging deep into the pockets of orphan nuclear receptors: insights from structural studies,” Trends in Cell Biology, vol. 14, no. 7, pp. 369–376, 2004. View at Publisher · View at Google Scholar · View at PubMed
34. Y. Zhu, L. Kan, C. Qi, et al., “Isolation and characterization of peroxisome proliferator-activated receptor (PPAR) interacting protein (PRIP) as a coactivator for PPAR,” Journal of Biological Chemistry, vol. 275, no. 18, pp. 13510–13516, 2000. View at Publisher · View at Google Scholar
35. R. T. Nolte, G. B. Wisely, S. Westin, et al., “Ligand binding and co-activator assembly of the peroxisome proliferator- activated receptor-$\gamma$,” Nature, vol. 395, no. 6698, pp. 137–143, 1998. View at Publisher · View at Google Scholar · View at PubMed
36. K. Lee, “Transactivation of peroxisome proliferator-activated receptor $\alpha$ by green tea extracts,” Journal of Veterinary Science, vol. 5, no. 4, pp. 325–330, 2004.
37. S. A. Kliewer, K. Umesono, D. J. Noonan, R. A. Heyman, and R. M. Evans, “Convergence of 9-cis retinoic acid and peroxisome proliferator signalling pathways through heterodimer formation of their receptors,” Nature, vol. 358, no. 6389, pp. 771–774, 1992. View at Publisher · View at Google Scholar · View at PubMed
38. C. Qi, Y. Zhu, and J. K. Reddy, “Peroxisome proliferator-activated receptors, coactivators, and downstream targets,” Cell Biochemistry and Biophysics, vol. 32, pp. 187–204, 2000. View at Publisher · View at Google Scholar
39. B. M. Spiegelman, P. Puigserver, and Z. Wu, “Regulation of adipogenesis and energy balance by PPAR$\gamma$ and PGC-1,” International Journal of Obesity, vol. 24, pp. S8–S10, 2000.
40. A. Sapone, J. M. Peters, S. Sakai, et al., “The human peroxisome proliferator-activated receptor $\alpha$ gene: identification and functional characterization of two natural allelic variants,” Pharmacogenetics, vol. 10, no. 4, pp. 321–333, 2000. View at Publisher · View at Google Scholar
41. D. M. Flavell, I. T. Pineda, Y. Jamshidi, et al., “Variation in the PPAR$\alpha$ gene is associated with altered function in vitro and plasma lipid concentrations in type II diabetic subjects,” Diabetologia, vol. 43, no. 5, pp. 673–680, 2000. View at Publisher · View at Google Scholar
42. C. Lacquemant, F. Lepretre, I. T. Pineda, et al., “Mutation screening of the PPAR$\alpha$ gene in type 2 diabetes associated with coronary heart disease,” Diabetes & Metabolism, vol. 26, no. 5, pp. 393–401, 2000.
43. M.-C. Vohl, P. Lepage, D. Gaudet, et al., “Molecular scanning of the human PPAR$\alpha$ gene: association of the L162V mutation with hyperapobetalipoproteinemia,” Journal of Lipid Research, vol. 41, no. 6, pp. 945–952, 2000.
44. E. S. Tai, S. Demissie, L. A. Cupples, et al., “Association between the PPARA L162V polymorphism and plasma lipid levels: the framingham offspring study,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 22, no. 5, pp. 805–810, 2002. View at Publisher · View at Google Scholar
45. T. Sparsø, M. S. Hussain, G. Andersen, et al., “Relationships between the functional PPAR$\alpha$ Leu162Val polymorphism and obesity, type 2 diabetes, dyslipidaemia, and related quantitative traits in studies of 5799 middle-aged white people,” Molecular Genetics and Metabolism, vol. 90, no. 2, pp. 205–209, 2007. View at Publisher · View at Google Scholar · View at PubMed
46. T. Jørgensen, K. Borch-Johnsen, T. F. Thomsen, H. Ibsen, C. Glümer, and C. Pisinger, “A randomized non-pharmacological intervention study for prevention of ischaemic heart disease: baseline results Inter99 (1),” European Journal of Cardiovascular Prevention and Rehabilitation, vol. 10, no. 5, pp. 377–386, 2003. View at Publisher · View at Google Scholar · View at PubMed
47. E. S. Tai, D. Corella, S. Demissie, et al., “Polyunsaturated fatty acids interact with the PPARA-L162V polymorphism to affect plasma triglyceride and apolipoprotein C-III concentrations in the framingham heart study,” Journal of Nutrition, vol. 135, no. 3, pp. 397–403, 2005.
