References

1. A. Sanz, R. Pamplona, and G. Barja, “Is the mitochondrial free radical theory,” Antioxidants & Redox Signaling, vol. 8, no. 3-4, pp. 582–599, 2006.

   View at: Publisher Site | Google Scholar

2. J. A. Knight, “The biochemistry of aging,” Advances in Clinical Chemistry, vol. 35, pp. 1–62, 2001.

   View at: Publisher Site | Google Scholar

3. J. Youssef and M. Badr, “Biology of senescent liver peroxisomes: role in hepatocellular aging and disease,” Environmental Health Perspectives, vol. 107, no. 10, pp. 791–797, 1999.

   View at: Publisher Site | Google Scholar

4. P. A. Parsons, “From the stress theory of aging to energetic and evolutionary expectations for longevity,” Biogerontology, vol. 4, no. 2, pp. 63–73, 2003.

   View at: Publisher Site | Google Scholar

5. D. Harman, “Aging: a theory based on free radical and radiation chemistry,” Journal of Gerontology, vol. 11, no. 3, pp. 298–300, 1956.

   View at: Google Scholar

6. T. M. Hagen, “Oxidative stress, redox imbalance, and the aging process,” Antioxidants & Redox Signaling, vol. 5, no. 5, pp. 503–506, 2003.

   View at: Publisher Site | Google Scholar

7. K. C. Kregel and H. J. Zhang, “An integrated view of oxidative stress in aging: Basic mechanisms, functional effects, and pathological considerations,” American Journal of Physiology—Regulatory Integrative and Comparative Physiology, vol. 292, no. 1, pp. R18–R36, 2007.

   View at: Publisher Site | Google Scholar

8. A. Navarro and A. Boveris, “The mitochondrial energy transduction system and the aging process,” American Journal of Physiology—Cell Physiology, vol. 292, no. 2, pp. C670–C686, 2007.

   View at: Publisher Site | Google Scholar

9. A. Sanz, P. Caro, and J. Ibanñez, “Dietary restriction at old age lowers mitochondrial oxygen radical production and leak at complex I and oxidative DNA damage in rat brain,” Journal of Bioenergetics and Biomembranes, vol. 37, no. 2, pp. 83–90, 2005.

   View at: Publisher Site | Google Scholar

10. B. P. Yu, “Aging and oxidative stress: modulation by dietary restriction,” Free Radical Biology and Medicine, vol. 21, no. 5, pp. 651–668, 1996.

    View at: Publisher Site | Google Scholar

11. H. Y. Chung, H. J. Kim, and J. W. Kim et al., “The inflammation hypothesis of aging: molecular modulation by calorie restriction,” Annals of The New York Academy of Sciences, vol. 928, pp. 327–335, 2001.

    View at: Google Scholar

12. M. Masternak, K. A. Al-Regaiey, and M. M. D. R. Lim et al., “Caloric restriction results in decreased expression of peroxisome proliferators-activated receptor/binding protein knockout mice,” The Journal of Gerontology. Series A, Biological Sciences and Medical Sciences, vol. 60, pp. 1238–1245, 2005.

    View at: Google Scholar

13. J. F. Oram, S. L. Bennetch, and J. R. Neely, “Regulation of fatty acid utilization in isolated perfused rat hearts,” Journal of Biological Chemistry, vol. 248, no. 15, pp. 5299–5309, 1973.

    View at: Google Scholar

14. J. D. McGarry and N. F. Brown, “The mitochondrial carnitine palmitoyltransferase system. From concept to molecular analysis,” European Journal of Biochemistry, vol. 244, no. 1, pp. 1–14, 1997.

    View at: Publisher Site | Google Scholar

15. D. E. Kelley, B. Goodpaster, R. R. Wing, and J. A. Simoneau, “Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss,” American Journal of Physiology—Endocrinology and Metabolism, vol. 277, no. 6 40-6, pp. E1130–E1141, 1999.

    View at: Google Scholar

16. C. M. R. LeMoine, G. B. McClelland, and C. N. Lyons et al., “Control of mitochondrial gene expression in the aging rat myocardium,” Biochemistry and Cell Biology, vol. 84, no. 2, pp. 191–198, 2006.

    View at: Publisher Site | Google Scholar

17. J. C. Chen, J. B. Warshaw, and D. R. Sanadi, “Regulation of mitochondrial respiration in senescence,” Journal of Cellular Physiology, vol. 80, no. 1, pp. 141–148, 1972.

    View at: Publisher Site | Google Scholar

18. R. G. Hansford, “Lipid oxidation by heart mitochondria from young adult and senescent rats,” Biochemical Journal, vol. 170, no. 2, pp. 285–295, 1978.

    View at: Google Scholar

19. T. Gulick, S. Cresci, T. Caira, D. D. Moore, and D. P. Kelly, “The peroxisome proliferator-activated receptor regulates mitochondrial fatty acid oxidative enzyme gene expression,” Proceedings of the National Academy of Sciences of the United States of America, vol. 91, no. 23, pp. 11012–11016, 1994.

    View at: Publisher Site | Google Scholar

20. S. Y. Park, Y. W. Kim, J. E. Kim, and J. Y. Kim, “Age-associated changes in fat metabolism in the rat and its relation to sympathetic activity,” Life Sciences, vol. 79, no. 23, pp. 2228–2233, 2006.

    View at: Publisher Site | Google Scholar

21. K. F. Petersen, D. Befroy, and S. Dufour et al., “Mitochondrial dysfunction in the elderly: possible role in insulin resistance,” Science, vol. 300, no. 5622, pp. 1140–1142, 2003.

    View at: Publisher Site | Google Scholar

22. K. F. Petersen, S. Dufour, D. Befroy, R. Garcia, and G. I. Shulman, “Impaired mitochondrial substrate oxidation in muscle of insulin-resistant offspring of type 2 diabetic patients,” The New England Journal of Medicine, vol. 350, pp. 664–671, 2004.

    View at: Google Scholar

23. K. Kannisto, A. Chibalin, and B. Glinghammar et al., “Differential expression of peroxisomal proliferator activated receptors alpha and delta in skeletal muscle in response to changes in diet and exercise,” International Journal of Molecular Medicine, vol. 17, no. 1, pp. 45–52, 2006.

    View at: Google Scholar

24. Y. Guan, Y. Zhang, and M. D. Breyer, “The role of PPARs in the transcriptional control of cellular processes,” Drug News and Perspectives, vol. 15, no. 3, pp. 147–154, 2002.

    View at: Publisher Site | Google Scholar

25. J. C. Corton, S. P. Anderson, and A. Stauber, “Central role of peroxisome proliferator-activated receptors in the actions of peroxisome proliferators,” Annual Review of Pharmacology and Toxicology, vol. 40, pp. 491–518, 2000.

    View at: Publisher Site | Google Scholar

26. V. D. Yumuk, “Targeting components of the stress system as potential therapies for the metabolic syndrome: the peroxisomal-proliferator-activated receptors,” Annals of the New York Academy of Sciences, vol. 1083, pp. 306–318, 2006.

    View at: Publisher Site | Google Scholar

27. R. Stienstra, C. Duval, M. Müller, and S. Kersten, “PPARs, obesity, and inflammation,” PPAR Research, vol. 2007, Article ID 95974, 10 pages, 2007.

    View at: Publisher Site | Google Scholar

28. B. Sung, S. Park, B. P. Yu, and H. Y. Chung, “Modulation of PPAR in aging, inflammation, and calorie restriction,” Journals of Gerontology—Series A, Biological Sciences and Medical Sciences, vol. 59, no. 10, pp. 997–1006, 2004.

    View at: Google Scholar

29. S. A. Kliewer, B. M. Forman, and B. Blumberg et al., “Differential expression and activation of a family of murine peroxisome proliferator-activated receptors,” Proceedings of the National Academy of Sciences of the United States of America, vol. 91, no. 15, pp. 7355–7359, 1994.

    View at: Publisher Site | Google Scholar

30. P. Howroyd, C. Swanson, C. Dunn, R. C. Cattley, and J. C. Corton, “Decreased longevity and enhancement of age-dependent lesions in mice lacking the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARalpha),” Toxicologic Pathology, vol. 32, no. 5, pp. 591–599, 2004.