48. T. Tanaka, J. M. Ordovas, J. Delgado-Lista, et al., “Peroxisome proliferator-activated receptor $\alpha$ polymorphisms and postprandial lipemia in healthy men,” Journal of Lipid Research, vol. 48, no. 6, pp. 1402–1408, 2007. View at Publisher · View at Google Scholar · View at PubMed
49. A.-M. Paradis, B. Fontaine-Bisson, Y. Bossé, et al., “The peroxisome proliferator-activated receptor $\alpha$ Leu162Val polymorphism influences the metabolic response to a dietary intervention altering fatty acid proportions in healthy men,” American Journal of Clinical Nutrition, vol. 81, no. 2, pp. 523–530, 2005.
50. D. M. Flavell, Y. Jamshidi, E. Hawe, et al., “Peroxisome proliferator-activated receptor $\alpha$ gene variants influence progression of coronary atherosclerosis and risk of coronary artery disease,” Circulation, vol. 105, no. 12, pp. 1440–1445, 2002. View at Publisher · View at Google Scholar
51. M. H. Frick, M. Syvänne, M. S. Nieminen, et al., “Prevention of the angiographic progression of coronary and vein-graft atherosclerosis by gemfibrozil after coronary bypass surgery in men with low levels of HDL cholesterol. Lopid Coronary Angiography Trial (LOCAT) Study Group,” Circulation, vol. 96, no. 7, pp. 2137–2143, 1997.
52. M. Syvänne, M.-R. Taskinen, M. S. Nieminen, et al., “A study to determine the response of coronary atherosclerosis to raising low high density lipoprotein cholesterol with a fibric-acid derivative in men after coronary bypass surgery. The rationale, design, and baseline characteristics of the LOCAT study. Lopid Coronary Angiography Trial,” Controlled Clinical Trials, vol. 18, no. 1, pp. 93–119, 1997. View at Publisher · View at Google Scholar
53. M. H. Frick, O. Elo, and K. Haapa, “Helsinki heart study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease,” New England Journal of Medicine, vol. 317, no. 20, pp. 1237–1245, 1987.
54. V. Manninen, L. Tenkanen, P. Koskinen, et al., “Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki heart study. Implications for treatment,” Circulation, vol. 85, no. 1, pp. 37–45, 1992.
55. L. Tenkanen, M. Mänttäri, and V. Manninen, “Some coronary risk factors related to the insulin resistance syndrome and treatment with gemfibrozil: experience from the Helsinki heart study,” Circulation, vol. 92, no. 7, pp. 1779–1785, 1995.
56. Y. Bossé, A. Pascot, M. Dumont, et al., “Influences of the PPAR$\alpha$-L162V polymorphism on plasma ${\text{HDL}}_2$-cholesterol response of abdominally obese men treated with gemfibrozil,” Genetics in Medicine, vol. 4, no. 4, pp. 311–315, 2002.
57. S. J. Robins, D. Collins, J. T. Wittes, et al., “Relation of gemfibrozil treatment and lipid levels with major coronary events. VA-HIT: a randomized controlled trial,” Journal of the American Medical Association, vol. 285, no. 12, pp. 1585–1591, 2001. View at Publisher · View at Google Scholar
58. H. B. Rubins, S. J. Robins, D. Collins, et al., “Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group,” New England Journal of Medicine, vol. 341, no. 6, pp. 410–418, 1999. View at Publisher · View at Google Scholar · View at PubMed
59. H. B. Rubins, J. Davenport, V. Babikian, et al., “Reduction in stroke with gemfibrozil in men with coronary heart disease and low HDL cholesterol the Veterans Affairs HDL Intervention Trial (VA-HIT),” Circulation, vol. 103, no. 23, pp. 2828–2833, 2001.
60. S. J. Robins, H. B. Rubins, F. H. Faas, et al., “Insulin resistance and cardiovascular events with low HDL cholesterol: the Veterans Affairs HDL Intervention Trial (VA-HIT),” Diabetes Care, vol. 26, no. 5, pp. 1513–1517, 2003. View at Publisher · View at Google Scholar
61. H. B. Rubins, S. J. Robins, D. Collins, et al., “Diabetes, plasma insulin, and cardiovascular disease: subgroup analysis from the Department of Veterans Affairs high-density lipoprotein intervention trial (VA-HIT),” Archives of Internal Medicine, vol. 162, no. 22, pp. 2597–2604, 2002. View at Publisher · View at Google Scholar
62. E. S. Tai, D. Collins, S. J. Robins, et al., “The L162V polymorphism at the peroxisome proliferator activated receptor $\alpha$ locus modulates the risk of cardiovascular events associated with insulin resistance and diabetes mellitus: the Veterans Affairs HDL Intervention Trial (VA-HIT),” Atherosclerosis, vol. 187, no. 1, pp. 153–160, 2006. View at Publisher · View at Google Scholar · View at PubMed
63. C.-Q. Lai, D. K. Arnett, D. Corella, et al., “Fenofibrate effect on triglyceride and postprandial response of apolipoprotein A5 variants: the GOLDN study,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 27, no. 6, pp. 1417–1425, 2007. View at Publisher · View at Google Scholar · View at PubMed
64. D. K. Arnett, M. A. Province, I. B. Borecki, et al., “The PPAR$\alpha$ L162V polymorphism predicts triglyceride lowering response to fenofibrate: the GOLDN study,” Circulation, vol. 112, no. 17, p. II-509, 2005.
65. K. Yamakawa-Kobayashi, H. Ishiguro, T. Arinami, R. Miyazaki, and H. Hamaguchi, “A Val227 ala polymorphism in the peroxisome proliferator activated receptor $\alpha$ (PPAR$\alpha$) gene is associated with variations in serum lipid levels,” Journal of Medical Genetics, vol. 39, no. 3, pp. 189–191, 2002. View at Publisher · View at Google Scholar
66. E. Chan, C. S. Tan, M. Deurenberg-Yap, K. S. Chia, S. K. Chew, and E. S. Tai, “The V227A polymorphism at the PPARA locus is associated with serum lipid concentrations and modulates the association between dietary polyunsaturated fatty acid intake and serum high density lipoprotein concentrations in Chinese women,” Atherosclerosis, vol. 187, no. 2, pp. 309–315, 2006. View at Publisher · View at Google Scholar · View at PubMed
67. Y. Jamshidi, H. E. Montgomery, H.-W. Hense, et al., “Peroxisome proliferator-activated receptor $\alpha$ gene regulates left ventricular growth in response to exercise and hypertension,” Circulation, vol. 105, no. 8, pp. 950–955, 2002. View at Publisher · View at Google Scholar
68. G. Steiner, D. Stewart, and J. D. Hosking, “Baseline characteristics of the study population in the Diabetes Atherosclerosis Intervention Study (DAIS). World Health Organization Collaborating Centre for the Study of Atherosclerosis in Diabetes,” American Journal of Cardiology, vol. 84, no. 9, pp. 1004–1010, 1999. View at Publisher · View at Google Scholar
69. “Effect of fenofibrate on progression of coronary-artery disease in type 2 diabetes: the diabetes atherosclerosis intervention study, a randomised study,” The Lancet, vol. 357, no. 9260, pp. 905–910, 2001. View at Publisher · View at Google Scholar
70. J.-C. Ansquer, C. Foucher, S. Rattier, M.-R. Taskinen, and G. Steiner, “Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS),” American Journal of Kidney Diseases, vol. 45, no. 3, pp. 485–493, 2005. View at Publisher · View at Google Scholar · View at PubMed