    View at: Publisher Site | Google Scholar

31. J. A. Youssef and M. Z. Badr, “Aging and enhanced heatocarcinogenicity by peroxisome proliferators-activated receptor alpha agonists,” Ageing Research Reviews, vol. 4, no. 1, pp. 103–118, 2005.

    View at: Publisher Site | Google Scholar

32. K. T. Coschigano, A. N. Holland, M. E. Riders, E. O. List, A. Flyvbjerg, and J. J. Kopchick, “Deletion, but not antagonism, of the mouse growth hormone receptor results in severely decreased body weights, insulin, and insulin-like growth factor I levels and increased life span,” Endocrinology, vol. 144, no. 9, pp. 3799–3810, 2003.

    View at: Publisher Site | Google Scholar

33. M. S. Bonkowski, J. S. Rocha, M. M. Masternak, K. A. Al Regaiey, and A. Bartke, “Targeted disruption of growth hormone receptor interferes with the beneficial actions of calorie restriction,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 20, pp. 7901–7905, 2006.

    View at: Publisher Site | Google Scholar

34. A. Erol, “Insulin resistance is an evolutionarily conserved physiological mechanism at the cellular level for protection against increased oxidative stress,” BioEssays, vol. 29, no. 8, pp. 811–818, 2007.

    View at: Publisher Site | Google Scholar

35. M. M. Masternak and A. Bartke, “PPARs in calorie restricted and genetically long-lived mice,” PPAR Research, vol. 2007, Article ID 28436, 7 pages, 2007.

    View at: Publisher Site | Google Scholar

36. R. G. Cutler, “Oxidative stress profiling: part I. Its potential importance in the optimization of human health,” Annals of The New York Academy of Sciences, vol. 1055, pp. 93–135, 2005.

    View at: Publisher Site | Google Scholar

37. H. Y. Chung, B. Sung, K. J. Jung, Y. Zou, and B. P. Yu, “The molecular inflammatory process in aging,” Antioxidants & Redox Signaling, vol. 8, no. 3-4, pp. 572–581, 2006.

    View at: Publisher Site | Google Scholar

38. H. Y. Chung, H. J. Kim, J. W. Kim, and B. P. Yu, “The inflammation hypothesis of aging: Molecular modulation by calorie restriction,” Annals of the New York Academy of Sciences, vol. 928, pp. 327–335, 2001.

    View at: Google Scholar

39. Y. Lavrovsky, B. Chatterjee, R. A. Clark, and A. K. Roy, “Role of redox-regulated transcription factors in inflammation, aging and age-related diseases,” Experimental Gerontology, vol. 35, no. 5, pp. 521–532, 2000.

    View at: Publisher Site | Google Scholar

40. M. Ricote, A. C. Li, T. M. Wilson, J. Kelly, and C. K. Glass, “The peroxisome proliferator-activated receptor-gamma is a negative regulator of macrophage activation,” Nature, vol. 391, no. 6662, pp. 79–82, 1998.

    View at: Publisher Site | Google Scholar

41. C. Jiang, A. T. Ting, and B. Seed, “PPAR-gamma agonists inhibit production of monocyte inflammatory cytokines,” Nature, vol. 39, pp. 82–88, 1998.

    View at: Google Scholar

42. M. E. Poynter and R. A. Daynes, “Peroxisome proliferators-activated receptor alpha activation modulates cellular redox status, represses nuclear factor-kappa B signaling, and reduces inflammatory cytokine production in aging,” The Journal of Biological Chemistry, vol. 273, no. 49, pp. 32883–32841, 1998.

    View at: Publisher Site | Google Scholar

43. A. Erol, “Interleukin-6 (IL-6) is still the leading biomarker of the metabolic and aging related disorders,” Medical Hypotheses, vol. 69, no. 3, p. 708, 2007.

    View at: Publisher Site | Google Scholar

44. R. E. Law, S. Goetze, and X. P. Xi et al., “Expression and function of PPAR$\gamma$ in rat and human vascular smooth muscle cells,” Circulation, vol. 101, no. 11, pp. 1311–1318, 2000.