71. C. Foucher, S. Rattier, D. M. Flavell, et al., “Response to micronized fenofibrate treatment is associated with the peroxisome-proliferator-activated receptors $\alpha$ G/C intron7 polymorphism in subjects with type 2 diabetes,” Pharmacogenetics, vol. 14, no. 12, pp. 823–829, 2004. View at Publisher · View at Google Scholar
72. L. Andrulionyte, J. Zacharova, J.-L. Chiasson, and M. Laakso, “Common polymorphisms of the PPAR-$\gamma 2$ (Pro12Ala) and PGC-$1\alpha$ (Gly482Ser) genes are associated with the conversion from impaired glucose tolerance to type 2 diabetes in the STOP-NIDDM trial,” Diabetologia, vol. 47, no. 12, pp. 2176–2184, 2004. View at Publisher · View at Google Scholar · View at PubMed
73. L. Andrulionyte, P. Peltola, J.-L. Chiasson, and M. Laakso, “Single nucleotide polymorphisms of PPARD in combination with the Gly482Ser substitution of PGC-1A and the Pro12Ala substitution of PPARG2 predict the conversion from impaired glucose tolerance to type 2 diabetes: the STOP-NIDDM trial,” Diabetes, vol. 55, no. 7, pp. 2148–2152, 2006. View at Publisher · View at Google Scholar · View at PubMed
74. L. Andrulionyte, T. Kuulasmaa, J.-L. Chiasson, and M. Laakso, “Single nucleotide polymorphisms of the peroxisome proliferator-activated receptor-$\alpha$ gene (PPARA) influence the conversion from impaired glucose tolerance to type 2 diabetes: the STOP-NIDDM trial,” Diabetes, vol. 56, no. 4, pp. 1181–1186, 2007. View at Publisher · View at Google Scholar · View at PubMed
75. S. S. Deeb, L. Fajas, M. Nemoto, et al., “A Pro12Ala substitution in $PPAR\gamma 2$ associated with decreased receptor activity, lower body mass index and improved insulin sensitivity,” Nature Genetics, vol. 20, no. 3, pp. 284–287, 1998. View at Publisher · View at Google Scholar · View at PubMed
76. L.-M. Chuang, C. Hsiung, Y.-D. Chen, et al., “Sibling-based association study of the PPAR$\gamma$2 Pro12Ala polymorphism and metabolic variables in Chinese and Japanese hypertension families: a SAPPHIRe study. Stanford Asian-Pacific Program in Hypertension and Insulin Resistance,” Journal of Molecular Medicine, vol. 79, no. 11, pp. 656–664, 2001. View at Publisher · View at Google Scholar · View at PubMed
77. R. Meshkani, M. Taghikhani, B. Larijani, et al., “Pro12Ala polymorphism of the peroxisome proliferator-activated receptor-$\gamma$2 PPAR-$\gamma$2 gene is associated with greater insulin sensitivity and decreased risk of type 2 diabetes in an Iranian population,” Clinical Chemistry and Laboratory Medicine, vol. 45, no. 4, pp. 477–482, 2007. View at Publisher · View at Google Scholar · View at PubMed
78. R. Buzzetti, A. Petrone, A. M. Caiazzo, et al., “PPAR-$\gamma$2 Pro12Ala variant is associated with greater insulin sensitivity in childhood obesity,” Pediatric Research, vol. 57, no. 1, pp. 138–140, 2005. View at Publisher · View at Google Scholar · View at PubMed
79. J. L. González Sánchez, M. Serrano Ríos, C. Fernández Pérez, M. Laakso, and M. T. Martínez Larrad, “Effect of the Pro12Ala polymorphism of the peroxisome proliferator-activated receptor $\gamma$-2 gene on adiposity, insulin sensitivity and lipid profile in the Spanish population,” European Journal of Endocrinology, vol. 147, no. 4, pp. 495–501, 2002.
80. A. Tönjes, M. Scholz, M. Loeffler, and M. Stumvoll, “Association of Pro12Ala polymorphism in peroxisome proliferator-activated receptor $\gamma$ with pre-diabetic phenotypes: meta-analysis of 57 studies on nondiabetic individuals,” Diabetes Care, vol. 29, no. 11, pp. 2489–2497, 2006. View at Publisher · View at Google Scholar · View at PubMed
81. R. Jaziri, S. Lobbens, R. Aubert, et al., “The PPARG Pro12Ala polymorphism is associated with a decreased risk of developing hyperglycemia over 6 years and combines with the effect of the APM1 G-11391A single nucleotide polymorphism: the Data from an Epidemiological Study on the Insulin Resistance Syndrome (DESIR) study,” Diabetes, vol. 55, no. 4, pp. 1157–1162, 2006. View at Publisher · View at Google Scholar
82. “The diabetes prevention program: design and methods for a clinical trial in the prevention of type 2 diabetes,” Diabetes Care, vol. 22, no. 4, pp. 623–634, 1999. View at Publisher · View at Google Scholar
83. D. Altshuler, J. N. Hirschhorn, M. Klannemark, et al., “The common PPAR$\gamma$Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes,” Nature Genetics, vol. 26, no. 1, pp. 76–80, 2000. View at Publisher · View at Google Scholar · View at PubMed
84. K. E. Lohmueller, C. L. Pearce, M. Pike, E. S. Lander, and J. N. Hirschhorn, “Meta-analysis of genetic association studies supports a contribution of common variants to susceptibility to common disease,” Nature Genetics, vol. 33, no. 2, pp. 177–182, 2003. View at Publisher · View at Google Scholar · View at PubMed
85. J. C. Florez, K. A. Jablonski, M. W. Sun, et al., “Effects of the type 2 diabetes-associated PPARG P12A polymorphism on progression to diabetes and response to troglitazone,” Journal of Clinical Endocrinology & Metabolism, vol. 92, no. 4, pp. 1502–1509, 2007. View at Publisher · View at Google Scholar · View at PubMed
86. T. Pischon, J. K. Pai, J. E. Manson, et al., “Peroxisome proliferator-activated receptor-$\gamma$2 P12A polymorphism and risk of coronary heart disease in US men and women,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 25, no. 8, pp. 1654–1658, 2005. View at Publisher · View at Google Scholar · View at PubMed
87. A. S. F. Doney, B. Fischer, G. Leese, A. D. Morris, and C. N. A. Palmer, “Cardiovascular risk in type 2 diabetes is associated with variation at the PPARG locus: a go-DARTS study,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 24, no. 12, pp. 2403–2407, 2004. View at Publisher · View at Google Scholar · View at PubMed
88. P. M. Ridker, N. R. Cook, S. Cheng, et al., “Alanine for proline substitution in the peroxisome proliferator-activated receptor $\gamma$-2 $(pparg2)$ gene and the risk of incident myocardial infarction,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 23, no. 5, pp. 859–863, 2003. View at Publisher · View at Google Scholar · View at PubMed
89. “Final report on the aspirin component of the ongoing physicians' health study,” New England Journal of Medicine, vol. 321, no. 3, pp. 129–135, 1989.
90. E. J. Rhee, C. H. Kwon, W. Y. Lee, et al., “No association of Pro12Ala polymorphism of PPAR-$\gamma$ gene with coronary artery disease in Korean subjects,” Circulation Journal, vol. 71, no. 3, pp. 338–342, 2007. View at Publisher · View at Google Scholar
91. E. Iwata, I. Yamamoto, T. Motomura, et al., “The association of Pro12Ala polymorphism in $PPAR\gamma 2$ with lower carotid artery IMT in Japanese,” Diabetes Research and Clinical Practice, vol. 62, no. 1, pp. 55–59, 2003. View at Publisher · View at Google Scholar
92. K. Z. Al-Shali, A. A. House, A. J. G. Hanley, et al., “Genetic variation in PPARG encoding peroxisome proliferator-activated receptor $\gamma$ associated with carotid atherosclerosis,” Stroke, vol. 35, no. 9, pp. 2036–2040, 2004. View at Publisher · View at Google Scholar · View at PubMed
93. E. S. Kang, S. Y. Park, H. J. Kim, et al., “Effects of Pro12Ala polymorphism of peroxisome proliferator-activated receptor $\gamma$2 gene on rosiglitazone response in type 2 diabetes,” Clinical Pharmacology and Therapeutics, vol. 78, no. 2, pp. 202–208, 2005. View at Publisher · View at Google Scholar · View at PubMed