    View at: Google Scholar

45. P. Tontonoz, L. Nagy, and J. G. Alvarez et al., “PPAR$\gamma$ promotes monocyte/macrophage differentiation and uptake of oxidized LDL,” Cell, vol. 93, pp. 241–252, 1998.

    View at: Publisher Site | Google Scholar

46. C. Jiang, A. T. Ting, and B. Seed, “ PPAR-$\gamma$ agonists inhibit production of monocyte inflammatory cytokines,” Nature, vol. 391, pp. 82–86, 1998.

    View at: Google Scholar

47. J. Minamikawa, “Potent inhibitory effect of triglitazone on carotid arterial wall thickness in type 2 diabetes,” The Journal of Clinical Endocrinology and Metabolism, vol. 83, no. 5, pp. 1818–1820, 1998.

    View at: Publisher Site | Google Scholar

48. H. Takano, H. Hasegawa, Y. Zou, and I. Komuro, “Pleiotropic actions of PPAR gamma activators thiazolidinediones in cardiovascular disease,” Current Pharmaceutical Design, vol. 10, pp. 2779–2786, 2004.

    View at: Google Scholar

49. S. E. Nissen and K. Wolski, “Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes,” The New England Journal of Medicine, vol. 356, no. 24, pp. 2457–2471, 2007.

    View at: Publisher Site | Google Scholar

50. C. A. Argmann, T. A. Cock, and T. A. Auwerx, “Peroxisome proliferators-activated receptor$\gamma$: the more the merrier? ,” European Journal of Clinical Investigation, vol. 35, no. 2, pp. 82–92, 2005.

    View at: Publisher Site | Google Scholar

51. M. J. Toth and A. Tehernof, “Lipid metabolism in elderly,” European Journal of Clinical Nutrition, vol. 54, pp. S121–S125, 2000.

    View at: Google Scholar

52. G. A. Francis, J.-S. Annicotte, and J. Auwerx, “PPAR-$\alpha$ effects on the heart and other vascular tissues,” American Journal of Physiology. Heart and Circulatory Physiology, vol. 285, pp. H1–H9, 2003.

    View at: Google Scholar

53. D. Auboeuf, J. Rieusset, and L. Fajas et al., “Tissue distribution and quantification of the expression of PPARs and LXR$\alpha$ in humans: no alterations in adipose tissue of obese and NIDDM patients,” Diabetes, vol. 46, pp. 1319–1327, 1997.

    View at: Publisher Site | Google Scholar

54. I. Isseman, R. A. Prince, J. D. Tugwood, and S. Green, “The peroxisome proliferators-activated receptor: retinoic X receptor heterodimer is activated by fatty acids and fibrate hypolipdaemic drugs,” Journal of Molecular Endocrinology, vol. 11, pp. 37–47, 1993.

    View at: Google Scholar

55. T. Lemberger, R. Saladin, and M. Vazquez et al., “Expression of the peroxisome proliferators-activated receptor alpha gene is stimulated by stress and follows a diurnal rhytm,” The Journal of Biological Chemistry, vol. 271, pp. 1764–1769, 1996.

    View at: Publisher Site | Google Scholar

56. T. Gulick, S. Cresci, T. Caira, D. D. Moore, and D. P. Kelly, “The peroxisome proliferator-activated receptor regulates mitochondrial fatty acid oxidative enzyme gene expression,” Proceedings of the National Academy of Sciences of the United States of America, vol. 91, pp. 11012–11016, 1994.

    View at: Publisher Site | Google Scholar

57. D. M. Muoi, P. S. Maclean, and D. B. Lang et al., “Fatty acid homeostasis and induction of lipid regulatory genes in skeletal muscles of peroxisome proliferator activated receptor (PPAR)$\alpha$ ?knock-out mice,” The Journal of Biological Chemistry, vol. 277, no. 29, pp. 26089–26097, 2002.

    View at: Publisher Site | Google Scholar

58. T. Tanaka, J. Yamamoto, and S. Iwasaki et al., “Activation of peroxisome proliferator-activated receptor $\delta$ ?induces fatty acid $\beta$-oxidationin 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 Site | Google Scholar

59. S. Luquet, J. Lopez-Soriano, and D. Holst et al., “Peroxisome proliferators-activated receptor $\delta$ ?controls muscle development and oxidative capacity,” FASEB Journal, vol. 17, pp. 2299–2230, 2003.

    View at: Google Scholar

60. C. Gaudel and P. A. Grimaldi, “Metabolic functions of peroxisome proliferator-activated receptor $\beta$ / $\delta$ in skeletal muscle,” PPAR Research, vol. 2007, Article ID 86394, 6 pages, 2007.

    View at: Publisher Site | Google Scholar

61. A. J. Gilde and M. Van Bilsen, “Peroxisome proliferator-activated receptors (PPARS): regulators of gene expression in heart and skeletal muscle,” Acta Physiologica Scandinavica, vol. 178, no. 4, pp. 425–434, 2003.

    View at: Publisher Site | Google Scholar

62. O. Braissant, F. Foufelle, C. Scotto, M. Dauça, and W. Wahli, “Differential expression of peroxisome proliferator activated receptors (PPARs): tissue distribution of PPAR-$\alpha$, -$\delta$, and -$\gamma$ in adult rat,” Endocrinology, vol. 137, pp. 354–366, 1996.

    View at: Publisher Site | Google Scholar

63. L. Teboul, D. Gaillard, and L. Staccini et al., “Thiazelidinediones and fatty acids convert myogenic cells into adipose-like cells,” The Journal of Biological Chemistry, vol. 270, no. 47, pp. 28183–28187, 1995.

    View at: Publisher Site | Google Scholar

64. K. R. Short, M. L. Bigelow, and J. Kahl et al., “Decline in skeletal muscle mitochondrial function with aging in humans,” Proceedings of the National Academy of Sciences of the United States of America, vol. 102, pp. 5618–5623, 2005.

    View at: Publisher Site | Google Scholar

65. A. Erol, “Energy dense high-carbohydrate and low-fat diets are the reason for the epidemic of metabolic syndrome-Novel approach to etiopathogenesis of metabolic syndrome,” Turkish Journal of Endocrinology and Metabolism, vol. 1, pp. 1–16, 2001.

    View at: Google Scholar

66. C. R. Carvalho, S. L. Brenelli, and A. C. Silva et al., “Effect of aging on insulin receptor, insulin receptor substrate-1, and phosphatidylinositol 3-kinase in liver and muscle of rats,” Endocrinology, vol. 137, pp. 151–159, 1996.

    View at: Publisher Site | Google Scholar

67. H. Yki-Jarvinen, “Thiazolidinediones,” The New England Journal of Medicine, vol. 351, pp. 1106–1118, 2004.

    View at: Google Scholar

68. J. J. Nolan, B. Ludvik, P. Beerden, M. Joyce, and J. Olefsky, “Improvement in glucose tolerance and insulin resistance in obese subjects treated with troglitazone,” The New England Journal of Medicine, vol. 331, no. 18, pp. 1188–1193, 1994.

    View at: Publisher Site | Google Scholar

69. E. Sanguino, N. Roglans, and M. Alegret et al., “Different response of senescent female Sprague-Dawley rats to gemfibrozil and rosiglitazone administration,” Experimental Gerontology, vol. 40, no. 7, pp. 588–598, 2005.

    View at: Publisher Site | Google Scholar

70. The DREAM Trial Investigators, “Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomized controlled trial,” Lancet, vol. 368, no. 9541, pp. 1096–1105, 2006.

    View at: Publisher Site | Google Scholar

71. J. L. Kirkland, C. H. Hollenberg, and W. S. Gillon, “Age, anatomic site, and the replication and differantiation of adipocyte precursors,” American Journal of Physiology—Cell Physiology, vol. 258, pp. C206–C210, 1990.

    View at: Google Scholar

72. W. Guo, T. Pirtskhalava, and T. Tchkonia et al., “Aging results in paradoxical susceptibility of fat cell progenitors to lipotoxicity,” American Journal of Physiology. Endocrinology and Metabolism, vol. 292, pp. 1041–1051, 2006.