94. A. Meirhaeghe, L. Fajas, N. Helbecque, et al., “A genetic polymorphism of the peroxisome proliferator-activated receptor $\gamma$ gene influences plasma leptin levels in obese humans,” Human Molecular Genetics, vol. 7, no. 3, pp. 435–440, 1998. View at Publisher · View at Google Scholar
95. X. L. Wang, J. Oosterhof, and N. Duarte, “Peroxisome proliferator-activated receptor $\gamma$ C161$\to$T polymorphism and coronary artery disease,” Cardiovascular Research, vol. 44, no. 3, pp. 588–594, 1999. View at Publisher · View at Google Scholar
96. T.-H. Chao, Y.-H. Li, J.-H. Chen, et al., “The 161TT genotype in the exon 6 of the peroxisome-proliferator-activated receptor $\gamma$ gene is associated with premature acute myocardial infarction and increased lipid peroxidation in habitual heavy smokers,” Clinical Science, vol. 107, no. 5, pp. 461–466, 2004. View at Publisher · View at Google Scholar · View at PubMed
97. J. A. Herd, M. S. West, C. Ballantyne, J. Farmer, and A. M. Gotto, Jr., “Baseline characteristics of subjects in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) with fluvastatin,” American Journal of Cardiology, vol. 73, no. 14, pp. D42–D49, 1994. View at Publisher · View at Google Scholar
98. M. S. West, J. A. Herd, C. M. Ballantyne, et al., “The Lipoprotein and Coronary Atherosclerosis Study (LCAS): design, methods, and baseline data of a trial of fluvastatin in patients without severe hypercholesterolemia,” Controlled Clinical Trials, vol. 17, no. 6, pp. 550–583, 1996. View at Publisher · View at Google Scholar
99. J. A. Herd, C. M. Ballantyne, J. A. Farmer, et al., “Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study [LCAS]),” American Journal of Cardiology, vol. 80, no. 3, pp. 278–286, 1997. View at Publisher · View at Google Scholar
100. S. Chen, N. Tsybouleva, C. M. Ballantyne, A. M. Gotto, Jr., and A. J. Marian, “Effects of PPAR$\alpha$, $\gamma$ and $\delta$ haplotypes on plasma levels of lipids, severity and progression of coronary atherosclerosis and response to statin therapy in the lipoprotein coronary atherosclerosis study,” Pharmacogenetics, vol. 14, no. 1, pp. 61–71, 2004. View at Publisher · View at Google Scholar
101. S. P. Azen, R. K. Peters, K. Berkowitz, S. Kjos, A. Xiang, and T. A. Buchanan, “TRIPOD (TRoglitazone In the Prevention Of Diabetes): a randomized, placebo-controlled trial of troglitazone in women with prior gestational diabetes mellitus,” Controlled Clinical Trials, vol. 19, no. 2, pp. 217–231, 1998. View at Publisher · View at Google Scholar
102. T. A. Buchanan, A. H. Xiang, R. K. Peters, et al., “Preservation of pancreatic $\beta$-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk Hispanic women,” Diabetes, vol. 51, no. 9, pp. 2796–2803, 2002. View at Publisher · View at Google Scholar
103. S. Snitker, R. M. Watanabe, I. Ani, et al., “Changes in insulin sensitivity in response to troglitazone do not differ between subjects with and without the common, functional Pro12Ala peroxisome proliferator-activated receptor-$\gamma$2 gene variant: results from the troglitazone in prevention of diabetes (TRIPOD) study,” Diabetes Care, vol. 27, no. 6, pp. 1365–1368, 2004. View at Publisher · View at Google Scholar
104. J. K. Wolford, K. A. Yeatts, S. K. Dhanjal, et al., “Sequence variation in PPARG may underlie differential response to troglitazone,” Diabetes, vol. 54, no. 11, pp. 3319–3325, 2005. View at Publisher · View at Google Scholar
105. J. Skogsberg, K. Kannisto, L. Roshani, et al., “Characterization of the human peroxisome proliferator activated receptor $\delta$ gene and its expression,” International Journal of Molecular Medicine, vol. 6, no. 1, pp. 73–81, 2000.
106. J. Skogsberg, K. Kannisto, T. N. Cassel, A. Hamsten, P. Eriksson, and E. Ehrenborg, “Evidence that peroxisome proliferator-activated receptor $\delta$ influences cholesterol metabolism in men,” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 23, no. 4, pp. 637–643, 2003. View at Publisher · View at Google Scholar · View at PubMed
107. J. Skogsberg, A. D. McMahon, F. Karpe, A. Hamsten, C. J. Packard, and E. Ehrenborg, “Peroxisome proliferator activated receptor $\delta$ genotype in relation to cardiovascular risk factors and risk of coronary heart disease in hypercholesterolaemic men,” Journal of Internal Medicine, vol. 254, no. 6, pp. 597–604, 2003. View at Publisher · View at Google Scholar