    View at: Publisher Site | Google Scholar

73. P. D. K. Miles, Y. Barak, and W. He et al., “Improved insulin-sensitivity in mice heterozygous for PPAR-$\gamma$ deficiency,” European Journal of Clinical Investigation, vol. 105, pp. 287–292, 2000.

    View at: Google Scholar

74. P. D. G. Miles, Y. Barak, R. M. Evans, and J. M. Olefsky, “Effect of heterozygous PPAR$\gamma$ deficiency and TZD treatment on insulin resistance associated with age and high-fat feeding,” American Journal of Physiology. Endocrinology and Metabolism, vol. 284, pp. E618–E626, 2003.

    View at: Google Scholar

75. T.-A. Cock, S. M. Houten, and J. Auwerx, “Peroxisome proliferator-activated receptor-$\gamma$ too much of a good thing causes harm,” EMBO Reports, vol. 5, no. 2, pp. 142–147, 2004.

    View at: Publisher Site | Google Scholar

76. R. Mukherjee, P. A. Hoener, and L. Jow et al., “A selective peroxisome proliferator-activated receptor-gamma (PPARgamma) modulator blocks adipocyte differentiation but stimulates glucose uptake in 3T3-L1 adipocytes,” Journal of Molecular Endocrinology, vol. 14, no. 9, pp. 1425–1433, 2000.

    View at: Publisher Site | Google Scholar

77. A. V. Schwartz, “Diabetes, TZDs, and bone: a review of the clinical evidence,” PPAR Research, vol. 2006, Article ID 24502, 6 pages, 2006.

    View at: Publisher Site | Google Scholar

78. S. O. Rzonca, L. J. Suva, D. Gaddy, D. C. Montague, and B. Lecka-Czernik, “Bone is a target for antidiabetic compound rosiglitazone,” Endocrinology, vol. 145, no. 1, pp. 401–406, 2004.

    View at: Publisher Site | Google Scholar

79. O. P. Lazarenko, S. O. Rzonca, W. R. Hogue, and F. L. Swain et al., “Rosiglitazone induces decreases in bone mass and strength that are reminiscent of aged bone,” Endocrinology, vol. 148, no. 6, pp. 2669–2680, 2007.

    View at: Publisher Site | Google Scholar

80. G. L. Rubin, Y. Zhao, A. M. Kalus, and E. R. Simpson, “Peroxisome proliferators-activated receptor gamma ligands inhibit estrogen biosynthesis in human breast adipose tissue: possible implications for breast cancer therapy,” Cancer Research, vol. 60, pp. 1604–1608, 2000.

    View at: Google Scholar

81. S. E. Kahn, S. M. Haffner, and M. A. Heise et al., “Glycemic durability of rosiglitazone, metfornin, or glyburide monotherapy,” The New England Journal of Medicine, vol. 355, no. 23, pp. 2427–2443, 2006.

    View at: Publisher Site | Google Scholar

82. R. V. James, “Diabetes and other coronary heart disease risk equivalents,” Current Opinion in Lipidology, vol. 12, pp. 425–431, 2001.

    View at: Google Scholar

83. E. Sanguino, M. Ramón, and L. Michalik et al., “Lack of hypotriglyceridemic effect of gemfibrozil as a consequence of age-related changes in rat liver PPAR$\alpha$,” Biochemical Pharmacology, vol. 67, no. 1, pp. 157–166, 2004.

    View at: Publisher Site | Google Scholar

84. A. Keech, R. J. Simes, and P. Barter et al., “Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomized controlled trial,” Lancet, vol. 366, no. 9500, pp. 1849–1861, 2005.

    View at: Publisher Site | Google Scholar

85. E. Sanguino, N. Roglans, M. Alegret, R. M. Sánchez, M. Vázquez-Carrera, and J. C. Laguna, “Atorvastatin reverses age-related reduction in rat hepatic PPAR$\alpha$ and HNF-4,” British Journal of Pharmacology, vol. 145, no. 7, pp. 853–861, 2005.

    View at: Publisher Site | Google Scholar

86. B. Sung, S. Park, B. P. Yu, and H. Y. Chung, “Amelioration of age-related inflammation and oxidative stress by PPAR$\gamma$ activator: suppression of NF-$\kappa$B by 2,4-thiazolidinedione,” Experimental Gerontology, vol. 41, no. 6, pp. 590–599, 2006.

    View at: Publisher Site | Google Scholar

87. J. C. Corton and H. M. Brown-Borg, “Peroxisome proliferator-activated receptor $\gamma$ coactivator 1 in caloric restriction and other models of longevity,” Journals of Gerontology—Series A, Biological Sciences and Medical Sciences, vol. 60, no. 12, pp. 1494–1509, 2005.

    View at: Google Scholar

88. A. J. Stauber, H. Brown-Borg, and J. Liu et al., “Constitutive expression of peroxisome proliferator-activated receptor $\alpha$-regulated genes in dwarf mice,” Molecular Pharmacology, vol. 67, no. 3, pp. 681–694, 2005.

    View at: Publisher Site | Google Scholar

89. M. M. Masternak, K. Al-Regaiey, and M. S. Bonkowski et al., “Divergent effects of caloric restriction on gene expression in normal and long-lived mice,” Journals of Gerontology—Series A, Biological Sciences and Medical Sciences, vol. 59, no. 8, pp. 784–788, 2004.

    View at: Google Scholar

90. M. E. Poynter and D. A. Daynes, “PPAR$\alpha$ activation modulates cellular redox status, represses NF$\kappa$B signalling and reduces inflammatory cytokine production in aging,” The Journal of Biological Chemistry, vol. 273, no. 49, pp. 32833–32841, 1998.

    View at: Publisher Site | Google Scholar

91. E. J. Masoro, “Overview of caloric restriction and ageing,” Mechanisms of Ageing and Development, vol. 126, no. 9, pp. 913–922, 2005.

    View at: Publisher Site | Google Scholar

92. A. Erol, “PPAR$\alpha$ activators may be good candidates as antiaging agents,” Medical Hypotheses, vol. 65, no. 1, pp. 35–38, 2005.

    View at: Publisher Site | Google Scholar

93. L. Guarente and F. Picard, “Calorie restriction-the SIR2 connection,” Cell, vol. 120, no. 4, pp. 473–482, 2005.

    View at: Publisher Site | Google Scholar

94. T. Yang, M. Fu, R. Pestell, and A. A. Sauve, “SIRT1 and endocrine signaling,” Trends in Endocrinology & Metabolism, vol. 17, no. 5, pp. 186–191, 2006.

    View at: Publisher Site | Google Scholar

95. F. Picard, M. Kurtev, and N. Chung et al., “SIRT1 promotes fat mobilization in white adipocytes by repressing PPAR$\gamma$,” Nature, vol. 429, pp. 771–776, 2004.

    View at: Publisher Site | Google Scholar

96. N. Klöting and M. Blüher, “Extended longevity and insulin signaling in adipose tissue,” Experimental Gerontology, vol. 40, no. 11, pp. 878–883, 2005.

    View at: Publisher Site | Google Scholar

97. J. M. Gimble, C. E. Robinson, and X. Wu et al., “Peroxisome proliferator-activated aeceptor-$\gamma$ activation by thiazolidinediones induces adipogenesis in bone marrow stromal cells,” Molecular Pharmacology, vol. 50, no. 5, pp. 1087–1094, 1996.

    View at: Google Scholar

98. A. Erol, “Adipobiology-based pharmacology,” Biomedical Review, vol. 17, pp. 73–87, 2006.

    View at: Google Scholar

99. G. N. Chaldakov, M. Fiore, and A. B. Tonchev et al., “Homo obesus: A metabotrophin-deficient species. Pharmacology and nutrition insight,” Current Pharmaceutical Design, vol. 13, no. 21, pp. 2176–2179, 2007.

    View at: Publisher Site | Google Scholar

100. M. Iemitsu, T. Miyauchi, and S. Maeda et al., “Aging-induced decrease in the PPAR-$\alpha$ level in hearts is improved by exercise training,” American Journal of Physiology—Heart and Circulatory Physiology, vol. 283, no. 5, pp. H1750–H1760, 2002.

     View at: Google Scholar